Liver Of Diabetic Rats Research Articles

Evaluation of Antioxidant Effects of Coenzyme Q10 against Hyperglycemia-Mediated Oxidative Stress by Focusing on Nrf2/Keap1/HO-1 Signaling Pathway in the Liver of Diabetic Rats.

Hyperglycemia-induced oxidative stress can damage the liver and lead to diabetes complications. Coenzyme Q10 (CoQ-10) reduces diabetes-related oxidative stress. However, its molecular mechanisms are still unclear. This study aimed to examine CoQ-10's antioxidant capabilities against hyperglycemia-induced oxidative stress in the livers of diabetic rats, specifically targeting the Nrf2/Keap1/ARE signaling pathway. This study was conducted between 2020-2021 at Arak University of Medical Sciences. A total of 30 male adult Wistar rats (8 weeks old) weighing 220-250 g were randomly assigned to five groups (n=6 in each group): control healthy, sesame oil (CoQ-10 solvent), CoQ-10 (10 mg/Kg), diabetic, and diabetic+CoQ-10. Liver oxidative stress indicators, including malondialdehyde, catalase, glutathione peroxidase, and glutathione, were estimated using the spectrophotometry method. Nrf2, Keap1, HO-1, and NQO1 gene expressions were measured using real-time PCR tests in the liver tissue. All treatments were conducted for 6 weeks. Statistical analysis was performed using SPSS software. One-way ANOVA followed by LSD's or Tukey's post hoc tests were used to compare the results of different groups. P<0.05 was considered statistically significant. The findings showed that induction of diabetes significantly increased Keap1 expression (2.1±0.9 folds, P=0.01), and significantly inhibited the mRNA expression of Nrf2 (0.38±0.2 folds, P=0.009), HO-1 (0.27±0.1 folds, P=0.02), and NQO1 (0.26±0.1 folds P=0.01), compared with the healthy group. In the diabetic group, the activity of glutathione peroxidase, catalase enzymes, and glutathione levels was decreased with an increase in malondialdehyde level. CoQ-10 supplementation significantly up-regulated the expressions of Nrf2 (0.85±0.3, P=0.04), HO-1 (0.94±0.2, P=0.04), NQO1 (0.88±0.5, P=0.03) genes, and inhibited Keap1 expression (1.1±0.6, P=0.02). Furthermore, as compared to control diabetic rats, CoQ-10 ameliorated oxidative stress by decreasing malondialdehyde levels and increasing catalase, glutathione peroxidase activities, and glutathione levels in the liver tissues of the treated rats in the treatment group. The findings of this study revealed that CoQ-10 could increase the antioxidant capacity of the liver tissue in diabetic rats by modulating the Nrf2/Keap1/HO-1/NQO1 signaling pathway.

AMELIORATION OF LIVER AND KIDNEY FUNCTION PARAMETERS IN ALLOXAN-INDUCED DIABETIC RATS TREATED WITH 3-[2-(1,5-Dimethyl-3-oxo-2-Phenyl-2,3-Dihydro- 1H-Pyrazol-4-yl) Hydrazinylidene]-1-Phenylbutanedione, and its Ni(II) Complex.

This hydrazone: 3-[2-(1,5-Dimethyl-3-oxo-2-Phenyl-2,3-Dihydro-1H-Pyrazol-4-yl) Hydrazinylidene]-1-Phenylbutanedione (HL), and its Ni (II) Complex ([Ni(HL)2]Cl2) have been reported to possess hypoglycaemic property but the effects of their use on kidney and liver functions in diabetic animals have not been investigated. The study investigated some biochemical parameters in the liver and kidney of alloxan-induced diabetic rats treated with these hydrazone compounds. Diabetes was induced by a single intraperitoneal dose of alloxan (150 mg/kg). Data showed that these compounds induced a significant decrease in serum glucose levels in the diabetic rats. Diabetic rats were administered orally with compounds for fourteen days after which some biochemical indices in the serum, liver and kidney were measured and compared with the control. Serum alkaline phosphatase (ALP), alanine aminotransferase (ALT), aspartate aminotransferase (AST), urea, total protein and creatinine of untreated diabetic group was significantly elevated when compared with the normal control group. The ALP, AST concentrations of diabetic rats treated with low and high doses of HL was observed to be non-significantly (p &gt; 0.05) higher compared with rats in the normal control group A. A significantly (p &lt; 0.05) decrease in the ALT, AST and ALP concentrations of diabetic rats treated with 200 and 400 mg/kg b.w. of HL and [Ni(HL)2]Cl2 were observed when compared with untreated rats in group B. These results suggest that administration of these compounds to diabetic rats did not have any adverse effect on the liver and kidney functions in rats showing that the compounds are not toxic to man.

