Biochemical and Histological Effects of Moringa oleifera Extract against Valproate-Induced Kidney Damage.

Valproic acid is an effective treatment for generalized seizure and related neurological defects. Despite its efficacy and acceptability, its use is associated with adverse drug effects. Moringa oleifera leaves are rich in phytochemical and nutritional components. It has excellent antioxidant and ethnobotanical benefits, thus popular among folk medicines and nutraceuticals. In the present study, 70% ethanol extract of moringa leaves was assessed for its in vivo biochemical and histological effects against valproate-induced kidney damage. Female Sprague-Dawley rats were randomly divided into four groups: Group I: control animals given physiological saline (n = 8); Group II: Moringa extract-administered group (0.3 g/kg b.w./day, n = 8); Group III: valproate-administered animals (0.5 g/kg b.w./day, n = 15); and Group IV: valproate + moringa extract (given similar doses of both valproate and moringa extract, n = 12) administered group. Treatments were administered orally for 15 days, the animals were fasted overnight, anesthetized, and then tissue samples harvested. In the valproate-administered experimental group, serum urea and uric acid were elevated. In the kidney tissue of the valproate rats, glutathione was depleted, antioxidant enzyme activities (superoxide dismutase, catalase, glutathione reductase, glutathione S-transferase, and glutathione peroxidase) disrupted, while oxidative stress biomarker, inflammatory proteins (Tumor necrosis factor-alpha and interleukin-6), histological damage scores, and the number of PCNA-positive cells were elevated. M. oleifera attenuated all these biochemical defects through its plethora of diverse antioxidant and therapeutic properties.

Glycoprotein Levels and Oxidative Stomach Damage in Diabetes and Prostate Cancer Model: Protective Effect of Metformin.

Men with diabetes have a higher risk of prostate cancer and people with prostate cancer are prone to stomach metastases. Therefore, researchers are continuing in order to find new approaches in the treatment of individuals with both diseases at the same time. The protective effect of metformin (which is used in the treatment of diabetes) on cancer continues to be supported by studies. The present study aimed that the protective effect of metformin in the stomach tissue of diabetic and/or prostate cancer rats was investigated through biochemical parameters. In the study, it was determined that the biochemical parameters studied showed a protective effect on stomach tissues with the administration of metformin to cancer and diabetic+cancer groups, and as a result of the principal component analysis, it was determined that the biochemical parameters studied in the stomach tissue showed a correlation.

The protective effect of metformin against testicular damage in diabetes and prostate cancer model.

Individuals with diabetes have an increased risk of breast, colorectal, pancreatic and prostate cancer. Metformin, an oral biguanide used to treat diabetes, has anti-hyperglycaemic, anti-hyperinsulinemic and antioxidant activities. The effects of metformin on testicular tissue damage in cancer and diabetic + cancer rat models were evaluated histologically, immunohistochemically and biochemically. The diabetic model was produced in Copenhagen rats using a single dose of streptozotocin (65 mg/kg), while prostate cancer was induced through subcutaneous inoculation of 2 × 104 Mat-LyLu cells into the animals. At the end of the experimental period, testicular tissues with a close functional relationship to the prostate were collected. Histological evaluation found moderate to severe damage to testes following the diabetes and cancer process. Histopathological and biochemical impairments were observed in the early stage of prostate cancer, which were increased in the diabetic animals. Metformin administration reversed these injuries and provided substantial protection of the testes. In particular, metformin had protective effects on tissue damage, apoptosis, oxidative stress and antioxidant capacity. This suggests that metformin should be further investigated as a targeted protective drug against prostate cancer-related damage to the testes.

Histological and biochemical investigation of the renoprotective effects of metformin in diabetic and prostate cancer model.

