R. Rukkumani

Protective effects of ferulic acid on hyperlipidemic diabetic rats

Abstract.Diabetes, when uncontrolled, causes dyslipidemia often followed by atherogenic abnormalities. The present study was focused to determine whether ferulic acid (FA), a flavonoid, has any role to play in diabetes-induced dyslipidemia. Diabetes in rats was induced with streptozotocin. The levels of blood glucose and plasma triglycerides (TG), free fatty acids (FFA), cholesterol and phospholipids were elevated during diabetes. Treatment with FA significantly reduced the elevated plasma lipid and blood glucose levels; a more pronounced effect was found with low-dose ferulic acid than with high dose. Thus, our study demonstrates that ferulic acid lowers the lipid levels in diabetic rats and hence prevents further complications.

Ferulic acid, a natural protector against carbon tetrachloride-induced toxicity

The present work is aimed at evaluating the protective effect of ferulic acid (FA), a naturally occurring phenolic compound on CCl4 induced toxicity. The activities of liver markers (alanine transaminase, aspartate transaminase, alkaline phosphatase, γ‐glutamyl transferase), lipid peroxidative index (thiobarbituric acid‐reactive substances, hydroperoxides, nitric oxide, protein carbonyl content), the antioxidant status (superoxide dismutase, catalase, glutathione peroxidase and reduced glutathione) were used as biomarkers to monitor the protective role of FA. The liver marker enzymes in plasma and lipid peroxidative index in liver and kidney were increased in CCl4‐treated groups, which were decreased significantly on treatment with FA. The antioxidants, which were depleted in CCl4‐treated groups, were improved significantly by FA treatment. Administration of FA to normal rats did not produce any harmful effects. Thus our results show that FA is an effective antioxidant without any side‐effects and may be a great gain in the current search for natural therapy.

Ferulic Acid, a Natural Phenolic Antioxidant Modulates Altered Lipid Profiles During Alcohol and Thermally Oxidized Sunflower Oil Induced Toxicity

Abstract Ethanol is a powerful inducer of hyperlipidemia in both animals and humans. Lipid abnormalities seen after ethanol consumption include alterations in the levels of free cholesterol, cholesteryl esters, fatty acids, phospholipids and triacylglycerol. Intake of high fat diet along with ethanol primes the hyperlipidemic effects of ethanol. Alcohol induced disturbances in lipid pattern were found to be exacerbated when the fat is thermally oxidized. In the present communication, we have investigated the influence of ferulic acid, a naturally occurring nutritional component on alcohol and thermally oxidized sunflower oil (?PUFA) induced hyperlipidemia. To evaluate the antihyperlipidemic potential of ferulic acid (FA), we analyzed the variation in lipid profiles cholesterol, triglycerides (TG), phospholipids (PL) and free fatty acids (FFA) in plasma, liver, heart and kidney. The results showed that there was a significant elevation in the levels of cholesterol, TG and FFA in alcohol, ?PUFA, alcohol + ?PUFA administered rats, which was effectively abrogated by FA treatment. In contrast, the phospholipids were significantly decreased in liver and kidney, but increased in plasma and heart during alcohol, ?PUFA and alcohol + ?PUFA ingestion, which were positively modulated by FA. Inspite of lipid accumulation, the gain in body weight was less in alcohol, ?PUFA and alcohol + ?PUFA groups compared to control rats. FA treated groups showed a significant improvement in the weight. Thus from the results obtained, we conclude that FA effectively protects the system against alcohol and ?PUFA induced tox-icity and can be developed as a potent drug for the treatment of hyperlipidemia.

FV peptide induces apoptosis in HEp 2 and HeLa cells: an insight into the mechanism of induction.

The present study is an attempt to evaluate the antiproliferative potential of peptide (7.6 kDa) from lionfish (Pterios volitans) venom on cultured HEp2 and HeLa cells. Different dose of purified peptide (1, 2 and 4 μg/ml) at different time points (12, 24 and 36 hrs) were tested for antiproliferative index of the peptide. Among them, 2 μg/ml at 24 hrs was found to effectively inhibit cancer cell growth in vitro and did not cause any adverse effect on normal human lymphocytes. Apoptosis was examined by propidium iodide staining, confirmed by the expression of caspase-8 and caspase-3, down regulation of Bcl-2 expression and DNA fragmentation in treated cells, when compared to untreated HEp2 and HeLa cells. Thus fish venom peptide was found to selectively induce apoptosis in cancer cell.

