Administration of Fenugreek Seed Extract Produces Better Effects in Glibenclamide-Induced Inhibition in Hepatic Lipid Peroxidation: An in vitro Study.

OBJECTIVE: To evaluate the comparative effects of fenugreek (Trigonella foenum graecum) seed extract (FSE) alone and in combination with an antidiabetic conventional medicine, glibenclamide (GLB), on the inhibition of in vitro lipid peroxidation (LPO) in liver, the major target organ of a drug. METHODS: LPO was induced by ferrous sulphate (FeSo4), hydrogen peroxide (H2O2) and carbon tetrachloride (CCl4) and the effects of test seed extract and/or GLB were evaluated. RESULTS: While FeSo4, H2O2 and CCl4 markedly enhanced the hepatic LPO, simultaneous administration of FSE reduced it in a concentration dependent manner. However, when both FSE and GLB were added to the incubation mixture, chemically induced hepatic LPO was further inhibited. The test extract also exhibited high antioxidative activity in 1,1-diphenyl-2-picrylhydrazyl radical and in 2,2'-azinobis, 3-ethylbenzothiazoline-6-sulphonic acid radical scavenging assays. CONCLUSION: FSE therapy in moderate concentration along with a hypoglycemic drug may prove to be advantageous in ameliorating diabetes mellitus and other diseases that are LPO mediated.

Beneficial Effect of Vitamin E in Rotenone Induced Model of PD: Behavioural, Neurochemical and Biochemical Study

Parkinson's disease (PD) a neurodegenerative disorder for which no preventive or long-term effective treatment strategies are available. Epidemiologic studies have failed to identify specific environmental, dietary or lifestyle risk factors for PD. However, oxidative stress in the SN is the most broadly accepted hypothesis for the etiopathology of PD. The Symptoms do not appear until there is a decline of striatal dopamine levels by 80% making it difficult to have early therapeutic interventions. Thus, the present experiment was designed to track down the sequential changes starting from the initiation of motor dysfunction and associated biochemical abnormality in rotenone based PD model. The study also evaluated the neuroprotective efficacy of vitamin E. Rats were treated with rotenone 2 mg/kg b.wt (s.c.) for 35 days. The level of dopamine decreased by 70~80% which was in turn reflected by marked deterioration in motor function such as (Total locomotor activity and catalepsy). Along with these the level of GSH and SOD declined significantly which was associated with elevated lipid peroxidation levels as much as by 60%.Vitamin E co-administration at a dose of 100 I.U/kg b.wt (i.m.) ameliorated rotenone induced changes in motor functions i.e Total locomotor activity and Catalepsy at the end of 5th week. Further, vitamin E supplementation significantly decreased lipid peroxidation and improved associated biochemical parameters i.e SOD and GSH level. Most interestingly the changes appeared as early as 3rd week suggesting that supplementation of vitamin E right at the beginning should be neuroprotective in PD.