ABSTRACT
Lead (Pb) poisoning is an environmental substance that accumulates in the hepato-renal tissue, which is hazardous to health, while Anacardium occidentale L. is a tropical herb used to treat oxidative stress and inflammatory diseases. The aim of this study was to investigate the antagonistic effect of Anacardium occidentale leaf extract on lead acetate exposure-induced hepatorenal toxicity in rats. Thirty-six adult Wistar rats were split into six equal groups (n = 6). Group I served as a control, and groups II and III were administered lead acetate (50 mg/kg) and Anacardium occidentale leaf extract (400 mg/kg), respectively, while rats in groups IV-VI were administered Anacardium occidentale (L) extract (200 mg/kg and 400 mg/kg) and 10 mg/kg of Succimer, respectively, and were then administered lead acetate (50 mg/kg). When compared to the group I, rats administered lead acetate showed an increase in hepatic enzymes, urea, creatinine, MDA, TNF-α, and IL-1ß (p < 0.001) levels and decreased levels of SOD, CAT, and GSH, whereas Anacardium occidentale prevented the increase in hepatorenal function parameters, oxidative stress, and inflammatory markers (TNF-α and IL-1ß) induced by lead acetate. Rats administered only lead acetate had a marked increase in hepatic Pb concentration, severe hepatic steatosis, and renal glomerulus degeneration. However, treatment with Anacardium occidentale extract and succimer decreases the Pb concentration, oxidative stress, and inflammation, and also reduces histological liver steatosis and glomerular cytoarchitecture deterioration in the kidney. The results of this study revealed that Anacardium occidentale extract protects against lead acetate-induced liver and kidney toxicity by decreasing oxidative stress and inflammation.
ABSTRACT
Purpose: The purpose of the study was to determine how camel milk affects hyperglycemia, beta-cell function, oxidative stress, and inflammatory markers in type 2 diabetic pigs. Methods: Twenty-five (25) pigs were separated into five (5) groups of five pigs each, with five (5) non-diabetic and twenty (20) diabetic pigs in each group. Groups 1 and 2 received distilled water as the standard control and diabetic control groups, respectively, while Groups 3 and 4 received camel milk at 250 mL/day and 500 mL/day, respectively, and Group 5 received metformin at 500 mg/day. The experiment lasted ten weeks. At the end of the ten weeks, all the pigs were euthanized. Results: Treatments with camel milk substantially enhance glucose fasting levels by reducing hyperglycemia in diabetic pigs, significant level at (p < 0.05). When pigs given camel milk were compared with untreated diabetic pigs, there was a substantial rise (p < 0.05) in superoxide dismutase (SOD), catalase (CAT), and reduced glutathione (GSH) levels. Also, camel milk substantially lowered the levels of interleukin (IL-1ß) and tumour necrosis factor-alpha (TNF-α) in diabetic pig serum. Similarly, immunohistochemical analysis of islet cells revealed an increase in insulin production, implying improved glycemic control and the eventual commitment of glucose to glycolysis. Conclusion: The bioactive-mediated anti-hyperglycemic and insulin release potential of camel milk treatments contributed to improving type 2 diabetes mellitus. Camel milk improved beta-cell function while reducing oxidative stress and inflammation in type 2 diabetic pigs.
ABSTRACT
Mercury chloride (HgCl2) is a neurotoxicant that remains a health hazard despite numerous efforts to reduce its levels in the environment. The use of medicinal plants in treating various diseases and other toxic agents has grown popular owing to their effectiveness and affordable rates. Andrographis paniculata (A. paniculata) is a plant with astringent and detoxifying characteristics and is widely used worldwide for its medicinal and antioxidant benefits. This study aimed to investigate the possible protective effects of A. paniculata aqueous extract against HgCl2-induced memory impairment, oxidative stress, and brain damage. Twenty-five adult Wistar rats were randomly divided into five groups: control, HgCl2 0.5 mg/kg, HgCl2+AP 250 mg/kg, HgCl2+AP 500 mg/kg, or HgCl2+Ascorbic acid 200 mg/kg. For 28 days, administrations were given through oral gavage once a day. HgCl2 injection resulted in memory impairment, increased glutamate concentrations in the brain, and the production of oxidative stress. Memory impairment was prevented in A. paniculata-treated groups by balancing the levels of AChE and dopamine activities, which then lowered glutamate concentration, avoided oxidative stress, and improved histopathological alterations in the brain. A. paniculata alleviated HgCl2-induced memory impairment in Wistar rats by increasing the memory index, regulating neurotransmitter levels, and reducing oxidative stress.
