Caralluma fimbriata and metformin protection of rat pancreas from high fat diet induced oxidative stress.

A high fat diet promotes oxidative stress, which contributes to the development of pancreatic fibrosis. We compared the protective effects of a hydroalcoholic extract of Caralluma fimbriata (CFE) to metformin (Met) in the pancreas of Wistar rats fed a high fat diet. The experimental animals were divided into five groups: control (C), treated with CFE (C + CFE), treated with high fat diet (HFD), high fat diet treated with CFE (HFD + CFE), and high fat diet treated with metformin (Met) (HFD + Met). CFE was administered orally to groups C + CFE and HFD + CFE rats for 90 days. Met was given to the HFD + Met group. After 90 days, oxidative stress markers in the pancreas including reduced glutathione (GSH), lipid oxidation (LO), protein oxidation (PO), and activities of antioxidant and polyol pathway enzymes, aldose reductase (AR) and sorbitol dehydrogenase (SDH) were assayed and tissue histology was examined. Establishment of oxidative stress in high fat diet fed rats was verified by elevated LO and PO, decreased GSH, decreased activities of antioxidants and increased activities of polyol pathway enzymes. Oxidative stress was prevented in HFD + CFE and HFD + Met groups. Group C + CFE exhibited improved antioxidant status compared to group C. CFE treatment prevented high fat diet induced acinar cell degeneration, necrosis, edema and hemorrhage. CFE could be used as adjuvant therapy for preventing or managing high fat diet induced pancreatic damage.

Beneficial effects of hydro-alcoholic extract of Caralluma fimbriata against high-fat diet-induced insulin resistance and oxidative stress in Wistar male rats.

The main aim of this study was to investigate the beneficial effects of hydro-alcoholic extract of Caralluma fimbriata (CFE) on the effects of high-fat diet feeding on insulin resistance and oxidative stress in Wistar rats. High-fat diet (60% of fat) and CFE (200 mg/kg body weight/day) were given concurrently to the rats for a period of 90 days. Feeding with high-fat diet resulted in the development of hyperglycemia, hyperinsulinemia, hyperleptinemia, and hypertriglyceridemia and impaired insulin sensitivity (P < 0.05). Administration of CFE to high-fat diet-fed rats for 90 days resulted in a significant improvement in plasma glucose, insulin, leptin, and triglycerides. Regarding liver antioxidant status, high-fat fed rats showed higher levels of lipid peroxidation, protein oxidation and lower GSH levels and lower activities of enzymatic antioxidants, while CFE treatment prevented all these observed abnormalities. In conclusion, intake of CFE may be beneficial for the suppression of high-fat diet-induced insulin resistance and oxidative stress.

Ethanolic extract of Commiphora mukul gum resin attenuates streptozotocin-induced alterations in carbohydrate and lipid metabolism in rats.

The purpose of this study was to investigate the effects of Commiphora mukul gum resin ethanolic extract (CMEEt) administration against altered activities of key enzymes of carbohydrate metabolism, lipid metabolism and changes in glycogen content (liver and muscle) and lipids (liver and heart) in streptozotocin (STZ) induced insulin deficient diabetic Wistar albino rats. Diabetes was induced by intraperitoneal injection of STZ (55 mg/kg body wt) to male Wistar rats. The animals were divided into four groups: Control (C), control-treated (C+CM), diabetic (D) and diabetic-treated group (D+CM). Diabetic-treated and control-treated rats were treated with C. mukul gum resin ethanolic extract (CMEEt) in 2 ml distilled water, orally (200 mg/kg body weight/day for 60 days). At the end of the experimental period, biochemical parameters related to carbohydrate and lipid metabolism were assayed. The significant enhancement in tissue lipids (heart and liver) total cholesterol, triglycerides, phospholipids and free fatty acids of diabetic rats were nearer to normalized in diabetic treated rats (D+CM). Alterations in the activities of enzymes of glucose metabolism (hexokinase, phosphofructokinase, pyruvate kinase, and glucose-6-phosphatase, fructose-1,6-bisphosphatase and glucose-6-phosphate dehydrogenase) and lipid metabolism (fatty acid synthase, malic enzyme and lipoprotein lipase) as observed in diabetic (D) rats were prevented with CMEEt administration. In conclusion, our findings indicate improvement of glucose and lipid metabolisms in STZ induced diabetic rats by treatment with Commiphora mukul and suggest that the plant can be used as an adjuvant for the prevention and/or management of insulin deficiency and disorder related to it.

