Flavanoid rich ethyl acetate fraction of Musa paradisiaca inflorescence down-regulates the streptozotocin induced oxidative stress,hyperglycaemia and mRNA levels of selected inflammatory genes in rats

Musa paradisiaca inflorescence is a commonly used vegetable. The purpose of this study was to evaluate the antioxidant; hypoglycaemic and anti-inflammatory activities of flavanoid rich fraction of M. paradisiaca inflorescence (MPIF) in streptozotocin (STZ) induced diabetes mellitus. Diabetic rats were treated with MPIF (200 mg/kg body weight/day) for 60 days. Diabetic rats showed significant (p < 0.05) increase in blood glucose, HbA₁C and lipid peroxidation products (LPO) and reduction in the activities of antioxidant enzymes in liver. The activities of inflammatory markers COX-2 and 5-LOX in monocytes and mRNA expressions of NF-κB, TGF-β₁, TNF-α and IL-6 in liver were significantly (p < 0.05) increased in diabetic group. In addition, the histopathological analysis of liver showed that severe steatosis and inflammation in diabetic group. But all these parameters were significantly (p < 0.05) reduced to near normal level and restored the histopathological alterations in MPIF treated group. In addition, HPLC and ESI-MS analysis of MPIF revealed that the presence of gallic acid (4.49 g%), quercetin (1.13 g%) and epicatechin. This indicates that the supplementation of MPIF may be beneficial as food supplement for the prevention or attenuation of diabetic complications.     

Reactive oxygen species may influence the heat shock response and stress tolerance in the yeast Saccharomyces cerevisiae

Moderate levels of reactive oxygen species (ROS) have been implicated as second messengers in a number of biochemical pathways, and in animal cells have been associated with the activation of the heat shock response (HSR). Here, using an intracellular probe, we demonstrate that differential accumulation of ROS in the yeast Saccharomyces cerevisiae is strongly associated with differential induction of an HS reporter gene over a range of heat shock temperatures. There was a good correlation between cellular ROS levels and the levels of HS-induced reporter gene expression between 37 degrees C and 44 degrees C, both reaching maximal values at 41 degrees C. Furthermore, the addition of 150 microM H2O2 to the yeast cells during heat treatment resulted in a 3 degrees C decrease in the temperature required for maximal induction of the HS expression vector--an increased HS sensitivity that corresponded to a concomitant increase in ROS levels at these lower HS temperatures. Conversely, cells treated with 10 mM of the antioxidant ascorbic acid required a temperature that was 2 degrees C above that required in untreated controls for maximal induction of the HS expression vector. This decreased HS sensitivity corresponded to a decrease in ROS levels at these higher HS temperatures. Finally, cell viability assays reveal that intrinsic thermotolerance remains high in control cells despite concomitant decreases in HS-reporter gene expression and ROS accumulation between 41 degrees C and 44 degrees C. We conclude that the sensitivity of the yeast HSR is strongly associated with ROS accumulation, and suggest that ROS-mediated signalling ensures cooperation between the HS and the antioxidant responses.