Search

This study evaluated the individual and combined effects of L. plantarum and L. reuteri on the growth performance, digestive enzymes, antioxidant, and immunity-related genes in zebrafish. Six hundred zebrafish (38.19±1.4 mg) were randomized into twelve tanks (50 fish per), and fed prepared diets comprising unsupplemented (T0), 1×108 CFU/g L. plantarum (T1), 1×1011 CFU/kg L. reuteri (T2), and 1×108 CFU/g L. plantarum + 1×1011 CFU/kg L. reuteri (T3) for 8 weeks. Experimental diets had meaningful effects on weight gain (WG), final weight (FW), and the highest WG and FW were seen in T3. Fish-fed supplemented diets had higher amylase and lipase activities. No significant differences were seen in protease, pepsin, chymotrypsin, and trypsin activities between treatments. The supplemented groups showed a significant increase in lysozyme activity and total immunoglobulin levels. Meaningful differences were noticed in ACH50, lysozyme activity, total immunoglobulin, and IgM levels. ALT levels were markedly higher in T2 and T3. Catalase (CAT), total antioxidant, and glutathione peroxidase (GPX) activity were significantly impacted by the experimental diets. The experimental diets showed no marked impact on superoxide dismutase (SOD) activity, and malondialdehyde (MDA) values. Relative expressions of CAT, GPX, and SOD genes were notably upper in T3. Moreover, IL1, LYZ, and TNFα gene expressions were significantly enhanced in T3 diets. The challenge test with A. hydrophila showed that zebrafish fed L. plantarum and L. reuteri had a lower mortality rate than the control. Consequently, the combination of L. reuteri and L. plantarum is proposed to improve growth efficiency, immunity, and reduce the negative effects of A. hydrophila infection in zebrafish. [ABSTRACT FROM AUTHOR]

Objective: The article studies how Melissa officinalis L. extract and rosmarinic acid (RA) affect lung inflammation, pathology, and oxidative stress in rats with ovalbumin-induced asthma. Materials and Methods: Asthma was induced in rats using ovalbumin injection and inhalation. The study assessed lung inflammation, pathological changes, and oxidative stress in control, untreated asthmatic rats and three treatment groups. These groups received M. officinalis extract (50, 100, 200 mg/kg), RA (0.5, 1, 2 mg/kg), or dexamethasone (Dex) 1 mg/kg. Results: In the sensitized group, white blood cell counts, malondialdehyde, and nitrite levels increased significantly, while thiol levels and the activity of superoxide dismutase and catalase decreased (p<0.001). However, all treatment groups with the extract, RA, and Dex showed a significant reduction in total white blood cells, eosinophils, monocytes, malondialdehyde, and nitrite levels compared to the asthma group (p<0.001 in all groups). Thiol levels and catalase and superoxide dismutase activity were significantly higher in all treated groups with RA and high extract doses (p<0.001). Lung pathological changes were also significantly less severe in the treated groups with dexamethasone, plant extract, and RA compared to the asthma group (p<0.05 to p<0.001). Conclusion: This study showed that M. officinalis and RA have antioxidant and anti-inflammatory effects in an animal asthma model, suggesting their potential for treating asthma symptoms. [ABSTRACT FROM AUTHOR]

Sericin (Ser) is a natural neuroactive macromolecule with diverse pharmacological properties, and our previous findings have shown its neuroprotective potentials. This study aimed to investigate the therapeutic potential of Ser on cognitive dysfunction induced by transient global cerebral ischemia/reperfusion (tGI/R) and its mechanism of action. The tGI/R was induced in BALB/c mice by bilateral occlusion of the common carotid arteries for two 5 min followed by a 10-min reperfusion period. After 24 h, mice were treated with normal saline or different doses of Ser (100, 200, and 300 mg/kg) for 10 days. Cognitive performances were assessed using the Barnes maze and social interaction tasks. Oxidative stress markers including superoxide dismutase (SOD), glutathione peroxidase (GPx), total antioxidant capacity (TAC), and malondialdehyde (MDA) as well as pro-inflammatory cytokines (interleukin (IL)-6 and tumor necrosis factor-alpha) and anti-inflammatory cytokine (IL-10) were assessed in the hippocampus. Markers of apoptosis (pro- and cleaved caspase-9 and 3, Bax, and Bcl-2) were assessed by Western blotting. Besides, transferase-mediated dUTP nick end-labeling assay was used to detect apoptotic cell death. We show here that Ser administration improved tGI/R-induced cognitive deficits, enhanced the activity of SOD and GPx, increased TAC levels, while reduced MDA levels. Notably, Ser decreased neuronal apoptotic cell death in the hippocampal dentate gyrus (DG) region, accompanied by suppression of neuroinflammation, downregulation of pro-apoptotic proteins (caspase-9, caspases-3, and Bax), and upregulation of anti-apoptotic protein, Bcl-2. Taken together, Ser administration protected hippocampal neurons from apoptotic cell death by impeding oxidative stress and inflammatory responses and, in turn, improved cognitive function in the tGI/R mice. [ABSTRACT FROM AUTHOR]

Alzheimer's disease (AD) is a progressive neurodegenerative disease characterized by cognitive decline and memory loss. Imipramine, a tricyclic antidepressant, has potent anti-inflammatory and antioxidant properties in the central nervous system. The aim of this study was to investigate the neuroprotective effects of imipramine on streptozotocin (STZ)-induced memory impairment. Male Wistar rats received an intracerebroventricular injection of STZ (3 mg/kg, 3 μl/ventricle) using the stereotaxic apparatus. The Morris water maze and passive avoidance tests were used to evaluate cognitive functions. 24 h after the STZ injection, imipramine was administered intraperitoneally at doses of 10 or 20 mg/kg for 14 consecutive days. The mRNA and protein levels of neurotrophic factors (BDNF and GDNF) and pro-inflammatory cytokines (IL-6, IL-1β, and TNF-α) were measured in the hippocampus using real-time PCR and ELISA techniques, respectively. In addition, real-time PCR was used to evaluate the mRNA levels of markers associated with neurogenesis (Nestin, DCX, and Ki67) and mitochondrial biogenesis (PGC-1α, NRF-1, and TFAM). The results showed that imipramine, especially at a dose of 20 mg/kg, effectively improved STZ-induced memory impairment. This improvement was associated with an increase in neurogenesis and neurotrophic factors and a decrease in neuroinflammation and mitochondrial biogenesis dysfunction. Based on these results, imipramine appears to be a promising therapeutic option for improving cognitive functions in neurodegenerative diseases such as AD. • Imipramine improved streptozotocin (STZ)-induced cognitive deficits in rats. • Imipramine increased neurogenesis and neurotrophic factors in STZ- injected rats. • Imipramine reduced neuroinflammation in the STZ- injected rats. • Imipramine increased mitochondrial biogenesis in the STZ- injected rats. [ABSTRACT FROM AUTHOR]