Polydatin from Polygoni Cuspidati Rhizoma et Radix regulates glucolipid metabolism in the liver of diabetic rats: Multiscale analysis of network pharmacology and multiomics

BackgroundPolygoni Cuspidati Rhizoma et Radix (Huzhang in Chinese), refers to the root and rhizome of Polygonum cuspidatum Sieb. et Zucc. Huzhang is commonly used in clinical practice for the prevention and treatment of diabetes and its complications, but its active components and regulatory mechanisms have not yet been thoroughly analyzed. PurposeThe network pharmacology combined with multi-omics analysis will be employed to dissect the substance basis and action mechanism of Huzhang in exerting its anti-diabetic activity. MethodsThis study employed phenotypic indicators for baseline assessment, followed by integrated analysis using network pharmacology, metabolomics, transcriptomics, and qPCR technology to elucidate the active components and pharmacological mechanisms of Huzhang. ResultsThe analysis of network pharmacology revealed that polydatin is a potential active component responsible for the anti-T2DM pharmacological effects of Huzhang. In vivo experimental results demonstrated that polydatin significantly regulates blood glucose, lipid levels, liver function, and liver pathological damage in diabetic rats. Analysis results from transcriptomics, metabolomics, and qPCR validation showed that polydatin comprehensively regulates glucose and lipid metabolism in T2DM by modulating bile acid metabolism, fatty acid oxidation, and lipogenesis. ConclusionPolydatin is a key component of Huzhang in treating T2DM, and its regulatory mechanisms are diverse, indicating significant development potential.

Effects of the Aquatic Extract of Cinnamon Zeylanicum on STZ-Induced Diabetic Rats: A Molecular and Histopathological Study

Background: The prevalence of diabetes mellitus has increased over the past few decades, making it a significant public health challenge of the twenty-first century. Cinnamon, as a traditional medicine, has been used in several regions of the world for its anti-diabetic properties. Objectives: The current study was conducted to determine the effect of Cinnamon Zeylanicum extract on blood glucose levels, oxidative stress markers, and antioxidant enzyme gene expression in diabetic rats. Methods: Forty Sprague-Dawley rats were divided into four groups, each containing 10 rats. A single dose of streptozotocin (50 mg/kg, IP) was used to induce diabetes. In this investigation, 40 mg/kg body weight of cinnamon extract was administered orally. After eight weeks, the levels of glucose, malondialdehyde (MDA), and reduced glutathione (GSH) were determined using biochemical methods. Additionally, the expression levels of catalase and glutathione reductase in the rat liver homogenate were evaluated using real-time PCR. The effect of cinnamon extract on histopathological changes in the rats' liver was also investigated. Results: The findings indicated that the administration of cinnamon extract resulted in a considerable reduction in blood glucose (210 ± 29.9 vs. 449 ± 48.4 mg/dL; P &lt; 0.001) and liver MDA levels (2.01 ± 0.35 vs. 3.05 ± 0.47; P &lt; 0.001) in diabetic rats after eight weeks. However, this extract had no significant effect on GSH levels (4.71 ± 0.25 vs. 4.75 ± 0.42; P = 0.79) in diabetic rats compared to diabetic control rats. The mRNA expression of catalase and glutathione reductase genes in the liver of diabetic control rats (0.73 ± 0.23 and 0.90 ± 0.18, respectively) was significantly lower than that of the healthy control group (1.33 ± 0.37 and 1.46 ± 0.54, respectively) (P = 0.001, P = 0.012). Administration of cinnamon extract increased the expression levels of these antioxidant enzyme genes, but these changes were statistically not significant (P = 0.72 and P = 0.48, respectively). Furthermore, the creation of hyperglycemia led to slight hypertrophic degeneration and lymphocyte infiltration in hepatocytes. Notably, the administration of cinnamon extract was unable to reverse these abnormalities. Conclusions: The findings of our study support cinnamon's anti-diabetic and antioxidant properties in diabetic rats. However, the histological abnormalities in the diabetic rats' livers could not be altered by the administration of cinnamon.

