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After myocardial infarction, the heart undergoes adverse remodeling characterized by a series of pathological changes, including inflammation, apoptosis, fibrosis, and hypertrophy. In addition to cardiac catheter-based re-establishment of blood flow, patients typically receive multiple medications that aim to address these different mechanisms underlying left ventricular remodeling. The current study aims to establish a versatile multi-drug delivery platform for the controlled and sequential delivery of multiple therapeutic agents in a single treatment. Toward this goal, we generated a microcapped microneedle patch carrying methylprednisolone, interleukin-10, and vascular endothelial growth factor. In vitro characterization demonstrated a time-sequenced release pattern of these drug: methylprednisolone for the first 3 days, interleukin-10 from day 1 to 15, and vascular endothelial growth factor from day 3 to 25. The therapeutic effects of the microneedle patch were evaluated in a rat model of acute myocardial infarction induced by permanent ligation of left anterior descending coronary artery. Heart function was measured using trans-thoracic echocardiography. Heart inflammation, apoptosis, hypertrophy and angiogenesis were evaluated using histology. Our data indicated that, at 28 days after patch transplantation, animals receiving the microneedle patch with sequential release of these three agents showed reduced inflammation, apoptosis and cardiac hypertrophy compared to the animals receiving control patch without sequential release of these agents, which is associated with the improved angiogenesis and heart function. In conclusion, the microneedle patch can be utilized to deliver multiple therapeutic agents in a controlled and sequential manner that aligns with the pathological phases following myocardial infarction. The post-myocardial infarction heart remodeling is characterized by a series of pathological events including acute inflammation, apoptosis, fibrosis, cardiac hypertrophy, and depressed heart function. In current clinical practice, multiple procedures and drugs given at different time points are necessary to combat these series of pathological events. In this study, we developed a novel microcapped microneedle patch for the controlled sequential delivery of triple cardioprotective drugs aiming to combat acute inflammation and cardiac hypertrophy, and promote angiogenesis. This study presents a comprehensive therapeutic approach, with the microneedle patch addressing multifaceted pathological processes during post-myocardial infarction left ventricular remodeling. This cardiac drug delivery system has the potential to improve patient treatment by delivering drugs in alignment with the series of time-dependent pathological phases following myocardial infarction, ultimately improving clinical outcomes. [Display omitted] [ABSTRACT FROM AUTHOR]

The complex arborization of the feto-placental vasculature is crucial for optimal fetal nutrition, waste exchange and ultimately, development. Ethical and experimental limitations constrain research into the human placenta, hence experimental animal models such as mice and rats, are crucial to understand placental function. It is unclear how well the mouse and rat feto-placental vascular structure emulates human. Moreover, the implications of differences in vascular structure, especially in arborization, for placental function remain unclear. We use micro-computed tomography imaging, high frequency Doppler ultrasound and computational fluid dynamics to characterize feto-placental vasculature structure and haemodynamics in mice, rats, and human. Our data suggest that despite structural differences between rat and mouse placenta, haemodynamics are similar and that both hold applicability to investigating feto-placental structure and function. We show that human cotyledons demonstrate vascularity-dependent haemodynamic behaviour (including flow deceleration and oxygen exchange) similar to rodents and can be analysed in the same spectrum as rodents. Finally, we show strong structure-function relationships when interspecies datasets are combined; notably, we demonstrate that surrogate measures such as vascularity, can be used to estimate placental oxygen exchange function. Pre-clinical placental research utilising rat and mouse placentae to understand the impact of feto-placental arborization on placental function and fetal development can inform the human context. • We compared feto-placental vascular structure of mouse, rat, and human. • Feto-placental vascular interspecies variation does not impact oxygen delivery. • For feto-placental vasculature, the mouse and rat are useful preclinical models. [ABSTRACT FROM AUTHOR]

Introduction: Astrocytes, specialized glial cells, are essential for maintaining the central nervous system homeostasis. Inflammatory conditions can disrupt neurotrophic factors and receptor expression in astrocytes, leading to potential central nervous system damage. Itaconate, recently identified for its anti-inflammatory properties, was investigated in this study for its effects on neurotrophic factors in LPS-stimulated primary rat astrocytes. Methods: Primary rat astrocyte cells were isolated from one-day-old Wistar rats and exposed to 1 µg/ml lipopolysaccharide (LPS) for 6 h to stimulate inflammation. The effect of DMI (62.5, 125, and 250 µM for 18 h) on the cell viability of astrocyte cells exposed to LPS was evaluated by the MTT assay. The effects of DMI on the mRNA and protein levels of NGF, BDNF, and GDNF were evaluated using ELISA and qRT-PCR assays. Protein and mRNA levels of neurotrophic factor receptors (TrkA, TrkB, and P75) were evaluated using qRT-PCR and Western blot analyses. Results: The results showed that DMI suppressed astrocytes cell death induced by LPS in a dose-dependent manner. DMI dose-dependently restored the reduced mRNA and protein levels of NGF, BDNF, GDNF, and TrkA and TrkB receptors in LPS-treated astrocytes, but it significantly decreased the p75 expression in the same condition. Conclusion: In conclusion, DMI may be able to support astrocyte survival and functions based on the restoration of neurotrophic factors and their receptors expression in LPS-stimulated astrocyte cells. This suggests that DMI could be a promising therapeutic option for neurodegenerative diseases characterized by inflammation-induced astrocyte dysfunction. [ABSTRACT FROM AUTHOR]

Coral atoll islands are important breeding sites for tropical seabird species, but on many of these islands, disturbances from humans and introduced mammals have extirpated breeding colonies. In the Republic of the Maldives (Indian Ocean), little published information exists on the location and extent of seabird breeding colonies. Here, we document what appears to be a regionally significant breeding site for White-tailed Tropicbirds Phaethon lepturus on Kurehdhoo, the northern-most inhabited island of Lhaviyani Atoll in the central Maldives. We systematically surveyed the entire island on two separate occasions, six months apart, to count the number of White-tailed Tropicbird nests, their breeding stage, and habitat. We counted 128 and 202 nests at all breeding stages, indicating year-round breeding and an estimated population size of about 800 adults. This population is most likely the outcome of 14 y of sustained rat control across the entire island in the presence of native atoll vegetation. The effort has allowed White-tailed Tropicbirds to rapidly increase in numbers and a small population of Tropical Shearwaters Puffinus bailloni to establish on the island. These discoveries demonstrate that land-based seabird conservation opportunities exist in association with island resort land use in the Republic of the Maldives. [ABSTRACT FROM AUTHOR]

