Sida cordifolia is a plant belonging to the Malvaceae family used in many ayurvedic preparations. This study aimed at assessing the effects of ethanolic extract of Sida cordifolia root on quinolinic acid (QUIN) induced neurotoxicity and to compare its effect with the standard drug deprenyl in rat brain. Rats were divided into six groups: (1) control group (2) QUIN (55 microg/100 g bwt/day) (3) 50% ethanolic plant extract treated group (50 mg/100 g bwt/day) (4) Deprenyl (100 microg/100 g bwt/day) (5) QUIN (55 microg/100 g bwt/day) + 50% ethanolic plant extract treated group (50 mg/100 g bwt/day) (6) QUIN (55 microg/100 g bwt/day) + Deprenyl (100 microg/100 g bwt/day). At the end of the experimental period a status of lipid peroxidation products, protein peroxidation product, activities of the scavenging enzymes and the activities of the inflammatory markers were analyzed. Results revealed that the lipid peroxidation products decreased and the activities of the scavenging enzymes increased significantly in the brain of the plant extract treated group, deprenyl treated group and also in the coadminstered groups. The activities of markers of inflammatory responses such as cyclooxygenase and lipoxygenase were found to be significantly increased in the QUIN treated rats and this was decreased upon the administration of plant extract and deprenyl. In short, the study revealed that 50% ethanolic extract of Sida cordifolia has got potent antioxidant and antiinflammatory activity and the activity is comparable with the standard drug deprenyl.

NFκB is a major transcription factor that controls the expression of various genes. Its activation is a complex process that can be triggered by many agents and one among them is reactive oxygen species. The aim of this study was to investigate the effect of selenium on NFκB activation in rats induced with myocardial infarction by isoproterenol (ISP). The markers of myocardial infarction showed increased activity in the serum of rats induced with ISP compared to the group that was pretreated with selenium along with ISP. Cellular selenium status was also found to be very low in the ISP-induced group of rats. The concentration of cytosolic NFκB was comparatively lower in the ISP group than in the group treated with selenium and ISP. Whereas higher levels of NFκB were found in the nuclear extract of the ISP-treated animals than in the selenium + ISP group. Elevated levels of malondialdehyde, hydroperoxides, and conjugated diens in the ISP-treated rats revealed the higher levels of oxidative stress in this group. Thus, our studies reveal the inhibitory effect of selenium in the nuclear translocation of NFκB during myocardial infarction. Histopathological studies of the heart also support the cardioprotective role of selenium.

Selenium (Se), an essential micronutrient, exerts its biological functions through selenoproteins. There are evidences that show Se to have an impact on the course and outcome of a number of etiologically inflammatory diseases. Leukotriene B(4) (LTB(4)) is an inflammatory mediator, and its production is mediated through two specific enzymes--lipooxygenase (LOX) and leukotriene A(4) hydrolase (LTA(4)H). We examined the effect of Se on LTB(4) synthesis during isoproterenol (ISP)-induced myocardial infarction (MI) in rats. Rats were divided as: control, ISP, Se, and Se + ISP. Sodium selenite was administered at dose of 8 μg/100 g/day. ISP was injected subcutaneously twice (10 mg/100 g body weight). The rats pretreated with Se had increased concentration of phospholipids and enhanced biosynthetic enzymes compared with that of ISP. The activities of phospholipases decreased on Se treatment. The level of calcium was increased in ISP group whereas, on Se treatment, it was near normal levels. Activities of LOX and expression of LTA(4)H were down-regulated in the case of Se-pretreated rats. Our study shows the anti-inflammatory mechanism of selenium during MI.

The measurement of LTB4 and TXB2 levels may therefore be useful to distinguish the chest pain leading to MI from that of non cardiac in origin and for the management of the disease.