Hepatoprotective potential of taxifolin in type 2 diabetic rats: modulation of oxidative stress and Bcl2/Bax/Caspase-3 signaling pathway.

Diabetes mellitus (DM) is a global metabolic problem. Several factors including hyperglycemia, oxidative stress, and inflammation play significant roles in the development of DM complications. Apoptosis is also an essential event in DM pathophysiology, -with B-cell lymphoma 2 (Bcl-2) and Bcl-2 associated X (Bax) determining apoptotic susceptibility. The present study aimed to elucidate the protective effects of two doses of taxifolin (TXF) on liver damage in diabetic rats and explore the possible mechanisms of action. DM was induced in eighteen rats through intraperitoneal injections of 50mg/kg streptozotocin and 110mg/kg nicotinamide. Diabetic rats received daily oral intubation of 25 and 50mg/kg TXF for 3 months. In the untreated diabetic group, there was a significant increase in fasting and postprandial glucose levels, glycosylated hemoglobin A1C (HbA1c), tumor necrosis factor-alpha (TNF-α), and interleukin-6 (IL-6), while insulin and adiponectin levels decreased significantly. Both TXF doses mitigated hyperglycemia, regulated cytokine production, and increased insulin level. Gene expressions and protein levels of Bax, caspase 3, and cytochrome c were significantly increased, while Bcl-2 was significantly decreased in the livers of diabetic rats, effects that were significantly ameliorated after TXF treatment. The results of the TUNEL assay supported the apoptotic pathway. Additionally, TXF significantly decreased lipid peroxidation and enhanced antioxidant enzyme activity in diabetic rats. Liver enzymes and histopathological changes also showed improvement. TXF mitigated diabetes-associated hepatic damage by reducing hyperglycemia, oxidative stress, inflammation, and modulating anti-/pro-apoptotic genes and proteins. A dose of 50mg/kg TXF was more effective than 25mg/kg and is recommended for consumption.

Comparative Evaluation of Diabetes Complication Using Liver Function Parameters as Indices between Male and Female Alloxan Induced Diabetic Rats

It is known that diabetes causes liver damage. On the other hand, because most cases of liver damage have been investigated in males, examining the relationship of this disease in both sexes is of great importance. This study was aimed at, comparatively evaluating diabetic complications using histopathological examination and liver function parameters as indices in alloxan-induced diabetic rats. A total of 24 male and female rats divided into four groups of six animals each were used for the experiment. Group A were female control, Group B were male control while group C and D were alloxan induced diabetic female and male rats respectively. Groups A and B were non diabetic rats fed with rat diet all through the experiment. Group C and D were diabetes induced with a single intraperitoneal injection of alloxan (120mg/kg). At the end of the inducement period, the rats were fasted overnight and sacrificed. Blood was collected by ocular puncture for the determination of fasting plasma glucose (FPG) and serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), total bilirubin (TB), direct bilirubin (DB), total protein (TP) and albumin (ALB) using spectrophotometric method. Histology of the liver was determined by H and E technique. The results showed the experimental group C (365.83±43.6mg/dl) and D (368.94±43.93mg/dl) had significantly elevated levels of FPG when compared with the controls group A (116.00±9.11mg/dl) and B (108.33±5.5mg/dl) confirming the induction of diabetes (P=0.000). The liver of both male and female diabetic rats showed ballooning degeneration. In the males, these were arranged in normal sheets and cord around central vein in some areas of the center, on the other hand, the central vein of the female diabetic rats appears slightly enlarged containing blood clots and the arrangement of the hepatocytes in sheets or cords around the central vein was completely distorted. There was no significant difference (p&gt;0.05) in the mean serum levels of ALP, AST, ALT, DB, TP and ALB in female diabetics when compared to male diabetic rats. The mean serum level of TB was significantly reduced (p=0.004) in female diabetics (0.53±0.05) than in the male diabetic albino rats (0.69±0.09). This study showed the liver histology and function are variably altered in diabetes mellitus. Further research on the causes of liver damage will help us to unravel the pathogenesis of diabetes and its complications.