BACKGROUND: Diabetes and cancer have common physiological and biochemical mechanisms. Metformin is the preferred drug of choice for the treatment of diabetes. Prostate cancer can be modeled in by injection of MAT-Lylu cells. A model of diabetes in rats is induced by streptozotocin injection. In the current study, we explored the mechanisms by which diabetes accelerates cancer, and evaluated the effects of metformin to know whether it has any impact against the damage caused by cancer and diabetic + cancer via histopathological and biochemical parameters of kidney tissue. METHODS: The experiment was carried out in rats. Groups 1-Control, 2- Diabetic, 3-Cancer, 4-Diabetic + cancer, 5-Diabetic + cancer + metformin, 6-Cancer + metformin. Metformin treatment was applied by gavage every day. The research ended on the 14th day. The collected kidney tissue sections were stained with Hematoxylin-Eosin. RESULTS: Histological evaluation showed moderate to severe damage to the kidney tissue following diabetic and cancer processess. In diabetic, cancer and diabetic + cancer groups, reduced glutathione levels, total antioxidant status, sodium/potassium-ATPase and paraoxonase1 activities were found to be significantly abated. While advanced oxidized protein products, lipid peroxidation, nitric oxide, tumor necrosis factor-alpha, reactive oxygen species levels, total oxidant status, catalase, superoxide dismutase, glutathione-related antioxidant enzymes, myeloperoxidase, and arginase activities were significantly raised. The administration of metformin reversed these defects. The outcome of the reveals that histopathological and biochemical damage in cancer and diabetes + cancer groups decreased in the groups that received metformin. CONCLUSION: In conclusion, metformin treatment can be considered an adjuvant candidate for kidney tissue in diabetes, prostate cancer and cancer therapy related damage.

Role of Exogenous Melatonin on Cell Proliferation and Oxidant/Antioxidant System in Aluminum-Induced Renal Toxicity.

Aluminum has toxic potential on humans and animals when it accumulates in various tissues. It was shown in a number of studies that aluminum causes oxidative stress by free radical formation and lipid peroxidation in tissues and thus may cause damage in target organs. Although there are numerous studies investigating aluminum toxicity, biochemical mechanisms of the damage caused by aluminum have yet to be explained. Melatonin produced by pineal gland was shown to be an effective antioxidant. Since kidneys are target organs for aluminum accumulation and toxicity, we have studied the role of melatonin against aluminum-induced renal toxicity in rats. Wistar albino rats were divided into five groups. Group I served as control, and received only physiological saline; group II served as positive control for melatonin, and received ethanol and physiological saline; group III received melatonin (10 mg/kg); group IV received aluminum sulfate (5 mg/kg) and group V received aluminum sulfate and melatonin (in the same dose), injected three times a week for 1 month. Administration of aluminum caused degenerative changes in renal tissues, such as increase in metallothionein immunoreactivity and decrease in cell proliferation. Moreover, uric acid and lipid peroxidation levels and xanthine oxidase activity increased, while glutathione, catalase, superoxide dismutase, paraoxonase 1, glucose-6-phosphate dehydrogenase, and sodium potassium ATPase activities decreased. Administration of melatonin mostly prevented these symptoms. Results showed that melatonin is a potential beneficial agent for reducing damage in aluminum-induced renal toxicity.

The role of vitamin C, vitamin E, and selenium on cadmium-induced renal toxicity of rats.

The aim of this study was to determine whether vitamin C, vitamin E, and selenium have protective effects against cadmium-induced renal toxicity of rats. Vitamin C (250 mg/kg/day), vitamin E (250 mg/kg/day), and sodium selenate (0.25 mg/kg/day) were given to rats orally for 8 days. Cadmium (2 mg/kg/day CdCl2) was given to rats intraperitoneally. Vitamin C, vitamin E, and selenium (in the same dose and time) were given 1 h prior to the administration of cadmium every day. The tissue and blood samples were taken from the rats for histological evaluation and biochemical analyses on the Day 9. Lipid peroxidation (LPO) and glutathione (GSH) determination were made in kidney tissue. In addition, urea and creatinine levels were determined in serum. The damage to the kidney tissue was moderate in the rats given cadmium. In this group, the distinctive changes in the proximal tubules were observed. Degenerative changes in kidney tissue were also observed in rats given vitamin C, vitamin E, selenium, and cadmium. LPO levels significantly increased and GSH levels decreased in kidney tissues following cadmium administration. Serum urea and creatinine levels were also increased in rats given cadmium. The administration of vitamin C, vitamin E, and selenium caused a significant decrease in LPO levels and an increase in GSH levels in the kidney of rats given cadmium. Serum urea and creatinine levels were decreased in rats given both the antioxidant and cadmium. It is concluded that vitamin C, vitamin E, and selenium showed some protective effect on the rat kidney.