To categorize the temporal progression of subchondral bone alterations induced by compromising meniscus integrity in mouse and rat models of knee osteoarthritis (OA). Scoping review of investigations reporting subchondral bone changes with appropriate negative controls in the different mouse and rat models of OA induced by compromising meniscus integrity. The available literature provides appropriate temporal detail on subchondral changes in these models, covering the entire spectrum of OA with an emphasis on early and mid-term time points. Microstructural changes of the subarticular spongiosa are comprehensively described; those of the subchondral bone plate are not. In mouse models, global subchondral bone alterations are unidirectional, involving an advancing sclerosis of the trabecular structure over time. In rats, biphasic subchondral bone alterations begin with an osteopenic degeneration and loss of subchondral trabeculae, progressing to a late sclerosis of the entire subchondral bone. Rat models, independently from the applied technique, relatively faithfully mirror the early bone loss detected in larger animals, and the late subchondral bone sclerosis observed in human advanced OA. Mice and rats allow us to study the microstructural consequences of compromising meniscus integrity at high temporal detail. Thickening of the subchondral bone plate, an early loss of thinner subarticular trabecular elements, followed by a subsequent sclerosis of the entire subchondral bone are all important and reliable hallmarks that occur in parallel with the advancing articular cartilage degeneration. Thoughtful decisions on the study design, laterality, selection of controls and volumes of interest are crucial to obtain meaningful data. [ABSTRACT FROM AUTHOR]

Copyright of China Journal of Oral & Maxillofacial Surgery is the property of Shanghai Jiao Tong University, College of Stomatology and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The study aims to elucidate the therapeutic mechanism of Baicalin (BAI) in alleviating cartilage injury in osteoarthritic (OA) rat models, concentrating on its regulation of the miR-766-3p/AIFM1 axis. An OA rat model was developed with unilateral anterior cruciate ligament transection (ACLT). Interventions comprised of BAI treatment and intra-articular administration of miR-766-3p inhibitor. For evaluation, histopathological staining was conducted to investigate the pathological severity of knee cartilage injury. The levels of oxidative stress (OS) indicators including MDA, SOD, and GSH-Px, were quantified using colorimetric assays. Inflammatory factors (IFs; TNF-α, IL-1β, and IL-6) in knee joint lavage fluids were assessed using ELISA, while RT-PCR was employed to quantify miR-766-3p expression. TUNEL apoptosis staining was utilized to detect chondrocyte apoptosis, and western blotting examined autophagy-related markers (LC3, Beclin, p62), extracellular matrix (ECM) synthesisassociated indices (COL2A, ACAN, MMP13), and apoptosisinducing factor mitochondrion-associated 1 (AIFM1). Histological examination revealed a marked amelioration of cartilage injury in the BAI-treated OA rat models compared to controls. BAI treatment significantly reduced inflammation and OS of knee joint fluid, activated autophagy, and decreased chondrocyte apoptosis and ECM degradation. Interestingly, the inhibitory effects of BAI on these pathological markers were significantly decreased by the miR-766-3p inhibitor. Further assessment revealed that BAI efficiently promoted miR-766-3p expression while inhibiting AIFM1 protein expression. BAI potentially mitigates articular cartilage injury in OA rats, likely through modulation of miR-766-3p/AIFM1 axis. [ABSTRACT FROM AUTHOR]

A new class of antidiabetic drugs - gliflozins (inhibitors of sodium glucose cotransporter-2; SGLT-2i) stimulate glucose and sodium excretion, thereby contributing to improved glycemic control, weight loss and blood pressure reduction in diabetic patients. Large clinical trials in patients with type 2 diabetes treated with empagliflozin, canagliflozin or dapagliflozin have demonstrated their excellent efficacy in improving many cardiovascular outcomes, including the reduction of death from cardiovascular diseases, non-fatal myocardial infarction or stroke, and hospitalization for heart failure. Moreover, the beneficial effects of SGLT-2i were also demonstrated in the decrease in proteinuria, which leads to a lower risk of progression to endstage renal disease and thus a delay in initiation of the renal replacement therapy. Unexpectedly, their cardioprotective and renoprotective effects have been demonstrated not only in patients with diabetes but also in those without diabetes. Recently, much effort has been focused on patients with heart failure (either with reduced or preserved ejection fraction) or liver disease. Experimental studies have highlighted pleiotropic effects of SGLT-2 inhibitors beyond their natriuretic and glycosuric effects, including reduction of fibrosis, inflammation, reactive oxygen species, and others. Our results in experimental nondiabetic models of hypertension, chronic kidney disease and heart failure are partially consistent with these findings. This raises the question of whether the same mechanisms are at work in diabetic and non-diabetic conditions, and which mechanisms are responsible for the beneficial effects of gliflozins under nondiabetic conditions. Are these effects cardio-renal, metabolic, or others? This review will focus on the effects of gliflozins under different pathophysiological conditions, namely in hypertension, chronic kidney disease, and heart failure, which have been evaluated in non-diabetic rat models of these diseases. [ABSTRACT FROM AUTHOR]

Few studies have investigated the hemodynamic mechanism whereby primary hyperaldosteronism causes hypertension. The traditional view holds that hyperaldosteronism initiates hypertension by amplifying salt-dependent increases in cardiac output (CO) by promoting increases in sodium retention and blood volume. Systemic vascular resistance (SVR) is said to increase only as a secondary consequence of the increased CO and blood pressure. Recently, we investigated the primary hemodynamic mechanism whereby hyperaldosteronism promotes salt sensitivity and initiation of salt-dependent hypertension. In unilaterally nephrectomized male Sprague-Dawley rats given infusions of aldosterone or vehicle, we found that aldosterone promoted salt sensitivity and initiation of salt-dependent hypertension by amplifying salt-induced increases in SVR while decreasing CO. In addition, we validated mathematical models of human integrative physiology, derived from Guyton’s classic 1972 model - Quantitative Cardiovascular Physiology-2005 and HumMod-3.0.4. Neither model accurately predicted the usual changes in sodium balance, CO, and SVR that normally occur in response to clinically realistic increases in salt intake. These results demonstrate significant limitations with the hypotheses inherent in the Guyton models. Together these findings challenge the traditional view of the hemodynamic mechanisms that cause salt-sensitive hypertension in primary aldosteronism. [ABSTRACT FROM AUTHOR]

