ISOLATION AND CHARACTERIZATION OF SECONDARY METABOLITE FROM HABENARIA INTERMEDIA D. DON FOR SCREENING OF HEPATOPROTECITVE POTENTIAL AGAINST CARBON TETRACHLORIDE INDUCED TOXICITY IN ALBINO RAT LIVER

The purpose of the study was to isolate the coumarin glycoside constituent from the ethyl acetate fraction of tubers of Habenaria intermedia D. Don by column chromatography using the gradient elution technique. The isolated coumarin glycoside was characterized by spectral studies and screened for hepatoprotecitve potential on CCl4 induced toxicity in rat liver. The coumarin glycoside (Scopoletin) protective activity was evaluated by the assay of liver function biochemical parameters such as SGOT, SGPT, Bilirubin, total protein and histopathological studies of the liver. Results showed that the toxic effect of CCl4 was controlled significantly by restoration of the levels of serum bilirubin, proteins and enzymes as compared to the normal and standard drug Silymarin treated groups. Histology of the liver sections of the rats treated with isolated coumarin glycoside showed the presence of normal hepatic cords, absence of necrosis and fatty infiltration, which further substantiated hepatoprotecitve activity. Therefore, outcome of the present study ascertains that the isolated coumarin glycoside possesses significant hepatoprotecitve activity

The role of sulfoglucuronosyl glycosphingolipids in the pathogenesis of monoclonal IgM paraproteinemia and peripheral neuropathy

In IgM paraproteinemia and peripheral neuropathy, IgM M-protein secretion by B cells leads to a T helper cell response, suggesting that it is antibody-mediated autoimmune disease involving carbohydrate epitopes in myelin sheaths. An immune response against sulfoglucuronosyl glycosphingolipids (SGGLs) is presumed to participate in demyelination or axonal degeneration in the peripheral nervous system (PNS). SGGLs contain a 3-sulfoglucuronic acid residue that interacts with anti-myelin-associated glycoprotein (MAG) and the monoclonal antibody anti-HNK-1. Immunization of animals with sulfoglucuronosyl paragloboside (SGPG) induced anti-SGPG antibodies and sensory neuropathy, which closely resembles the human disease. These animal models might help to understand the disease mechanism and lead to more specific therapeutic strategies. In an in vitro study, destruction or malfunction of the blood-nerve barrier (BNB) was found, resulting in the leakage of circulating antibodies into the PNS parenchyma, which may be considered as the initial key step for development of disease