31% at 1000 μg/ml, followed by a moderate inhibition percentage and 43.41% at 500 μg/ml respectively. Hydrogen peroxide itself is not reactive, as it can sometimes be toxic to cell because it may give rise to OH radical in the cells. Addition of hydrogen peroxide to cells in culture can lead to transition metal ion dependent OH radicals mediated DNA damage. Scavenging of hydrogen peroxide by our crude endophytic extract

may be attributed to their phenolic nature, which can donate electrons to H2O2, thus find more neutralizing it to water.21 Nitric oxide scavenging activity of EEA is listed Table 4. In case of nitric oxide scavenging activity, EEA showed high activity 69.24% at 1000 μg/ml followed by a moderate activity 35.40% at 400 μg/ml. BHT and Ascorbic acid were used as the positive control. Nitric oxide is a diffusible free radical, which plays many roles as an effector molecule including neuronal signaling, and regulation of cell mediated toxicity. Nitric oxide (NO) is generated in different cell types by at least three

isoforms of NO synthase (NOS). Neuronal NOS (nNOS) and endothelial NOS (eNOS) are constitutively expressed and their enzymatic activity is Ca2+/calmodulin-dependent.22 Suppression of NO released may be partially attributed to direct NO scavenging, as the extract decreased the amount of nitrite generated from the decomposition of sodium nitroprusside in vitro. Based on the results obtained from the in vitro α-glucosidase inhibition, EEA was found Panobinostat research buy to show high activity. Hence in vivo studies were carried out using EEA on lowering maltose and sucrose levels in the blood. At 30 min after maltose load, the normal control Rolziracetam animals had shown an increase in plasma glucose level; whereas the EEA treated as well as the Acarbose treated animals had not shown any significant rise in plasma glucose level. As shown in Table 5 incubation of the EEA at different concentrations with intestinal alpha glucosidase enzyme caused an increased

activity with 83.33% inhibition when incubated at 1000 μg/ml concentration. However, the inhibitory effect was equally comparable to that of the acarbose, which is well known alpha glucosidase inhibitor. With the interesting result obtained using EEA, further in vivo study of α-glucosidase inhibition was carried out. The study reveals that there is no significant rise in the plasma glucose level. At 30 min after administration of maltose and sucrose orally, the normal control animals had shown an increase in plasma glucose level 109.79 mg/dl at 120 min; whereas the EEA treated as well as the Acarbose treated animals had not shown any significant rise in plasma glucose level. At 60 min after sucrose load, the control animals had shown an increase in plasma glucose level 118.81 mg/dl whereas the EEA treated as well as the Acarbose treated animals had not shown any rise in plasma glucose level Tables 6 and 7.