Starting from simple clinical statistics, the spectrum of methods used in epilepsy research in the Institute of Physiology of the Czechoslovak (now Czech) Academy of Sciences progressively increased. Professor Servít used electrophysiological methods for study of brain activity in lower vertebrates, neuropathology was focused on electronmicroscopic study of cortical epileptic focus and ion-sensitive microelectrodes were used for studies of cortical direct current potentials. Developmental studies used electrophysiological methods (activity and projection of cortical epileptic foci, EEG under the influence of convulsant drugs, hippocampal, thalamic and cortical electrical stimulation for induction of epileptic afterdischarges and postictal period). Extensive pharmacological studies used seizures elicited by convulsant drugs (at first pentylenetetrazol but also other GABA antagonists as well as agonists of glutamate receptors). Motor performance and behavior were also studied during brain maturation. The last but not least molecular biology was included into the spectrum of methods. Many original data were published making a background of position of our laboratory in the first line of laboratories interested in brain development. [ABSTRACT FROM AUTHOR]

Studies have shown that dexmedetomidine (DEX, an a2-adrenoceptors agonist) provides a neuroprotective effect and influences blood glucose levels. Here, we evaluated the effect of prolonged treatment with low doses of DEX on the survival rate of dopaminergic (DAergic) neurons in the substantia nigra and also serum glucose levels in 6-hydroxydopamine (6-OHDA) – induced Parkinson's disease (PD) in the rat. The neurotoxin of 6-OHDA was injected into the medial forebrain bundle by stereotaxic surgery. DEX (25 and 50 µg/kg, i.p) and yohimbine, an a2-adrenoceptor antagonist (1 mg/kg, i.p) were administered before the surgery to the 13 weeks afterward. Apomorphine-induced rotational tests and blood sampling were carried out before the surgery and multiple weeks after that. Thirteen weeks after the surgery, the rats' brain was transcardially perfused to assess the survival rate of DAergic neurons using the tyrosine hydroxylase (TH) immunohistochemistry. DEX remarkably attenuated the severity of rotational behavior and reversed the progress of the PD. It also increased the number of TH-labeled neurons by up to 60%. The serum glucose levels in 6-OHDA-received rats did not change in the third and seventh weeks after the surgery but decreased significantly in the thirteenth week. Treatment with DEX prevented this decrement in glucose levels. On the other hand, Treatment with yohimbine did not affect PD symptoms and glucose levels. Our data indicate that DEX through neuroprotective activity attenuates the severity of 6-OHDA-induced PD in rats. DEX might also prevent hypoglycemia during the progress of the PD. [ABSTRACT FROM AUTHOR]

Copyright of Studia Slavica Academiae Scientiarum Hungaricae is the property of Akademiai Kiado and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Aseptic loosening around the prosthesis is a common cause of failure in total joint arthroplasty. Polyethylene wear particles trigger the release of inflammatory factors by macrophages. Key mediators involved in osteoclastogenesis include interleukin-6, tumor necrosis factor-α, receptor activator of nuclear factor kappa B (RANK), RANK ligand (RANKL), and bone protection hormone (Osteoprotegerin [OPG]). The purpose of our experiment was to see whether melittin can slow down the release of inflammatory mediators through the NF-kB pathway, regulate the RANKL/OPG ratio, reduce osteoclast formation, and delay the onset of arthritis in rats. A total of 20 male Sprague-Dawley rats (10 months, Specific Pathogen Free, 350 g ± 20 g) were randomly divided into 5 groups: sham group, model group, melittin concentration 1 group (0.2 mg/kg), concentration 2 group (0.4 mg/kg), and concentration 3 group (0.6 mg/kg). All rats were implanted with TA2 high-purity titanium rods. A drill was used to create a bone canal along the long axis of the femur in the intercondylar notch. The model group and experimental groups were exposed to polyethylene particles, while the sham group did not receive any particles. The melittin group exhibited significantly increased serum levels of serum P, calcium-phosphorus product, OPG, PINP, PINP/CTX-I, and OPG/RANKKL (P <.05). In the experimental group, micro computed tomography scanning results revealed a decrease in the amount of bone defect around the prosthesis. Immunofluorescence analysis demonstrated a decrease in the expression of IKKα and P65, while the expression of OPG showed an upward trend. Both Hematoxylin-Eosin and Tartrate-Resistant Acid Phosphatase staining revealed less osteoclast and inflammatory cell infiltration in bone resorption pits. Our study demonstrates that melittin has the ability to inhibit the NF-kB pathway in a rat model, and reduce the impact of RANKL/OPG, thereby delaying osteoclast activity and alleviating periprosthetic osteolysis. [ABSTRACT FROM AUTHOR]

Intact extraction of the mandibular first molar tooth is an interesting model for studies of alveolar bone healing. The aim of this study was to describe a new experimental technique for extraction of rat mandibular first molar teeth with crown and all 4 roots intact using controlled forces applied to the teeth. One hundred and twenty female Sprague-Dawley rats were used from a center for experimental animal research. Animals underwent general anesthesia and were then placed in a special dental unit (designed by Moghadam) for the extraction of rat teeth. After syndesmotomy, luxation of the tooth began with a tipping movement in the buccal direction with a very low range of motion for 1 s. A tipping movement in the lingual direction was then used to continue luxation. After a maximum of 10 repetitions, the tooth was left alone for 30 s. After 3-4 stages of this cycle, the tooth loosened. To complete the luxation, the same forces were applied in the buccal and lingual directions with larger amplitude for 3 s. After this step, the tooth was loose enough to be easily extracted. The alveolus was then sutured closed. The results showed no hemorrhage or fracture of crowns and mesial or distal roots, and only 8% of the buccal and lingual roots fractured. The technique designed and used in this study was shown to be an effective model for complete molar tooth extraction in the rat. This technique could also be used in the treatment of other rodents. [ABSTRACT FROM AUTHOR]