Hepatoprotective Effects of Curcumin on Liver Injury in Streptozocin-induced Diabetic Rats

Introduction: Type 2 diabetes mellitus is characterized by chronically elevated blood sugar levels associated with disruption of the inflammatory and oxidative state and dyslipidemia. Curcumin is a highly pleiotropic molecule with hypoglycemic, hypolipidemic, anti-inflammatory, and antioxidant properties. The aim of this study was to evaluate the effects of curcumin on the liver of streptozotocin-induced diabetic rats. Materials and Methods: Thirty-two adult male rats were used in the study. The rats were divided into four groups: Control (C), Diabetes (D), Curcumin (CUR), and Diabetes + Curcumin (D + CUR) (n = 8). The groups given curcumin were given 60 mg/kg curcumin by gavage once a day during the 14-day study period. At the end of the experiment, biochemical, stereological, histological, and immunohistochemical analyses were performed on blood and liver samples taken from rats sacrificed. Results: After curcumin treatment in diabetic rats, there was a significant decrease in blood glucose levels, hepatic markers, and levels of thiobarbituric acid reactive substances (P &lt; 0.01). Furthermore, a significant increase in enzymatic antioxidants such as superoxide dismutase, catalase, and glutathione peroxidase was observed after treatment (P &lt; 0.01). It was determined that curcumin decreased the apoptotic index and the number of dual-nucleated hepatocytes in the liver, and provided support for liver regeneration (P &lt; 0.01). Discussion and Conclusion: Based on the findings of this study, it can be concluded that curcumin has the potential to protect against hyperglycemia-induced oxidative stress and apoptosis in liver cells, and also induces regeneration in damaged liver.

Hydrazone-flavonol based oxidovanadium(V) complexes: Synthesis, characterization and antihyperglycemic activity of chloro derivative in vivo

Wet synthesis approach afforded four new heteroleptic mononuclear neutral diamagnetic oxidovanadium(V) complexes, comprising salicylaldehyde-based 2-furoic acid hydrazones and a flavonol coligand of the general composition [VO(fla)(L-ONO)]. The complexes were comprehensively characterized, including chemical analysis, conductometry, infrared, electronic, and mass spectroscopy, as well as 1D 1H and proton-decoupled 13C(1H) NMR spectroscopy, alongside extensive 2D 1H1H COSY, 1H13C HMQC, and 1H13C HMBC NMR analyses. Additionally, the quantum chemical properties of the complexes were studied using Gaussian at the B3LYP, HF, and M062X levels on the 6–31++g(d,p) basis sets. The interaction of these hydrolytically inert vanadium complexes and the BSA was investigated through spectrofluorimetric titration, synchronous fluorimetry, and FRET analysis in a temperature-dependent manner, providing valuable thermodynamic insights into van der Waals interactions and hydrogen bonding. Molecular docking was conducted to gain further understanding of the specific binding sites of the complexes to BSA. Complex 2, featuring a 5-chloro-substituted salicylaldehyde component of the hydrazone, was extensively examined for its biological activity in vivo. The effects of complex administration on biochemical and hematological parameters were evaluated in both healthy and diabetic Wistar rats, revealing antihyperglycemic activity at millimolar concentration. Furthermore, histopathological analysis and bioaccumulation studies of the complex in the brain, kidneys, and livers of healthy and diabetic rats revealed the potential for further development of vanadium(V) hydrazone complexes as antidiabetic and insulin-mimetic agents.

SARS-CoV-2 Spike Protein Enhances Carboxypeptidase Activity of Angiotensin-Converting Enzyme 2.

In this study, we investigated whether severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) spike protein may modify angiotensin-converting enzyme 2 (ACE2) activity in the plasma, heart, kidney, liver, lung, and six brain regions (amygdala, brain stem, cortex, hippocampus, hypothalamus, and striatum) of diabetic and hypertensive rats. We determine ACE2 activity in the plasma and lysates of heart, kidney, liver, lung, and six brain regions. MLN-4760 inhibits ACE2 activity in the plasma and all organs. On the other hand, soluble ACE2 (sACE2) activity increased in the plasma of diabetic rats, and there was no change in the plasma of hypertensive rats. ACE2 activity was augmented in the liver, brain stem, and striatum, while it decreased in the kidney, amygdala, cortex, and hippocampus of diabetic rats. ACE2 activity increased in the kidney, liver, and lung, while it decreased in the heart, amygdala, cortex, and hypothalamus of hypertensive rats. We measured the ACE2 content via enzyme-linked immunosorbent assay and found that ACE2 protein levels increased in the heart, while it decreased in the plasma, kidney, brain stem, cortex, hippocampus, hypothalamus, and striatum of diabetic rats. ACE2 protein levels decreased in the brain stem, cortex, hippocampus, and hypothalamus of hypertensive rats. Our data showed that the spike protein enhanced ACE2 activity in the liver and lungs of diabetic rats, as well as in the heart and three of the brain regions (cortex, hypothalamus, and striatum) of hypertensive rats.

