Swati N. Desai

Hepatoprotective potential of polyphenol rich extract of Murraya koenigii L.: an in vivo study.

The present study investigates hepatoprotective effects of polyphenol rich Murraya koenigii L. (MK) hydro-ethanolic leaf extract in CCl(4) treated hepatotoxic rats. Plasma markers of hepatic damage, lipid peroxidation levels, enzymatic, and non-enzymatic antioxidants in liver and histopathological changes were investigated in control and treated rats. MK pretreated rats with different doses (200, 400 and 600mg/kg body weight) showed significant decrement in activity levels of alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, total protein, and bilirubin. Also, MK treated rats recorded a dose dependent increment in hepatic super oxide dismutase, catalase, reduced glutathione and ascorbic acid and, a decrement in lipid peroxidation. Microscopic evaluations of liver revealed CCl(4)-induced lesions and related toxic manifestations that were minimal in liver of rats pretreated with MK extract. These results demonstrate that hydro-ethanolic leaf extract of MK possesses hepatoprotective potentials.

Cardio protective effect of Coriandrum sativum L. on isoproterenol induced myocardial necrosis in rats.

The preventive effect of Coriandrum sativum L. (CS) on cardiac damage was evaluated by Isoproterenol (IP) induced cardiotoxicity model in male Wistar rats. Rats were pretreated with methanolic extract of CS seeds at a dose of 100, 200 or 300 mg/kg orally for 30 days and they were subsequently administered (s.c.) with IP (85 mg/kg body weight) for the last two days. IP treated rats showed increased LPO, decreased levels of endogenous antioxidants and ATPases in the cardiac tissue together with increased plasma lipids and markers of cardiac damage. TTC staining showed increased infarct areas while HXE staining showed myofibrillar hypertrophy and disruption. CS (200 and 300 mg/kg body weight) pretreatment significantly prevented or resisted all these changes. Our results show that methanolic extract of CS is able to prevent myocardial infarction by inhibiting myofibrillar damage. It is also concluded that, the rich polyphenolic content of CS extract is responsible for preventing oxidative damage by effectively scavenging the IP generated ROS.

Coriandrum sativum L. seed extract mitigates lipotoxicity in RAW 264.7 cells and prevents atherogenic changes in rats.

This study was designed to assess the efficacy of Coriandrum sativum L. (CS) in preventing in vitro low density lipoprotein (LDL) oxidation mediated macrophage modification. Further, an in vivo study was also conducted to confirm upon the efficacy of CS seed extract in alleviating pathophysiological alterations of high cholesterol diet induced atherosclerosis in rats. Copper mediated cell free oxidation of LDL accounted for elevated indices of malondialdehyde (MDA), lipid hydroperoxide (LHP)and protein carbonyl (PC) and a progressive increment in conjugate diene (CD) levels whereas, reverse set of changes were recorded in presence of CS extract. Cell mediated LDL oxidation (using RAW 264.7 cells) accounted for lowered MDA production and oxidized LDL (Ox-LDL) mediated cell death in presence of CS extract and the same was attributed to its potent antioxidant and free radical scavenging potentials. High cholesterol fed atherogenic rats showed elevated lipid indices, evidences of LDL oxidation, plaque formation in thoracic aorta. The same was further validated with immunostaining of cell adhesion molecules and hematoxylin and eosin (HXE) staining. However, co-supplementation of CS to atherogenic rats recorded significant lowering of the above mentioned parameters further strengthening the claim that CS extract is instrumental in preventing onset and progression of atherosclerosis.

ACUTE AND SUB-CHRONIC TOXICOLOGICAL EVALUATION OF HYDRO-METHANOLIC EXTRACT OF CORIANDRUM SATIVUM L. SEEDS

Coriandrum sativum L. (CS) seeds are known to possess therapeutic potentials against a variety of physiological disorders. This study assesses acute and sub-chronic toxicity profile of hydro-methanolic extract of CS seeds using OECD guidelines. In acute toxicity study, mice were once orally administered 1000, 3000 and 5000 mg/kg body weight of CS extract. There were no any behavioral alterations or mortality recorded in CS treated groups. The LD50 value was more than 5000 mg/kg body weight. In the sub-chronic oral toxicity study, the animals were orally administered with CS extract (1000, 2000 and 3000mg/kg body weight) daily for 28 days whereas; vehicle control group received 0.5 % carboxy methyl cellulose. There was significant reduction in food intake, body weight gain and plasma lipid profiles of CS2 and CS3 (2000 and 3000 mg/kg body weight respectively) groups as compared to the control group. However, there were no alterations in haematological profile, relative organ weights, histology and plasma markers of damage of vital organs (heart, liver and kidney). The overall finding of this study indicates that CS extract is non-toxic up to 3000 mg/kg body weight and can be considered as safe for consumption.

Apoptotic potential of C-phycoerythrin from Phormidium sp. A27DM and Halomicronema sp. A32DM on human lung carcinoma cells

Phycobilisomes present in cyanobacteria are photosynthetic macromolecular protein complexes that are categorized into three types - phycoerythrins (high energy), phycocyanin (intermediate energy) and allophycocyanin (low energy). Structurally, they consist of α and β protein subunits and open chain tetrapyrrole prosthetic group (bilin chromophore), known for its antioxidant properties and therapeutic potential against a variety of physiological ailments. Phycoerythrins (C-PE) were purified from cyanobacterial strains Phormidium sp. A27DM and Halomicronema sp. A32DM and their respective apoptotic potentials were assessed on A549 human lung carcinoma cells. Both strains of cyanobacteria were cultured and the C-PE from each strain was extracted, quantified and characterized. C-PE accounted for a dose dependent decrement in cell viability, mitochondrial membrane potential and an increment in lactate dehydrogenase release. Higher doses of C-PE (of both strains) accounted for loss of cell viability and nuclear pycnosis. These findings were further substantiated with flow cytometry that revealed a cell arrest at G0/G1 phase and a high percentage of cells undergoing apoptosis following C-PE treatment. These results confirm the efficacy of C-PE from Phormidium sp. or Halomicronema sp. in triggering apoptotic cell death. This study is the first to report on apoptotic property of C-PE against A549 human lung carcinoma cells and warrants further studies to establish its anti-cancer potential.