Immunohistochemical methods were employed to investigate the morphological heterogeneity and localization of fibroblasts associated with the function of major salivary glands in rats. Histochemical and electron microscopic observations were made in rat parotid, submandibular, and sublingual glands and pancreas. Fibroblasts were immunostained using their specific marker, 47 kDa heat shock protein (Hsp47). Hsp47-immunopositive fibroblasts within the intralobular connective tissue exhibited a notably smaller size compared with the interlobular connective tissue. They were loosely distributed throughout the connective tissue. However, fibroblasts with elongated long processes were explicitly identified at the intercalated ducts in parotid, sublingual, and submandibular glands. Fibroblastic bodies and processes were tightly approximated with the basement membrane of the duct. Electron microscopy confirmed these findings, revealing a thin layer consisting of collagen fibers was found between the fibroblasts and the basement membrane. Double staining of Hsp47 and α-smooth muscle actin (αSMA) in parotid glands indicating that Hsp47-positive fibroblasts enveloped both the duct and αSMA-positive myoepithelial cells. Additionally, They projected long and thin processes longitudinally at the straight portion or circularly at the bifurcated portion of the duct. The three-dimensional reconstruction showed a frame-like structure of fibroblasts surrounding the intercalated duct with longitudinal myoepithelial cells. However, such specific localization of fibroblasts was not detected in the exocrine pancreas lacking myoepithelium. Small fibroblasts with long processes connecting or overwrapping each other and thin collagen layers surround the intercalated ducts in rat major salivary glands, presumably contributing to protecting the ducts from salivary flow and myoepithelial contraction. [Display omitted] • The morphological heterogeneity and localization of fibroblasts in rat major salivary glands were investigated immunohistochemically. • Fibroblasts with long processes connecting/overwrapping each other and thin collagen layers surrounded the intercalated ducts. • We termed tentatively this structure 'the peri-intercalated duct sheath'. • 'The peri-intercalated duct sheath' presumably protect the ducts from the myoepithelial contraction and salivary flow. [ABSTRACT FROM AUTHOR]

Copyright of Revista Cientifica de la Facultade de Veterinaria is the property of Universidad del Zulia, Facultad de Ciencias Veterinarias and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The pain-reducing effects of the exercise were exerted through different mechanisms. Knowing more clear mechanisms helps to find more approach that is therapeutic. The objective of the present study is the evaluation of cerebrospinal fluid (CSF) glutamate level alteration in neuropathic pain rats and whether physical activity could modulate it. In the present study 104 male Wistar rats weighing 180–220 g were randomly divided into 4 groups (Sham, Sham + Exe, Neuropathy, and Neuropathy + Exe) which in turn each group subdivided into 4 groups according to time points for behavioral testing and CSF sampling (Baseline, 2 weeks, 3 weeks, and 4 weeks). To induction of neuropathy (by chronic constriction injury,), after anesthetizing with a mixture of ketamine (80 mg/kg) and xylazine (10 mg/kg), the animal's right sciatic nerve was exposed and was ligated using four movable catgut chromic suture 4/0. The exercise protocol included 25 min of daily swimming, 5 days a week for 4 weeks. Thermal hyperalgesia and mechanical tactile threshold were detected using the plantar test and Von Frey filaments, respectively. CSF glutamate level was determined using high-performance liquid chromatography. Findings indicated that mechanical and thermal thresholds significantly (p < 0.01, p < 0.05 respectively) decreased in the neuropathy group against that in sham groups. On the other hand, exercise significantly increased mechanical tactile threshold (p < 0.0012) and thermal threshold (p < 0.05) compared to the neuropathy group. Moreover, CSF glutamate level prominently (p < 0.01) was increased in the neuropathy group compared to the sham group, and swimming exercise significantly (p < 0.001) reduced it. The present findings provide new evidence showing that medium-intensity swimming exercise attenuates pain-like behaviors in neuropathic pain animals, which is possibly due to decreasing CSF glutamate level and its neurotransmission. [ABSTRACT FROM AUTHOR]

Background: The nose can be damaged by environmental pollutants and foreign bodies, as well as a result of trauma, infection or surgical interventions. Proper healing of the damaged nasal mucosa is important for health. Objective: There is no study in the literature investigating the effects of rosmarinic acid on mucosal healing. The aim of this study was to investigate the effect of rosmarinic acid on nasal mucosal healing. Methods: 21 male, adult Spraque Dawley albino rats were divided into three groups as the control group, the local treatment group in which rosmarinic acid was applied locally to the nasal mucosa, and the systemic treatment group in which rosmarinic acid was injected intraperitoneally. The wound area was obtained by creating a trauma area by inserting a 10 mm interdental brush through the right nasal nostril into the right nasal cavities of all animals. For the following 15 days, the treatment agent was applied as indicated once a day and on the 15th day the animals were decapitated and tissue samples taken from the nasal mucosa were prepared for histopathological examination. The preparations were examined in terms of cellular hyperplasia, goblet cell hypertrophy and degeneration, leukocyte infiltration, cilia loss and degeneration, edema and vascular dilatation, and they have been classified into four categories as mild (+), moderate (++), severe (+++) and very severe (++++). Results: There was a significant difference between the groups in terms of all parameters evaluated, and there is a decrease in the intensity of the parameters with transition from the control group to the local group and from there to the systemic group. Conclusion: Systemic rosmarinic acid administration showed an enhancing effect on the healing of experimentally induced nasal mucosal injury due to its possible anti-inflammatory effect. [ABSTRACT FROM AUTHOR]

Background: Warm acupuncture (WA) has analgesic and anti-inflammatory effects. However, the underlying mechanism of these effects remain unclear. Objectives: To explore the analgesic and anti-inflammatory effects of WA and the potential underlying mechanism in male Sprague-Dawley rats with non-compressive lumbar disk herniation (LDH) caused by autologous nucleus pulposus (NP) transplantation. Methods: We used low-frequency (2 Hz) electrical stimulation and WA (40°C) to treat GB30 and BL54 acupoints in rats for 30 mins per day. We monitored the paw withdrawal threshold of rats during the experiment and measured serum cytokine levels using commercial kits. Dorsal root ganglion (DRG) tissue pathology was analyzed via H&E staining. We used qRT-PCR to measure the mRNA expression levels of IL-1β, IL-6, and TNF-α genes in DRG. Western blot was used to analyze the expression levels of IL-1β, IL-6, TNFα, P-p38MAPK, p38MAPK, P-κBα, IκBα, and NF-κB p65 proteins. Results: WA treatment significantly increased the pain threshold of rats, reduced serum IL-6, PEG2, NO, SP, NP-Y, and MMP-3 levels, and effected histopathological improvements in the DRG in rats. Moreover, WA treatment significantly downregulated the expression levels of inflammation-associated genes (Il-1β, Il-6, and Tnf-α) and proteins (IL-1β, IL-6, TNF-α, P-p38MAPK, P-κBα, and NF-κB p65) in the DRG of non-compressive LDH rats. Conclusion: WA can alleviate pain and inhibit inflammatory response in rats with non-compressive LDH caused by autologous NP transplantation, and these effects are likely associated with the inhibition of the p38MAPK/NF-κB pathway. [ABSTRACT FROM AUTHOR]