Protective Role of a Novel Curcuminoid on Alcohol and PUFA-Induced Hyperlipidemia

Alcohol use is contributing to an unprecedented decline in life expectancy. It induces hyperlipidemia when taken at higher concentrations. Alcoholics usually after a heavy binge of alcohols take fried food items normally made up of polyunsaturated fatty acids (PUFAs). The combined ingestion of alcohol and PUFAs is considered to be dangerous and known to result in hyperlipidemic conditions. Previous studies have shown that curcumin, an active principle of turmeric (Curcuma longa), has antihyperlipidemic properties. So in the present work we have synthesized an analog of curcumin and tested the protective role of that synthetic curcuminoid on alcohol and thermally oxidized sunflower oil-induced hyperlipidemia. Male Albino rats of Wistar strain were used for the experimental study. Antihyperlipidemic activity of the synthetic curcuminoid was evaluated by analyzing the levels of lipids (cholesterol, triglycerides [TGs], phospholipids [PLs], and free fatty acids [FFAs]) in different tissues and histopathological changes in the liver. The results showed that the levels of cholesterol, TGs, and FFAs were increased significantly in alcohol, thermally oxidized sunflower oil (Δ PUFA), and alcohol + Δ PUFAs treated groups. Administration of synthetic curcuminoid effectively reduced these levels. The phospholipid (PL) levels, which were decreased in the liver and kidney and increased in the heart in the alcohol, Δ PUFA, and alcohol + Δ PUFA groups, were positively modulated by treatment with synthetic curcuminoid (CA). Our histopathological observations were also in correlation with the biochemical parameters. From the results obtained, we could conclude that the synthetic curcuminoid effectively protects the system against alcohol and Δ PUFA-induced hyperlipidemia and may become an effective therapeutic agent for the treatment of hyperlipidemia.

Effect of Curcumin and its Analogue on Lipids in Carbon Tetrachloride-Induced Hepatotoxicity: A Comparative Study

Abstract Curcumin and its analogue (bis.demethoxy curcumin analogue [BDMC-A]) were studied for their possible lipid-lowering properties in carbon tetrachloride (CCl4)-induced hepatotoxicity in rats. Carbon tetrachloride (3 ml kg−1 wk−1) administration to albino Wistar rats increased the levels of hepatic marker enzymes such as aspartate transaminase (AST), alkaline phosphatase (ALP), and γ.-glutamyl transferase (GGT) in the plasma. The levels of lipids cholesterol, triglycerides, and free fatty acids were also increased in plasma and tissues (liver, kidney, heart, and brain). Phospholipid levels increased in plasma, heart, and brain but decreased in liver and kidney. Curcumin (80 mg/kg) and BDMC-A (80 mg/kg) administration to CCl4-treated rats for a period of 3 months significantly decreased the lipid levels. The effect exerted by BDMC-A was more prominent than that of curcumin. Studies on the histopathology of the liver are also in line with the biochemical parameters studied. These observations show the lipid-lowering efficacy of curcumin and its analogue in CCl4-induced hepatotoxicity.

Role of Cuminum cyminum on Ethanol and Preheated Sunflower Oil Induced Lipid Peroxidation

ABSTRACT Alcohol is a neurotoxin associated with significant mortality and morbidity. Ethanol is found to induce a dose-dependent increase in lipid peroxidation. The elevation in lipid peroxidative products and the loss of antioxidant defense potential are enhanced when alcohol is consumed along with polyunsaturated fatty acids. The present study evaluated the effect of Cuminum cyminum on lipid peroxidation induced by ethanol and preheated (to oxidize) sunflower oil. Hepatotoxicity, assessed by the activities of plasma aspartate transaminase (AST), alkaline phosphatase (ALP), and γ-glutamyl transferase (GGT), was apparent in rats fed alcohol and preheated oil as compared with control rats on a normal diet. The toxicity was associated with lipid peroxidation and a disruption in the antioxidant defense mechanism, as evidenced by increased levels of thiobarbituric acid reactive substances (TBARS), hydroperoxides, and free fatty acids (FFA) in the liver; decreased levels of glutathione, vitamin C, and vitamin E in the liver and kidney; and decreased activities of superoxide dismutase (SOD), catalase and glutathione peroxidase (GPx) in the liver. Treatment with cumin significantly reversed the metabolic trends associated with alcohol and preheated sunflower oil, bringing liver and kidney activities close to normal levels, indicating antioxidant properties of cumin.