Ameliorative Effect of Pigeon Pea Leaves and Ginger Extract on Oxidative Stress Condition in Kidney and Liver of Experimental Diabetic Rats

Ameliorative Effect of Pigeon Pea Leaves and Ginger Extract on Oxidative Stress Condition in Kidney and Liver of Experimental Diabetic Rats

Investigation of cytogenetic, electrophoretic, histopathological and biochemical effects of walnut (juglans regia l.) Leaf extract in rats experimentally induced diabetes by streptozotocin

In this study, the effects of Juglans regia L. (JR) leaf extract on histological damage and cytogenetic, electrophoretic, and biochemical parameters in the liver and kidney tissues of diabetic rats were investigated. In the study, 60 male rats (Sprague-Dawley) were separated into six groups. According to sodium dodecyl sulfate–polyacrylamide gel electrophoresis (SDS-PAGE) data, it was determined that there were increases and decreases in different serum protein expressions because of the treatment of JR leaf extract in the diabetes group. In the kidney tissue of the diabetes group, an increase in volume in the glomeruli and narrowing of the Bowman's space as well as thickening of the walls of tubules were detected. Vacuolization and shedding were observed in the epithelial cells of tubules in the cortical regions in kidney. In diabetic + JR extract groups administered JR leaf extract at doses of 250 mg/kg and 500 mg/kg, serum AST and ALT levels were reduced compared to the diabetic group. Diabetic rats' livers showed spotted necrosis and fibrosis in the portal area, biliary tract proliferation, mild inflammation, increased vascularization, unicellular necrosis in hepatocytes, and sinusoidal dilatation. The JR leaf extract group did not exhibit these problems. JR leaf extract influences reducing hepatotoxic and oxidative damage due to diabetes and increasing the level of antioxidant enzymes. As a result, it was concluded that the application of JR leaf extract may have a protective effect against damage caused by diabetes.

Effect of Aqueous Solanum macrocarpon Leaves Extract on Hyperglycemia, Liver Enzymes, and Liver and Pancreas Histology in Alloxan-Induced Diabetes

Solanum macrocarpon (SM) is frequently used for both medicinal and dietary purposes. It has been documented to have hypoglycemic properties in diabetes management. This research delved into the effect of aqueous Solanum macrocarpon leaves extract on blood glucose levels, liver enzymes, antioxidant enzymes, and histology of the liver and pancreas in alloxan-induced diabetic rats. A total of thirty male Wistar rats, with weights ranging from 150 to 200 g, were randomly divided into six groups, each containing five rats. The normal (A) and diabetic control (B) groups received distilled water. The diabetic treated groups (C, D, E, and F) were administered 5 mg of glibenclamide, 250 mg/kg, 500 mg/kg, and 750 mg/kg of Solanum macrocarpon extract orally for a period of 14 days. Significant reversal of the altered levels of liver enzymes was noted in the results. Positive alterations in blood glucose concentration and antioxidant enzyme activity were also observed. The histological examination showed damage to the hepatic and pancreatic cells of the diabetic untreated rat group, which was mitigated in diabetic rats treated with the aqueous extract. The findings indicate that the aqueous Solanum macrocarpon leaves extract serves as a valuable source of natural antioxidants, promoting both liver function and blood glucose regulation.