Endotoxins, products of Gram-negative bacteria, are the primary cause of blood-brain barrier (BBB) damage. In the present study, we aimed to investigate the possible neuroprotection mechanisms of melatonin on BBB damage induced by endotoxemia. Adult, female Sprague-Dawley rats (n = 42) were separated into four random groups as a control group and three treatment groups. Lipopolysaccharide (7,5 mg/kg/day) was administrated for a single dose to generate a 24-hour sepsis model on rats. Melatonin (10 mg/kg/day) was treated a week before sepsis. Afterward, the dissected brain tissues were examined by histopathological, biochemical, and molecular analyses. LPS caused weight loss in the groups. As a result, degenerated neurons with cytoplasmic vacuoles and irregular pyknotic nuclei, pale stained necrotic neurons, and vascular congestion were observed in LPS-exposed rats. However, MEL decreased the number of degenerated neurons in treated groups. MEL treatment increased ZO1 and Occludin immunoreactivity while decreasing TLR4 in brain tissues. MEL effect on protein expression was recorded for ZO1 increase and TLR4 decrease in brain tissue compared to LPS groups. MEL also decreased MDA levels in brain tissue. MEL recovered the degenerative damage of sepsis by contributing to blood-brain barrier integrity, and by decreasing inflammation, thus the neuroprotective effects of MEL might provide an experimental basis for clinical applications. [ABSTRACT FROM AUTHOR]

Copyright of Brazilian Journal of Biology is the property of Instituto Internacional de Ecologia and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Revista Cientifica de la Facultade de Veterinaria is the property of Universidad del Zulia, Facultad de Ciencias Veterinarias and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Revista Cientifica de la Facultade de Veterinaria is the property of Universidad del Zulia, Facultad de Ciencias Veterinarias and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Oral mucosal lesions are a common pathology that impact the quality of life due to pain, inappetence, weight loss, and low productivity. The purpose of this study is to evaluate the effects of Tarantula cubensis extract on wound healing in rats with buccal mucosal lesions. A total of 40 male Wistar albino rats weighing 250–300 g were used in the study. The rats were divided into four equal groups. A 3 mm diameter mucosal defect was created in the buccal mucosa of each rat. Groups one and three (controls) assessed spontaneous healing at 3 and 6 days post trauma, respectively. Groups two and four (treatment) received 0.2 ml T. cubensis extract subcutaneously. Group two was treated for 2 days and assessed at 3 days and group four was treated for 5 days and assessed at 6 days. All rats were euthanatized prior to tissue sample collection. Tissue samples were compared between control and treatment groups using histopathology and immunohistochemistry. Tissue samples taken from the defect areas were immunohistochemically evaluated for cytokeratin and collagen expressions. In both the 3 and 6 day treatment groups, the improvements were statistically different compared to the control groups. T. cubensis extract was found to increase cytokeratin and collagen in both epithelial and connective tissue and to have a significant healing effect on mucosa on both gross and microscopic findings. [ABSTRACT FROM AUTHOR]

Tadalafil is used to treat erectile dysfunction and improve exercise capacity in people with pulmonary arterial hypertension. It promotes blood circulation to the penis during sexual stimulation, thus facilitating the occurrence of an erection. This study examined tadalafil effects on the liver, focusing on potential hepatotoxicity and liver function adverse effects. It aims to contribute to knowledge on tadalafil misuse and abuse, promoting informed decision-making and raising awareness. The study was conducted using fifteen (15) adult Wistar rats randomly assigned into three groups consisting of 5 rats each. Group A was the control group while group B (10 mg/kg of tadalafil) and C (20 mg/kg of tadalafil) were the low dose and high dose groups respectively. Oral administration of tadalafil in treated rats showed evidence of vascular congestion and dilation in the liver tissue, at 20 mg/kg there was periportal hepatitis. Assay of liver function parameters showed increase in liver enzymes across treatment groups compared to control. The presence of periportal hepatitis indicates potential inflammation in the region surrounding the portal area of the liver which suggests that tadalafil may have an impact on hepatocyte morphology and may also influence the inflammatory response in the periportal region of the liver. Hence, Tadalafil should be taken with caution. [ABSTRACT FROM AUTHOR]

Lipofuscin accumulation has been observed in human coronary arteries but whether or not myocardial tissue can release lipofuscin generated within cardiomyocytes must be clarified, as this may provide indicators for future anti-ageing research. The hearts of Sprague Dawley rats, aged 6–24 months, were embedded in resin and ultrathin sections cut for electron microscopy. Lipofuscin granules were abundant in cardiomyocytes. Cardiomyocytes were seen to release lipofuscin granules into the myocardial interstitium as cytoplasmic fragments with irregular protrusions on the sarcolemma surface. The cytoplasmic fragments entering the stroma fused directly with the endothelial cells of adjacent capillaries, delivering lipofuscin to the vessel wall. These fragments were also seen to be engulfed by stromal macrophages or fused with fibroblasts, which then combined with capillary endothelial cells to deliver lipofuscin to the vessel wall. Some cytoplasmic fragments disaggregated and formed membrane-like waste, which travelled to the vessel wall from the myocardial stroma as soluble fine particles via diffusion or pinocytosis of capillary endothelial cells. Lipofuscin entered the vascular wall and endothelial cells, forming large and small protrusions or folds that transported the lipofuscin to the vascular lumen and bloodstream. [ABSTRACT FROM AUTHOR]

