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Objective To observe the alterations in lectin-like transcript 1(LLT1) expression within liver tissues of alveolar echinococcosis (AE) patients and to assess its correlation with clinical pathological parameters. Methods Thir‐ ty liver tissue samples from AE patients were collected, including 30 samples from proximal lesion tissues (CLT, < 2 cm form the lesion center) and 28 samples from distal tissues (DLT, > 2 cm from the lesion center). Immunohistochemistry was employed to determine the expression and localization of LLT1. The LLT1 expression changes in the liver tissues of AE patient with different clinical pathological parameters were analyzed. Data set GSE124362 from the GEO database, includ‐ ing 6 CTL and 6 matched DLT samples, was used to analyze the correlation between CLEC2D (the LLT1 coding gene) ex‐ pression and immune cell expression. Results LLT1 predominantly expressed in hepatocytes and inflammatory cells within the lesions' surrounding inflammatory zone. The expression scores for LLT1 in CLT and DLT were 3(2, 4) and 6 (4, 8), respectively, indicating significantly higher expression levels in CLT (both P<0. 05). LLT1 expression was relat‐ ed to the AE patients' P stage, ALT, AST, and γ-glutamyl transferase levels (all P<0. 05). CLEC2D expression showed a positive correlation with plasma cells, M2 macrophages, and activated dendritic cells (r=0. 83, 0. 87, 0. 74, respective‐ ly； all P<0. 01), and had a negative correlation with activated NK cells, M1 macrophages, and mast cells (r=–0. 73, –0. 60, –0. 74, respectively； all P<0. 01). Further analysis revealed that CLEC2D expression was negatively correlated with M1 mac‐ rophage markers CD1B and IL-6(r=–0. 65, –0. 89, respectively； both P<0. 05), and was positively correlated with M2 macrophage markers CD163, CLEC7A, and IL-10(r=0. 90, 0. 71, 0. 74, respectively； all P<0. 01). Conclusion The high expression of LLT1 in CLT of AE patients was related to P stage, liver function indices, and various immune cell ex‐ pression, suggesting LLT1 was involved in infiltration process of the AE liver lesions. [ABSTRACT FROM AUTHOR]

Diabetes mellitus (DM) causes an imbalance in the oxidative status of the human body. Three novel Dapagliflozin (Dapg) Zn (II), Cr (III) and Se (IV) complexes were prepared and characterized by elemental analysis, IR, electronic spectra, magnetic susceptibility, scanning electron microscopy (SEM) and X-ray diffraction. The molar conductance values confirmed the non-electrolytic nature of the Dapg complexes. According to spectral data, Dapg acts as a bidentate ligand. The thermal analyses of the complexes were studied using the DSC technique. The surface morphology and particle sizes of the Dapg complexes were investigated using SEM and XRD. XRD confirmed the crystalline structure for the complexity. This study investigated the effect of novel metal complexes of Dapg with the metals Zn (II), Cr (III) and Se (IV) on oxidative injury and tissue damage in the hepatic tissue of streptozotocin (STZ)-induced diabetic male rats. DM was experimentally induced in male rats. The diabetic rats received Dapg, Dapg/Zn, Dapg/Cr and Dapg/Se orally for 30 successive days. Male rats exposed to STZ showed multi-histopathological alterations in their hepatic tissue, including inflammatory and structural changes. STZ elevated oxidative stress markers in the hepatic tissue and lowered the antioxidant defense enzymes. Supplementation of Dapg with Zn, Cr or Se novel complexes significantly prevented hepatic injury and suppressed the generation of reactive oxygen species. The Dapg/Zn complex was highly effective against Bacillus subtilis and Streptococcus penumonia, while Dapg/Cr was highly effective against Escherichia coli and Pseudomonas aeruginosa, and Dapg/Se was highly effective against Staphylococcus aureas. In conclusion, Dapg novel metal complexes with Zn, Cr or Se protect against oxidative injury and the pathophysiological and bacterial complications of DM and hepatic tissue injury. The Dapg novel metal complexes improved hepatic functions, reduced blood glucose levels and enhanced the levels of antioxidant defense enzymes in diabetic male rats. [ABSTRACT FROM AUTHOR]