Effects of ethanolic extract of &lt;i&gt;Aristolochia repens&lt;/i&gt; on biochemical and histological changes in high-fat diet and streptozotocin-induced rats

The study evaluated the lipid profile, electrolytes and histological changes in diabetic Wistar rats treated with stem bark extract of Aristolochia repens. Type 2 diabetes was induced in rats with high-fat diet and low dose of streptozotocin (35 mg/kg body weight). A total of thirty-five Wistar rats were fed with high-fat diet for eight (8) weeks, while five (5) Wistar rats (Sham control) were fed with low-fat diet. Non-induced male Wistar rats were treated with distilled water (Sham control); while the induced male Wistar rats were treated with distilled water, metformin (100 mg/kg), 50, 100 and 200 mg/kg ethanolic extract of Aristolonchia repens stem bark for 28 days. The rats were sacrificed; liver, kidney and serum were collected and analyzed for serum glucose, lipid profile, electrolytes and histological changes. Treatment with ethanolic extract of Aristolonchia repens stem bark significantly reduced the body weight, glucose level, total cholesterol concentration, triglycerides, low-density lipoprotein concentration and atherogenic indices. Mild pathological alterations were observed in the liver and kidney of diabetic rats at dosage above 50 mg/kg. However, the extract reduced the blood glucose, lipids and improve the selected electrolyte balance. This study suggests that ethanolic extract of stem bark of A. repens possesses antihyperglycaemia and antilipidaemic potential and might not be safe at dosage above 50 mg/kg.

Theaflavin-3,3'-Digallate Protects Liver and Kidney Functions in Diabetic Rats by Up-Regulating Circ-ITCH and Nrf2 Signaling Pathway.

Theaflavin-3,3'-digallate (TFDG) in black tea has a strong antioxidant capacity. However, its effect on diabetic liver and kidney injury and the underlying mechanisms remain unclear. In the present study, our findings indicated that TFDG administration effectively lowers the fasting blood glucose and serum lipid concentrations and enhances the functionality and cellular architecture of the liver and kidney in rats with diabetes. The data also showed that TFDG mitigates oxidative harm in the liver and kidney of rats afflicted with diabetes. Additionally, metformin combined with TFDG was significantly more effective in reducing blood glucose and oxidative stress. Further studies suggested that TFDG upregulates the Nrf2 signal pathway and circ-ITCH (hsa_circ_0001141) expression. Silencing of circ-ITCH by transfection of the interfering plasmid apparently reduces the effects of TFDG on the Nrf2 signal pathway and oxidative stress in high-glucose-treated hepatic and renal cells. In conclusion, the present study highlights the great potential of TFDG in ameliorating diabetic liver and kidney injury by up-regulating circ-ITCH to promote the Nrf2 signal pathway and provides a potential option for the prevention and treatment of diabetic complications.

Histopathological effect of Buccholzia coricea on some liver and kidneys in alloxan-induced diabetic Wistar rats

Liver and kidneys are vital organs that play several important roles such as detoxification, storage of blood, blood filtration and purification, urine excretion and secretion of hormones among others. This study was conducted to determine the histopathological effects of Buccholzia coricea on the liver and kidneys of female wistar rats, Twenty-five female wistar rats were divided into five groups of five rats per group. The five rats in group one served as the normal control group and were fed with food and water without inducement and treatment. Test group two, the positive control were induced with alloxan (150 mg/kg) without any treatment throughout the study. Test group three, the known drug group were induced with diabetes (150 mg/kg) and administered metformin daily. Test group four were induced with diabetes and were treated with low dose of 250 mg/kg of Buccholzia coriacea seed extract daily throughout the study. Test group five were induced with diabetes and were treated with high dose of 1000 mg/kg of Buccholzia coriacea seed extract daily throughout the study for 14 days and the animal models were checked daily with glucometer to ascertain their blood sugar level before the animals were sacrificed and organs harvested and preserved for histological analysis. At the end of the 14 days, hematoxylin and eosin staining methods of histological methods were used. The results of the histology of the five groups showed that group one had normal liver and kidney tissues. Group two showed cytoplasmic vacoulation and cellular infiltration of liver but an inflammation of the kidney tissue. Group three had mild sinusoidal dilation in the liver and distention of the renal tubules with reduced inflammation of the kidney tissue. Group four had cytoplasmic vacoulation of liver and reduced inflammatory activities of the kidney tissue. Group five had mild cellular degeneration of liver, hemorrhage and inflammation of the kidney tissue. Thus, Buccholzia coriacea can improve the functioning of the liver and kidneys of a diabetic rats when it is consumed below 1000mg and its equivalent daily by mitigation of the histopathological alterations by alloxan-induced diabetes. Buccholzia coriacea is a natural panacea in the management of diabetes-related organ damage.

Resveratrol Has Histone 4 and Beta-Defensin 1-Mediated Favorable Biotherapeutic Effects on Liver and Other Target Organs in Diabetic Rats.