The present study aimed to histologically clarify the regional specificity of the mucosal enteric glial cells (mEGCs) in the rat intestine with serial block-face scanning electron microscopy (SBF-SEM). SBF-SEM analysis with the ileum, the cecum and the descending colon revealed that mEGC nuclei were more abundant in the data stacks from the apical portion of the villus and the lateral portion of the crypt of the ileum. mEGCs exhibited a high rate of coverage over the nerve bundle around the lateral portion of the ileal crypt, but showed an extremely low level of coverage in the luminal portion of the cecum. These findings evidenced regional differences in the localization of mEGCs and in their sheath structure in the rat intestine. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Diabetes mellitus and glucose regulation are important in deciding on surgical intervention in pre-surgical assessments. In our study, we aimed to investigate the correlations between the induction time of anesthesia, glucose level, and weight in a diabetic rat model. MATERIALS AND METHODS: Weightmatched adult male Wistar rats were grouped as control (n=8) and diabetic (n=8). In the latter group, diabetes was induced with a single intraperitoneal injection of 50 mg/kg streptozotosin. 72 hours after the injection, animals possessing a blood glucose concentration above 300 mg/kg were considered diabetic. The weights and blood glucose levels were observed for 7 days. In the end, 80 mg/kg ketamine and 12 mg/kg xylazine were administered to both groups, and the induction time of anesthesia was recorded. The success of anesthesia was confirmed with toe pinching by using a clamp. The Student's tand Pearson's correlation tests were used for statistical analyses. RESULTS: The induction time of anesthesia was significantly reduced in the diabetic group compared to the controls (p<0.01). Diabetic animals weighed less than the control group (p<0.01). The correlation analysis in the diabetic group showed that the weight and blood glucose level of animals did not influence the induction time of anesthesia (respectively, p=0.80, r: 0.150; p=0.68, r: -0.300). A negative correlation between blood glucose concentration and weight was found in diabetics (p<0.05, r: -0.828). CONCLUSIONS: The dosage of anesthetic agents is important in the effectiveness of anesthesia, and surgical complications. Since our results indicate the susceptibility of diabetics to anesthesia, we suggest that the dose of anesthetics should be finely adjusted considering the presence of diabetes. [ABSTRACT FROM AUTHOR]

Epigallocatechin-3-gallate (EGCG) is playing an increasingly important role in the treatment of oral diseases. However, its mechanisms remain to be clarified. This study aimed to investigate the effect of EGCG on oxidative and inflammatory stress and bone loss in experimental periodontitis. Periodontitis was induced in rats, followed by gavage using different concentrations of EGCG for 5 weeks. The levels of interleukin-1β (IL-1β), interleukin-18 (IL-18), tumor necrosis factor-α (TNF-α), superoxide dismutase (SOD) and malondialdehyde (MDA) in rats were measured. The degree of alveolar bone loss and the number of inflammatory cells were detected. The integrated optical density of nuclear factor erythroid 2-related factor (Nrf2), heme oxygenase-1 (HO-1), NLR pyrin domain-containing 3 (NLRP3) and nuclear factor-kappaB p65 (NF-κB p65) was measured. EGCG (200 mg/kg) significantly reduced alveolar bone loss in the ligated maxillary molars and the number of inflammatory cells in the EGCG-200 group compared with the periodontitis, EGCG-100 and EGCG-400 groups. 200 mg/kg was the optimal dose of EGCG and was used in subsequent experiments. The expression levels of IL-1β, IL-18, TNF-α and MDA were significantly lower and the expression level of SOD was significantly higher in the EGCG-200 group compared with the periodontitis group. The expression of NLRP3 and NF-κB p65 was significantly decreased, while the expression of Nrf2 and HO-1 was significantly increased in the EGCG-200 group compared with the periodontitis group. These results suggest that EGCG inhibits oxidative stress and inflammatory responses in the periodontitis model by modulating the Nrf2/HO-1/NLRP3/NF-κB p65 signaling pathway, thereby decreasing alveolar bone loss. [ABSTRACT FROM AUTHOR]

Rats are a common model for diabetes mellitus in humans, but spontaneous diabetes in pet rats has not been described. A 1-year, 5-month-old, intact male domestic rat (Rattus norvegicus) was evaluated for polydipsia and weight loss. Diagnostics revealed glucosuria and hyperglycemia (414 mg/dL; normal 89–165 mg/dL) consistent with diabetes mellitus. Hypercholesteremia and elevated liver enzymes were also noted. Treatment with glipizide (0.5–1 mg/kg, orally, every 12 hours), metformin (50–150 mg/kg, orally, every 12 hours), and intermediate-acting porcine insulin (1–3 units, subcutaneously, every 12 hours) were ineffective at producing normoglycemia. Long-acting glargine insulin (1 unit, subcutaneously, every 12 hours) resulted in improved body weight and longer periods of normoglycemia for 3 months. Eleven months after diagnosis, the rat presented with rapid weight loss and tail necrosis; euthanasia was elected. On histopathology of the pancreas, the few visible islets and lack of amyloid production was considered more consistent with insulin-dependent (type I) diabetes mellitus than insulin-independent (type II). Other necropsy findings included bronchopneumonia, radiculoneuropathy, skeletal muscle necrosis of the tail, and chronic renal disease. Although uncommon, diabetes mellitus should be considered in pet rats presenting with polydipsia, polyuria, and weight loss. Insulin therapy may be useful for treatment of diabetes mellitus in pet rats but requires careful monitoring and further evaluation. [ABSTRACT FROM AUTHOR]

The aim of this study was to investigate the potential of diffusion kurtosis imaging (DKI) to assess the early renal functional undulation of diabetic mellitus (DM). Fifty-seven Sprague-Dawley (SD) rats were randomly divided into two groups and eventually 48 rats were included in this study: the normal control (CON) group and diabetic mellitus (DM) group. Weeks 0, 4, 8, and 12 after the diabetes model was successfully established, all the rats were scanned on the 3.0T MRI. The DKI derived parameters of renal parenchyma, including fractional anisotropy (FA co , FA me), mean diffusivity (MD co , MD me), and mean kurtosis (MK co , MK me) were measured. Their alteration over time was analyzed and then correlated with urine volume (UV), blood urea nitrogen (BUN), and serum creatinine (Scr) using Pearson correlation analysis. Finally, hematoxylin and eosin (H&E) staining was performed on the kidneys of the two groups. There was a decreasing trend in FA, MK, and MD values over time in diabetic rats. Also, the gradually worsening histological damage of kidneys was noted over time in diabetic rats. The cortical FA and MK values and medullary FA, MK and MD values of diabetic rats were significantly lower than those of controls at most time points after DM induction. In addition, negative correlations were revealed between the BUN and FA co (r = -0.43, p = 0.03) or FA me value (r = -0.49, p = 0.01). The cortical MK value was moderately correlated with UV (r = -0.46, p = 0.03) and BUN (r = -0.55, p = 0.01). The preliminary findings suggest that DKI might be an effective and sensitive tool to assess the early changes of renal function impairment in diabetic rats. The FA values of the cortex and medulla and the MK value of the cortex are sensitive markers in detecting renal injury in diabetic rats. [ABSTRACT FROM AUTHOR]