Protective role of Melissa officinalis L. extract on liver of hyperlipidemic rats: a morphological and biochemical study.

In this study, the effects of Melissa officinalis L. extract on hyperlipidemic rats were investigated, morphologically and biochemically. The animals were fed a lipogenic diet consisting of 2% cholesterol, 20% sunflower oil and 0.5% cholic acid added to normal chow and were given 3% ethanol for 42 days. The plant extract was given by gavage technique to rats to a dose of 2 g/kg every day for 28, 14 days after experimental animals done hyperlipidemia. The degenerative changes were observed in hyperlipidemic rats, light and electron microscopically. There was a significant increase in the levels of serum cholesterol, total lipid, alanine transaminase (ALT), aspartate transaminase (AST) and alkaline phosphatase (ALP), a significant decrease in the levels of liver tissue glutathione (GSH), a significant increase in the levels of tissue lipid peroxidation (LPO) in this group. On the other hand, the administration of Melissa officinalis L. extract reduced total cholesterol, total lipid, ALT, AST and ALP levels in serum, and LPO levels in liver tissue, moreover increased glutathione levels in the tissue. As a result, it was suggested that Melissa officinalis L. extract exerted an hypolipidemic effect and showed a protective effect on the liver of hyperlipidemic rats.

Effects of chard (Beta vulgaris L. var cicla) on the liver of the diabetic rats: a morphological and biochemical study.

Chard (Beta vulgaris L. var cicla) is one of the medicinal herbs used by diabetics in Turkey. It has been reported to reduce blood glucose. We have investigated the effect of chard extracts on the liver by biochemical and morphological investigation. The plant extract was administered by the gavage technique to rats at a dose of 2 g/kg every d for 28 d, 14 d after experimental animals were made diabetic. In the diabetic group, some degenerative changes were observed by light and electron microscope examination, but degenerative changes decreased or were not observed in the diabetic group given chard. In the diabetic group, blood glucose levels, serum alanine, aspartate transaminase, alkaline phosphatase activities, total lipids, sialic and uric acid levels, liver lipid peroxidation (LPO), and nonenzymatic glycosylation (NEG) levels increased, while blood glutathione, body weight, and liver glutathione (GSH) levels decreased. The diabetic group given chard, serum alanine, aspartate transaminase, alkaline phosphatase activities, total lipid level, sialic and uric acid levels, blood glucose levels, and liver LPO and NEG levels decreased, but the other values increased. As a result of all the morphological and biochemical findings obtained, it was concluded that the extract of this plant has a protective effect on the liver in diabetes mellitus.

Effects of vanadyl sulfate on kidney in experimental diabetes.

The aim of this work was to investigate the biochemical and histological effects of vanadyl sulfate on blood glucose, urea, and creatinine in serum and nonenzymatic glycosylation and glutathione levels in kidney tissue of normal and streptozotocin (65 mg/kg) diabetic rats. Vanadyl sulfate was administered by gavage at a dose of 100 mg/kg. After 60 d of treatment, serum urea, creatinine, and blood glucose levels significantly increased in the diabetic group but not so in the vanadyl sulfate, which showed significantly reduced serum urea and blood glucose levels and a nonsignificant reduction of serum creatinine levels. Nonenzymatic glycosylation was increased and the glutathione level was decreased in the kidney tissue of diabetic rats. Treatment with vanadyl sulfate reversed these effects. Degenerative changes were detected in diabetic animals by electron and light microscopy. Although there are individual differences in diabetic animals given vanadium, some reduction of degenerative changes were observed.