It was aimed to investigate the biochemical and histopathological effects of resveratrol and melatonin, via histone H4 and β-defensin 1, in diabetic rats. Twenty-four Sprague-Dawley male rats were categorized into 4 groups, with 6 rats in each group (control, diabetes mellitus, melatonin - diabetes mellitus, and resveratrol+diabetes mellitus). Diabetes was formed by giving streptozotocin to all groups except the control group. Melatonin, 5 mg/kg/day, was given to the melatonin - diabetes mellitus group, and resveratrol, 5 mg/kg/day, was given to the resveratrol+diabetes mellitus group via intraperitoneally for 3 weeks. Interleukin-1 beta, tumor necrosis factor alpha, histone H4, and β-defensin 1 levels were measured in the blood of all rats. The lung, liver, and kidney tissue of all rats were performed as histopathological examinations. Whereas there was no difference between the other groups (P >.05), interleukin-1 beta levels of the diabetes mellitus group were found to be significantly higher compared with the control group (5.02 ± 2.15 vs. 2.38 ± 0.72 ng/mL; P < .05). Whereas histone H4 levels of the diabetes mellitus group were higher compared with the control and resveratrol+diabetes mellitus groups (7.53 ± 3.30 vs. 2.97 ± 1.57 and 3.06 ± 1.57 ng/mL; P <.05), the β-defensin 1 levels of the diabetes mellitus group were lower compared with control and resveratrol+diabetes mellitus groups (7.6 ± 2.8 vs. 21.6 ± 5.5 and 18.8 ± 7.4 ng/mL; P <.05). β-Defensin 1 levels were moderately inversely correlated with interleukin-1 beta and histone H4 levels (rs > -0.50, P < .01). Histopathological changes found in favor of target cell damage in the diabetes mellitus group were not observed in resveratrol+diabetes mellitus group. Resveratrol may be used as a biotherapeutic agent, which significantly reduces diabetes-induced histone H4 and interleukin-1 beta-mediated liver and other target organ damage.

Antidiabetic and Antioxidant Effect of Ethanolic Extract of Propolis from Meiganga (Cameroon) on Type 2 Diabetes in Rats

Diabetes mellitus is a metabolic disorder characterized by chronic hyperglycemia. In Cameroon, the traditional treatment of this pathology is based on the use of Propolis. The present study aims to evaluate the antidiabetic and antioxidant properties of the ethanoic extract of Meiganga propolis (Adamawa Region, Cameroon). To confirm the different properties of this extract, the glycaemia, lipid profile and oxidative stress parameters of different groups of animals were assessed in a type 2 diabetes model induced by the Hypercaloric Sucrose Diet combined with dexamethasone. Simultaneous administration of the ethanolic extract of Meiganga propolis (EEMP 300 mg/kg) and the hypercaloric sucrose diet to rats for 30 days prevented a significant increase in fasting blood glucose levels compared with animals in the diabetic control group, whose fasting blood glucose levels were 78.25 ± 2.29 and 156.5 ± 2.75 mg/dL respectively on day 30. In terms of lipid profile, the administration of propolis extract (300 mg/kg) prevented a significant increase in LDL-cholesterol and triglyceride levels compared with animals in the diabetic control groups. The values were 27±2.71 mg/dL and 97.8±2.92 mg/dL for LDL-cholesterol. In terms of oxidative stress, simultaneous administration of propolis extract (300 mg/kg) and a high calorie diet to rats for 30 days prevented a significant increase in malondialdehyde (MDA) and increased superoxide dismutase (SOD) levels compared with animals in the diabetic control group. Values for this superoxide dismutase in the liver were 81.72 U/g of organ for EEMP 300 mg/kg and 58.6 U/g of organ in the liver of diabetic rats. These results justify the use of ethanoic extract of Meiganga propolis in the prevention of type 2 diabetes in Cameroon.

Effects of Berberis vulgaris fruit extract on oxidative stress status in the kidney and liver of diabetic rats.