It has been demonstrated that in vivo brain ischemia induces activation and proliferation of astrocytes and microglia. However, the mechanism underlying the ischemia-induced activation and proliferation of these cells remains to be unclear. Oxygen-glucose deprivation (OGD), an in vitro ischemia mimic, has been extensively used to analyze the hypoxia response of various cell types. This study examined the OGD-induced changes in the expression level of astrocytes and microglia marker proteins and immunoreactivity for Ki-67, a marker protein for cell proliferation, using rat primary hippocampal neuron-glia co-culture (NGC) cells. Furthermore, OGD-induced changes in the expression of M1/M2 microglia phenotype-related genes were also examined. MTT assay indicated that 120 min of OGD decreased cell viability, and immunocytochemistry indicated that 120 min of OGD abolished most microtubule-associated protein 2 (MAP2)-immunopositive neurons. In contrast, glial fibrillary acidic protein (GFAP)-immunopositive astrocytes and ionized calcium-binding adapter protein-1 (Iba-l)-immunopositive microglia, and 2',3'-cyclic nucleotide-3'-phosphodiesterase (CNPase)-immunopositive oligodendrocytes survived OGD. Western blot assays and double-immunofluorescent staining indicated that OGD increased the GFAP expression level and the Ki-67-immunopositive/GFAP-immunopositive cells' ratio. Real-time PCR analysis showed that OGD altered M1 microglia phenotype-related genes. Specifically, OGD decreased the expression level of CD32 and interleukin-1ß (IL-1 ß) genes and increased that of the inducible nitric oxide synthase (iNOS) gene. Therefore, applying OGD to NGC cells could serve as a useful in vitro tool to elucidate the molecular mechanisms underlying brain ischemia-induced changes in GFAP expression, astrocyte proliferation, and M1 microglia phenotype-related gene expression. [ABSTRACT FROM AUTHOR]

Osteoarthritis (OA) is a chronic degenerative bone and joint disease that often occurs in aging animals. Currently, there are still no biomarkers that can effectively diagnose OA in the early stage. To identify possible biomarkers, here we examined changes in the expression of C‐telopeptide fragments of type II collagen (CTX‐II) and collagenase generated carboxy‐terminal neoepitope of type II collagen (C2C) in serum at different time points in an anterior cruciate ligament transection (ACLT)‐induced rat OA model. The serum levels of CTX‐II and C2C, and the OARSI score in the ACLT group were increased from week two until the end of the experiment. The AUC of the combined biomarkers was higher than that of CTX‐II or C2C alone. Moreover, serum levels of CTX‐II and C2C were positively correlated with the OARSI score. The results suggest that the combined detection of serum CTX‐II and C2C concentrations may have potential for assessing and diagnosing OA at early stages. [ABSTRACT FROM AUTHOR]

Objective: To comparatively investigate the ameliorative effect of Phellinus igniarius (P. igniarius) on renal aging in a rat model of focal and segmental glomerulosclerosis (FSGS). Methods: The FSGS model was established in rats by uninephrectomy combined with tail vein injection of doxorubicin. The FSGS rats were randomly divided into the model group, the P. igniarius decoction group, the P. igniarius polysaccharides group, and the P. igniarius polyphenols group. Molecular indicators of cell senescence, renal function indexes, and podocyte injury markers were tested after ten weeks of intragastric administration. Besides, the pathological renal lesions and the ultrastructural changes were observed. Results: FSGS developed in the model group within ten weeks and showed segmental glomerular scarring and renal aging. Following the 10-week intervention, 24 h proteinuria, serum creatinine, blood urea nitrogen, P16INK4α, thrombospondin-1, and transforming growth factor-β1 were decreased in each treatment group, whereas albumin, erythropoietin, nephrin, and podocin were increased; the pathological renal injury was alleviated, and the number of senescent cells was reduced, especially in rats treated with P. igniarius decoction. Conclusions: P. igniarius ameliorates renal aging and renal injury in the FSGS rat model. Compared with the effective constituents (polysaccharides and polyphenols), P. igniarius decoction has a better curative effect, which is expected to provide a new therapeutic idea for FSGS. [ABSTRACT FROM AUTHOR]

To investigate the regulatory effect of n-butylphthalide (NBP) on the nerve cells of rats with cerebral infarction (CI) through the JNK/p38MAPK signaling pathway, 135 SPF SD male rats were and randomly assigned into the control group (n=45, sham surgery + peanut oil gavage), model group (n=45, CI model + peanut oil gavage), and NBP group (n= 45, CI model + NBP gavage). The comparison of the neurological function score between the model group and the NBP group, as well as the integrated locomotor ability score, Slit2 expression level, blood-brain barrier permeability, microvessel density (MVD), CI volume, neuronal apoptosis rate of the brain tissue and expression levels of brain tissue p-JNK and p-p38MAPK protein among three groups was conducted. NBP inhibits the expression of JNK/p38MAPK signaling pathway, promotes the expression of Slit2 in CI rats, improves the neurological function and locomotor ability of CI rats, while promoting micro vascularization of the brain tissue, protecting the blood-brain barrier, reducing the volume of CI and the apoptosis of nerve cells. [ABSTRACT FROM AUTHOR]

Copyright of China Journal of Oral & Maxillofacial Surgery is the property of Shanghai Jiao Tong University, College of Stomatology and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Cukurova Medical Journal / Çukurova Üniversitesi Tip Fakültesi Dergisi is the property of Cukurova University, Faculty of Medicine and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Cukurova Medical Journal / Çukurova Üniversitesi Tip Fakültesi Dergisi is the property of Cukurova University, Faculty of Medicine and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Alzheimer's disease (AD) occurs in approximately 10% to 30% of individuals aged 65 or older worldwide. Novel therapeutic agents therefore need to be discovered in addition to traditional medications. Nimodipine appears to possess the potential to reverse cognitive impairment-induced dysfunction in learning and memory through its regulatory effect on the brain-derived neurotrophic factor (BDNF), acetylcholine (Ach), and acetylcholinesterase (AChE) pathway in the hippocampus and prefrontal cortex. Twenty-four male Sprague Dawley rats weighing 380 ± 10 g were used for behavioral and biochemical analyses. These were randomly and equally assigned into one of three groups. Group 1 received saline solution alone via the intraperitoneal (i.p) route, and Group 2 received 1 mg/kg/day i.p. scopolamine once a day for three weeks for induction of learning and memory impairments. In Group 3, 10 mg/kg/day nimodipine was prepared in tap water and administered orally every day for three weeks, followed after 30 min by 1 mg/kg/day scopolamine i.p. Behavior was evaluated using the Morris Water Maze test. BDNF, ACh, and AChE levels were determined using the ELISA test in line with the manufacturer's instructions. Nimodipine treatment significantly increased the time spent in the target quadrant and the number of entries into the target quadrant compared to the scopolamine group alone. Additionally, BDNF and ACh levels in the hippocampus and prefrontal cortex decreased following 20-day scopolamine administration, while AChE activation increased. Nimodipine exhibited potentially beneficial effects by ameliorating cognitive decline following scopolamine administration in the hippocampus and prefrontal cortex. [ABSTRACT FROM AUTHOR]