Diabetes mellitus (DM) causes an imbalance in the oxidative status of the human body. Three novel Dapagliflozin (Dapg) Zn (II), Cr (III) and Se (IV) complexes were prepared and characterized by elemental analysis, IR, electronic spectra, magnetic susceptibility, scanning electron microscopy (SEM) and X-ray diffraction. The molar conductance values confirmed the non-electrolytic nature of the Dapg complexes. According to spectral data, Dapg acts as a bidentate ligand. The thermal analyses of the complexes were studied using the DSC technique. The surface morphology and particle sizes of the Dapg complexes were investigated using SEM and XRD. XRD confirmed the crystalline structure for the complexity. This study investigated the effect of novel metal complexes of Dapg with the metals Zn (II), Cr (III) and Se (IV) on oxidative injury and tissue damage in the hepatic tissue of streptozotocin (STZ)-induced diabetic male rats. DM was experimentally induced in male rats. The diabetic rats received Dapg, Dapg/Zn, Dapg/Cr and Dapg/Se orally for 30 successive days. Male rats exposed to STZ showed multi-histopathological alterations in their hepatic tissue, including inflammatory and structural changes. STZ elevated oxidative stress markers in the hepatic tissue and lowered the antioxidant defense enzymes. Supplementation of Dapg with Zn, Cr or Se novel complexes significantly prevented hepatic injury and suppressed the generation of reactive oxygen species. The Dapg/Zn complex was highly effective against Bacillus subtilis and Streptococcus penumonia, while Dapg/Cr was highly effective against Escherichia coli and Pseudomonas aeruginosa, and Dapg/Se was highly effective against Staphylococcus aureas. In conclusion, Dapg novel metal complexes with Zn, Cr or Se protect against oxidative injury and the pathophysiological and bacterial complications of DM and hepatic tissue injury. The Dapg novel metal complexes improved hepatic functions, reduced blood glucose levels and enhanced the levels of antioxidant defense enzymes in diabetic male rats.

Background: Type 2 Diabetes Mellitus is a long term metabolic disorder that is characterized by high blood sugar, insulin resistance, and lack of insulin. Based on the understanding of the pathogenesis of T2DM, several distinct pharmacological therapies have been developed but many of them are producing significant adverse drug reactions. Objectives: The present study helps to understand the progression of hepatic degeneration in diabetes mellitus upon treatment with vildalgliptin and insulin. This study is aimed to evaluate the toxicity of combined therapy of vildagliptin and insulin in alloxan induced diabetic rats. Methods: Adult male albino Wistar rats were distributed among 5 groups, and induced diabetes with alloxan. The alterations in glucose metabolizing enzyme activities were determined spectrophotometrically in the liver homogenate and confirmed by histological study. The hematological count has been carried out in all experimental groups to understand the toxicity of combinatorial therapy. Results: The histopathological studies showed pathological changes in the cellular architecture and microcytic hepatic nuclei. The level of haemoglobin, red blood cells and platelet count has been lowered drastically when compared to the monotherapy showing that the combinatorial therapy makes the animal anaemic. The level of lymphocytes has been considerably reduced in the combinatorial therapy showing the loss of immunity. The glucose metabolizing enzymes have been significantly altered showing the glucose metabolism is severely affected in combinatorial therapy showing it was not properly metabolized. Conclusion: The above studies have clearly proves that vildagliptin and insulin drug therapy shows toxicity on metabolic organs and blood cells. So our studies will be really helpful for developing new drugs which are devoid of adverse effects. [ABSTRACT FROM AUTHOR]

Immunohistochemistry (IHC) is a method of routine use in histopathology for the diagnosis and differentiated diagnosis of liver diseases. IHC staining in human hepatic tissue is often obstructed by the presence of non-specific antibody interactions, the cause of high background staining. Cognizant of previous encounters with high levels of background in human hepatic tissue when using polyclonal antibodies, the potential causes were systemattically investigated by testing the impact of different antibody variants and assay conditions. Firstly, IHC was performed on hepatic tissue with immunized and non-immunized polyclonal antibodies and it was demonstrated that immunized antibodies pervaded the samples with non-specific staining, while non-immunized antibodies produced insignificant background. Following, the primary antibody was co-incubated with different concentrations of protein blocks, acid/base solutions, crystalline ionic compounds, and combinations of these individual components in order to assess their potency in removing background staining. Optimization of these assay conditions revealed that background could be significantly reduced by the addition of sodium chloride to primary antibody solution and/or protein block to sodium azide-stabilized Tris-HCl buffer, while little beneficial effect was observed from co-incubating the primary antibody with non-serum protein block/goat serum, hydrochloric acid/sodium hydroxide, or a higher concentration of peroxidase block. Together, the results suggest that hepatic background in IHC is mainly attributed to strong ionic interactions between the light chains of polyclonal antibodies and polar molecules specifically prevalent in hepatic tissue, which can be reduced by increasing the ionic strength of the antibody-antigen reaction microenvironment. Thus, the findings can enhance the specificity of hepatic tissue immunoassays and improve IHC studies in human liver tissues using polyclonal antibodies. [ABSTRACT FROM AUTHOR]