Oxidative stress has a key role in the diabetes pathogenesis and complications. Berberis vulgaris is known in folk medicine for curing several diseases. The current research aimed to assess the influences of Berberis vulgaris fruit extract against oxidative stress in streptozotocin-induced diabetic rats. Streptozotocin (60 mg/kg, ip) was injected to male rats. After diabetes confirmation, animals received the Berberis vulgaris fruit extract daily at amounts of 3.5 and 7.5 % of drinking water (v/v) for six weeks. Total thiol and lipid peroxidation levels were assessed in the serum, liver, kidney and spleen at the end of the study. Diabetic rats exhibited hyperglycemia along with enhancement of lipid peroxidation levels in the serum, liver, kidney and spleen, and decrement of total thiol content in the kidney and liver tissues. Chronic administration of Berberis vulgaris fruit extract at amount of 3.5 % of drinking water decreased the lipid peroxidation level in the serum and liver, and enhanced total thiol level in the liver and kidney. Berberis vulgaris fruit extract exerts antioxidant activity in the serum, liver and kidney organs of diabetic rats. Therefore, it might be used in the prevention and control of diabetes complications.

Effect of aminoguanidine on plasminogen activator inhibitor-1 and receptor of advanced glycation endproduct in the liver of streptozotocin-induced diabetic rats

Objectives: Advanced glycation end products (AGEs) play an important role in the development and progression of diabetic complications. The receptor for AGE (RAGE) is the ligand-binding site of AGE that initiates and accelerates the atherosclerotic process. Plasminogen activator inhibitor-1 (PAI-1) is a prothrombotic factor that has been proposed as a biological marker for prognostic assessment, monitoring of microvascular and macrovascular complications in diabetes. The purpose of this study is to investigate the effects of aminoguanidine on RAGE and PAI-1 expression levels in the liver of streptozotocin-induced diabetic rats.&#x0D; Methods: Diabetes was induced in rats by intraperitoneal injection of streptozocin (STZ, 50 mg/kg). On day 3, diabetic rats were administered 50, 100, and 200 mg/kg/day of aminoguanidine. The expression of PAI-1 and RAGE in the liver tissue was evaluated using real-time PCR.&#x0D; Results: PAI-1 and RAGE gene expression levels were higher in the liver of the diabetic rats compared to the control group. Aminoguanidine at 50, 100, and 200 mg/kg decreased PAI-1 and RAGE gene expression in the liver (p&lt;0.001 at all doses). However, these genes were downregulated only at a dose of 200 mg/kg in healthy rats (p&lt;0.0001). In addition, hepatic AGE protein levels were significantly decreased following treatment of the diabetic rats with aminoguanidine (p&lt;0.001). There was also a significant correlation between AGE protein concentration and the expression of PAI-1 and RAGE.&#x0D; Conclusion: In summary, the data of the present study suggest that aminoguanidine reduced the expression of PAI-1 and RAGE in the liver of the diabetic rats.

Antidiabetic and hepato-renal protective effects of medicinal plants in STZ induced diabetic rats.

The antidiabetic and hepato-renal protective effects of Citrullus colocynthis and Momordica charantia ethanol extracts were investigated in streptozotocin (STZ) induced diabetic male albino rats. Diabetic rats were treated with C. colocynthis, M. charantia or C. colocynthis + M. charantia mixed extract at a dose of 250 mg /kg body weight per oral per day for 21 days. The mean body weight of all the diabetic rat groups on day 1 of treatment (day 10 of diabetes) was significantly lower than the normal control rat group (P<0.05). The blood glucose level of all the diabetic rat groups on day 1 of treatment (day 10 of diabetes) was significantly (P<0.05) higher (> 200 mg/dl) than the normal control rat group (95.5 ± 2.7). At the end of treatment (day 21), the diabetic rats treated with plant extracts showed significant increase (P<0.05) in body weight and significant (P<0.05) reduction in blood glucose level when compared to diabetic control animals. Significant increase (< 0.05) was observed in the serum bilirubin, alanine transaminase (ALT), aspartate transaminase (AST), alkaline phosphatase (ALP), urea and creatinine levels of diabetic control rat group. The serum levels of these liver and kidney-related parameters of diabetic rats treated with plant extract were significantly lower when compared to diabetic control rat group (p < 0.05). Photomicrographs of liver and kidney microsections from diabetic rats treated with these plant extracts showed amelioration in the hepato-renal histoarchitectures. It was concluded that the C. colocynthis and M. charantia methanol extracts are antidiabetic and hepato-renal protective in STZ induced diabetic male rats. Treatment of the diabetic rats with C. colocynthis + M. charantia mixed extract is more effective in the amelioration of diabetes and hepato-renal injuries in STZ induced diabetic male rats.