Protective effect of ethanolic extract of Commiphora mukul gum resin against oxidative stress in the brain of streptozotocin induced diabetic Wistar male rats.

The objective of the study was to investigate the possible neuroprotective effect of ethanolic extract of Commiphora mukul gum resin (EtCMGR) against oxidative stress in the brain of streptozotocin (STZ) induced diabetic Wistar rats. The experimental animals were divided into four groups: control (C), control treated with EtCMGR (C+CM), diabetic (D) and diabetic treated with EtCMGR (D+CM). Diabetes was induced by a single intraperitoneal injection of STZ (55 mg/kg body weight). Plant extract treated groups (C+CM and D+CM) were administered EtCMGR at a dose of 200 mg/kg body weight/day by gavage for 60 days. Diabetic rats showed hyperglycemia, hypoinsulinemia with impaired insulin sensitivity. EtCMGR treatment to diabetic (D+CM group) rats prevented the rise in glucose level by 96.7 %, while enhancing insulin level (77.7 %) and improving insulin sensitivity (27.3 %) compared to D group. The brain antioxidant status of D group rats showed higher levels of lipid peroxidation (77.9 %), protein glycation (100 %), and increased activities of xanthine oxidase (47.1 %) and sorbitol dehydrogenase (101.9 %) and lowered concentration of reduced glutathione (38.2 %) and decreased activities of antioxidant enzymes i.e., glutathione reductase (24 %), glutathione peroxidase (24.4 %) and superoxide dismutase (42.1 %) and increased activities of catalase (87.4 %) and glutathione-S-transferase (45.3 %) compared to control group. While EtCMGR treatment for 60 days in D+CM group prevented the observed abnormalities of antioxidant status of D group. This study demonstrates that EtCMGR is a potent neuroprotective agent against oxidative damage induced under diabetes.

Protective effects of curcumin and vitamin E on carbon tetrachloride-induced nephrotoxicity in rats.

The present investigation reports the protective effects of curcumin (CMN) and vitamin E against CCl4 induced oxidative stress and nephrotoxicity in rats. The toxicant CCl4 was used to induce nephrotoxicity at a dose of 1 ml/kg as 1:1(v/v) mixture with liquid paraffin twice weekly for 8 weeks. Plasma total protein, albumin, urea and creatinine concentrations were measured to assess the renal function. Antioxidant status in the kidney was estimated by determining the activities of glutathione peroxidase (GPx), glutathione reductase (GR), glutathione-S-transferase (GST), catalase (CAT) and superoxide dismutase (SOD) as well as by histopathological examination. CCl4 caused elevated levels of urea and creatinine while it decreased levels of total protein and albumin in plasma. Furthermore, CCl4 treated rats showed marked depletion of renal endogenous antioxidant enzymes. Oral administration of curcumin (100 mg/kg, daily for 8 weeks) and in combination with vitamin E (three times weekly for 8 weeks) showed significantly attenuated renal dysfunction by increased activity of antioxidant enzymes in kidney. It also increased the concentrations of plasma total protein and albumin, while reducing the concentration of urea and creatinine. Kidney sections of CCl4 induced rats showed deleterious alterations in micro anatomy. However, curcumin and vitamin E treatment prevented kidney damage induced by CCl4. This study reveals that curcumin in combination with vitamin E possesses strong antioxidant and kidney protective activity compared to curcumin alone.