Abstract: The present study is to investigate the antioxidant activity in alloxan induced diabetic rats. The experimental rats were randomly divided into three groups: Group I: control; Group II: alloxan induced diabetic rats and Group III: alloxan induced diabetic rats were treated with ethanolic extract of Crinum asiaticum leaves (200mg/kg/bw). Diabetes mellitus was induced by alloxan in a single dose of 200mg/kg/bw. A significant decrease in blood sugar level was observed and also an increase in high density lipoprotein (HDL) level and a decrease (P <0.05) in cholesterol, triglyceride, low density lipoprotein (LDL) and very low density lipoprotein (VLDL) levels were observed after 15days of treatment with C. asiaticum extract. Besides, the activities of aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), acid phosphatase (ACP) and lactate dehydrogenase (LDH) (P <0.05) were diminished in the C. asiaticum leaves extract of the supplemented group. In addition, the activity of superoxide dismutase (SOD), catalase (CAT) and reduced glutathione (GSH) (P <0.05) was increased by the C. asiaticum leaves extract administration and increases in lipid peroxides (LPO) in liver were found to be ameliorated after treatment. The findings of the present investigation demonstrated the hepatocyte protective nature of C. asiaticum by attenuating markers of hyperglycemia-mediated oxidative stress and the antioxidant competence in hepatic tissues of diabetic rats. [Copyright &y& Elsevier]

Decoctions and infusions of Artocarpus communis (Forst.) (family: Moraceae) root-bark are commonly used traditionally among the Yoruba-speaking people of Western Nigeria as folk remedies for the management, control and/or treatment of an array of human diseases, including type 2, adult-onset diabetes mellitus. Although numerous bioactive flavonoids have been isolated from the roots, stem-bark and leaves of A. communis, to the best of our knowledge, the effects of the plant's root-bark extract on animal model of diabetes mellitus and on liver tissues have hitherto, not been reported in the biomedical literature. In view of this, the present study was undertaken to investigate the glycaemic effect of, and hepatic tissue ultrastructural, morphological and metabolic changes induced by A. communis root-bark aqueous extract (ACE) in Wistar rats. The ultrastructural, morphological and metabolic effects of ACE have been compared with those induced by streptozotocin (STZ) in rat experimental paradigms. Four groups (A, B, C and D) of Wistar rats, each group containing 10 rats, were used. Diabetes mellitus was induced in the diabetic groups B and C animals by intraperitoneal injections of STZ (75 mg/kg body weight), while group A rats received A. communis root-bark aqueous extract (ACE, 100 mg/kg body weight, i.p.) alone. Control group D rats received distilled water in quantities equivalent to the volume of ACE administered intraperitoneally. The rats in group C were additionally treated with ACE (100 mg/kg body weight i. p.) daily from day 3 to day 10 after STZ treatment. Hepatic glucokinase, hexokinase, glutamate dehydrogenase, succinate dehydrogenase, beta-hydroxybutyrate dehydrogenase, serum insulin and blood glucose levels of the animals were measured and recorded before and after ACE, STZ and STZ+ACE treatments. Hepatic tissues were also processed for transmission electron microscopy. Electron microscopic examinations showed toxic, deleterious alterations in the ultrastructures of groups A, B and C hepatic cells, the most prominent deleterious effects being on the hepatocytes. Ultrastructural changes observed within the hepatocytes of groups A, B and C rats include disrupted mitochondria with increase in lipid droplets, extensive hepatocellular vacuolation, scanty rough endoplasmic reticulum (RER) and ribosomes. Large glycogen clusters were also noticed displacing the mitochondria and RER in group A rats. Group A rats also developed significant hyperglycemia (p<0.05) immediately after ACE administration, while groups B and C rats developed hyperglycemia 24 hours after STZ treatment. When compared with the control group D rats, the activities of all the three subsystems were disrupted, leading to overall inhibition of oxidative phosphorylation of the liver mitochondria in groups A, B and C rats, but remain normal in the untreated group D control rats. The findings of the present study indicate that A. communis root-bark aqueous extract induces hyperglycaemia in the experimental animal model used, and that the plant's extract disrupts the ultrastructural characteristics and architecture of hepatocytes as well as oxidative energy metabolism.