It has been suggested that oxidative stress plays an important role in neural degeneration and Alzheimer's disease. Some studies have shown that metformin has some beneficial effects on the brain and reduces oxidative stress, while others reveal that metformin increases oxidative stress in diabetic patients. In this study acute and chronic effects of metformin and antioxidant protective effects of N-acetyl cysteine in Alzheimeric rats were investigated. Animals were divided into seven groups (n=8): Control, STZ, STZ + metformin (one, three and eleven weeks), STZ+ metformin (eleven weeks) +N-acetyl cysteine (eleven weeks) and N-acetyl cysteine (eleven weeks). ICV injections of saline (1μl/rat) or STZ (3mg/kg) and IP injections of Saline (1ml/kg), metformin (200mg/kg) and/or N-acetyl cysteine (100mg/kg) were done. Memory retrieval, CA1 neurons density and serums oxidative stress were investigated. STZ injections reduced memory retention, intact neurons and increased serum oxidative stress compared to the control (p<0/001). Metformin injection for one and three weeks (but not eleven weeks) improved the effects of STZ (p<0/001). Administration of N-acetylcysteine with metformin (eleven weeks) improved STZ bad effects (p<0/001). It seems that acute and chronic consumption of metformin have different effects on memory retrieval, CA1 neurons and serum oxidative stress factors in AD rats. [ABSTRACT FROM AUTHOR]

This study aims to examine the effects induced by lead acetate (Pb) using different experimental approaches, such as neurobehavioral, biochemical, and histological in young Wistar rats during gestation and lactation, and to test the probiotic effect of Lactobacillus rhamnosus (Prob) throughout correcting or not the harmful effects of the studied metal. Chronic exposure to 0.2% lead acetate in rats during the development period resulted in a decrease in body and brain weights compared to controls. Test results for depression (forced swimming test), anxiety (Elevated plus maze), and locomotor and exploratory activity (Open field) all show that Pb intoxication causes neurobehavioral disorders, leading to decreased locomotor activity and a reduction of the exploration behavior of the environment which reflects the establishment of a state of stress, anxiety, and depression. In fact, the histopathological analysis revealed significant lesions in the brain tissue. Furthermore, the administration of probiotics (Prob) allowed the rats to regain body and brain weight when compared to the intoxicated rats. In addition, the use of various behavioral test techniques reveals that the administration of Lactobacillus rhamnosus corrects the depressive state, locomotor hypoactivity, and anxiety observed in rats exposed to Pb. Blood antioxidant status analysis revealed that Prob restored the activity of different antioxidant enzymes (SOD, CAT, GPx, and GSH) and non-enzymatic enzymes (glutathione) in rats intoxicated and treated with Prob. In effect, the histological study showed a significant improvement in the brain histology in rats intoxicated and treated with Prob. This illustrates the important implications of probiotic lactobacilli and their therapeutic properties. [ABSTRACT FROM AUTHOR]

Copyright of Revista Cientifica de la Facultade de Veterinaria is the property of Universidad del Zulia, Facultad de Ciencias Veterinarias and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Ruboxistaurin (RBX) used to treat retinopathy in diabetic patients which caused by microvascular damage and leakage which contributes to visual loss. There are no published studies on the use of liquid chromatography-tandem mass spectrometry for development and validation of a simple, sensitive, and accurate method for measuring RBX in rat plasma. Chromatographic separation of RBX was achieved using ultra-performance liquid chromatography. Multiple-reaction monitoring quantification used RBX [M + H] + ion at m / z 469.18 and daughter ions at m / z 84, 58.12, and 98.10. Atorvastatin was used as internal standard (IS), has a single daughter ion, and was identified using m / z 559.6 → 249.9. Validation of the liquid chromatography-tandem mass spectrometry (LC-MS/MS) method for RBX in rat plasma for linearity (greater than0.997) was carried out at 25–1000 ng/mL. In rat plasma, the accuracy was within 3.4%, and the intra- and inter-day precision was within 11.8%. Stability, recovery, and matrix effect were all within acceptable limits. The drug retention time (0.85 ± 0.03 min) was remarkably short. The method developed in the current study is suitable to quantify RBX in plasma or bulk doses. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Botulinum toxin type A (BoNT/A) reversibly blocks neurotransmission at voluntary and autonomic cholinergic nerve terminals, inducing paralysis. The aim of this study was to block panenteric peristalsis in rats through BoNT/A administration into the superior mesenteric artery (SMA) and to understand whether the toxin's action is selectively restricted to the perfused territory. MATERIALS AND METHODS: Rats were infused through a 0.25-mm surgically inserted SMA catheter with different doses of BoNT/A (10 U, 20 U, 40 U BOTOX®, Allergan Inc.) or with saline for 24 h. Animals were free to move on an unrestricted diet. As a sign of bowel peristalsis impairment, body weight and oral/water intake were collected for 15 days. Statistical analysis was conducted with nonlinear mixed effects models to study the variation over time of the response variables. In three 40 U-treated rats, the selectivity of the intra-arterial delivered toxin action was studied by examining bowel and voluntary muscle samples and checking the presence of BoNT/Acleaved SNAP-25 (the smoking gun of the toxin action) using the Immunofluorescence (IF) method through a specific antibody recognition. RESULTS: While control rats exhibited an increasing body weight, treated rats showed an initial dose-dependent weight reduction (p<0.001 control vs. treated) with recovery after Day 11 for 10 and 20 U-treated rats. Food and water intake over time showed significantly different half-saturation constants with rats treated with higher doses who reached half of the maximum achievable in a greater number of days (p<0.0001 control vs. treated rats). BoNT/A-cleaved SNAP-25 was identified in bowel wall NMJs and not in voluntary muscles, demonstrating the remarkable selectivity of arterially infused BoNT/A. CONCLUSIONS: Blockade of intestinal peristalsis, can be induced in rats by slow infusion of BoNT/A into the SMA. The effect is long-lasting, dose-dependent and selective. BoNT/A delivery into the SMA through a percutaneous catheter could prove clinically useful in the treatment of entero-atmospheric fistula by temporarily reducing fistula output. [ABSTRACT FROM AUTHOR]