ABSTRACT
Type 2 diabetes occurs as a result of insulin resistance and dysfunction in insulin signaling. Controlling hyperglycemia and activation of insulin signaling are important in the management of type 2 diabetes. This study aimed to evaluate the effect of genistein and Momordica charantia L. fruit (MCF) on oxidative stress, markers of inflammation, and their role in proglucagon and insulin receptor messenger RNA (mRNA) expression by real-time PCR in diabetic rats. Thirty-five albino rats were divided into 7 groups (n = 5). Group I (non-diabetic) and group II (diabetic control) were treated with distilled water, and groups III and IV received 250 mg/kg and 500 mg/kg lyophilized MCF, respectively. Groups V and VI received 10 mg/kg and 20 mg/kg genistein, respectively, while group VII received 500 mg/kg metformin. The administration lasted for 28 days. MCF and genistein significantly reduced interleukin (IL)-1ß and tumor necrosis factor alpha (TNF-α) levels, which were elevated in the serum of diabetic rats. Treatment with MCF and genistein significantly increased the expression of proglucagon mRNA in the small intestine and insulin receptor mRNA in the liver of diabetic rats. In conclusion, MCF and genistein ameliorate type 2 diabetes complications by preventing the loss of insulin-positive cells, inhibiting IL-1ß and TNF-α, and upregulating proglucagon and insulin receptor mRNA expression. Novelty: MCF and genistein have an inhibitory effect on diabetic induced IL-1ß and TNF-α production. MCF and genistein upregulate proglucagon and insulin receptor mRNA expression.
ABSTRACT
PURPOSE: The present study was aimed at evaluating the role of Momordica charantia L. fruit and Genistein on beta cell, insulin resistance/sensitivity and lipid profile in type 2 diabetic rats. METHODS: Thirty-five (35) albino rats were divided into seven (7) groups of 5 rats each comprising of five (5) non-diabetic and thirty (30) diabetic rats. Groups 1 and 2 served as the normal control and diabetic control groups respectively and received distill water, groups 3 and 4 received Mormodica charantia L. at 250 mg/kg and 500 mg/kg respectively. Groups 5 and 6 received Genistein at 10 mg/kg and 20 mg/kg respectively while group 7 received Metformin at 500 mg/kg the experiment lasted for four weeks. All the rats were euthanized at the end of the fourth week. RESULTS: Lipid profile, glucose and insulin levels were determined from the analysis of serum parameters and the histology of the pancreas. A significant reduction (p < 0.05) in blood glucose levels was noticed in rats that received Momordica charantia L. (MC) and genistein when compared with diabetic control rats. A significant decrease (p < 0.05) in cholesterol, triglyceride, low density lipoprotein (LDL) and very low density lipoprotein (VLDL) levels were also noted in rats that received MC and Genistein when compared with the diabetic control rats. MC and Genistein significantly increased (P < 0.05) serum insulin level compared to the diabetic control rats. MC and Genistein significantly decreased (p < 0.05) homeostatic model assessment-insulin resistance (HOMA-IR) level compared with the diabetic control group. Pancreas of rats that received MC and Genistein showed regenerating beta-cells. CONCLUSION: Momordica charantia L. fruit and Genistein were able to enhance beta cell function and prevent lipid accumulation and insulin resistance in type 2 diabetic rats.
ABSTRACT
OBJECTIVES: The objective of this study was to evaluate the therapeutic effects of balanitoside in diabetic rats. METHODS: Twenty-five rats were divided into five groups. Rats in groups 2 to 5 were treated with streptozotocin to induce hyperglycemia. In addition, rats in groups 1 and 2 received 1 mL of distilled water, whereas those in groups 3, 4, and 5 received 10 and 20 mg/kg balanitoside and 6 U/kg insulin, respectively, for 14 days. All rats were sacrificed on day 15, blood samples were collected, and serum levels of alkaline phosphatase (ALP), alanine aminotransferase (ALT), and aspartate aminotransferase (AST) were measured. The liver was processed for examination under a light microscope. RESULTS: The results showed a significant decrease in liver protein concentrations in diabetic control rats, compared to those in the normal control rats and rats treated with 10 mg/kg balanitoside (p < 0.05). There was no significant difference in ALP levels among all groups. However, a significant increase in ALT and AST levels was observed in the diabetic control rats, compared to those in the normal control rats (p < 0.05). Photomicrographs of the liver of the diabetic control rats showed fat and glycogen droplets, vacuolated nuclei, and loss of cellular boundaries, whereas those of the rats treated with balanitoside or insulin showed a small amount of microvesicular fat droplets and slight infiltration of lymphocytes. CONCLUSION: The findings of this study suggest the therapeutic effects of balanitoside in the liver of diabetic rats.
