The stem bark extracts of Bauhinia rufescens Lam. (Fabaceae) yielded 6-methoxy-7-methyl-8-hydroxydibenz[b,f]oxepin, alpha-amyrin acetate, beta-sitosterol 3-O-beta-D-xylopyranoside, 4-(2'-Hydroxyphenethyl)-5-methoxy-2-methylphenol, menisdaurin and sequoyitol. Their structures were determined using spectroscopic methods and comparisons with the literature data. For the antimicrobial assay Gram-positive and Gram-negative bacterial and fungal strains were tested, while the tyrosinase inhibition assay utilized L-DOPA as a substrate for the tyrosinase enzyme. 6-Methoxy-7-methyl-8-hydroxydibenz[b,f]oxepin, a-amyrin acetate, beta-sitosterol 3-O-D-xylopyranoside, menisdaurin and sequoyitol showed weak to moderate activities with minimum inhibition concentration (MIC) values in the range of 112.5-900 microg/mL against all bacterial strains, while the MIC values for the fungal strains were in the range of 28.1-450 microg/mL. In the tyrosinase inhibition assay, a-amyrin acetate was found to be moderately active against tyrosinase with an inhibition of 62% at 0.1 mg/mL. This activity was lower than that of the positive control, kojic acid (85%).
The aim of the study was to evaluate the protective activity of D-Pinitol against carbon tetrachloride (CCl4)-induced hepatotoxicity in rats. The animals were divided into six groups, with each group consisting of six animals. Group I animals served as normal controls and received olive oil vehicle (1.0 ml/kg body weight intraperitoneally). Group II rats served as CCl4 controls, which received 30% CCl4 suspended in olive oil (3.0 ml/kg body weight intraperitoneally) twice a week for 4 weeks. Group III rats were treated with 30% CCl4 suspended in olive oil (3.0 ml/kg body weight intraperitoneally) twice a week for 4 weeks, followed by D-Pinitol (100 mg/kg body weight) given for 28 days intragastrically. Group IV rats received D-Pinitol alone at a concentration of 100 mg/kg body weight for 28 days intragastrically. At the end of the experimental period, serum marker enzymes and lipid peroxidation (LPO) levels were significantly increased in group II animals. On the other hand, D-Pinitol treatment significantly decreased marker enzymes and LPO levels and increased the antioxidant level. CYP expression was also investigated. Therefore, the present study revealed that D-Pinitol acts as a protective agent by decreasing metabolic activation of xenobiotics through its antioxidant nature.
Phylligenine, together with quebrachitol, stigmasterol and two aporphine alkaloids--oxoputerine and liriodenine--were isolated from the twigs of Mitrephora vulpina C.E.C. Fisch. They were evaluated for their ability to inhibit platelet activating factor (PAF) receptor binding to rabbit platelets using 3H-PAF as a ligand and their antiplatelet aggregation effect in human whole blood induced by arachidonic acid (AA), collagen and adenosine diphosphate (ADP). Of all the compounds tested, phylligenin and quebrachitol exhibited potent and concentration-dependent inhibitory effects on PAF receptor binding, with IC(50) values of 13.1 and 42.2 µM, respectively. The IC(50) value of phylligenin was comparable to that of cedrol (10.2 µM), a potent PAF antagonist. Phylligenin also showed strong dose-dependent inhibitory activity on platelet aggregation induced by AA and ADP.
Breast cancer is the most prevalent malignant neoplasm in the world, and chemoprevention through dietary intervention strategy is an emerging option to reduce the incidence. D-pinitol (DP), a major component of soya bean, possesses attractive biological actions. We have investigated whether D-pinitol have an effect on tumor growth in vivo against 7,12-dimethylbenz(a)anthracene (DMBA)-initiated rat mammary carcinogenesis and investigated its mechanism of action. Tumors were induced in Sprague-Dawley (SD) rats by a gastric dose of 20 mg/kg DMBA, and after 13 weeks of induction period, the rats were orally administered with D-pinitol for 45 days. At the end of the assay, animals in carcinogen control group prompted a tumor incidence of 100 % and developed a tumor volume of 8.35 ± 0.56, which was significantly reduced to 5.74 ± 0.32 for the animals treated with D-pinitol. The D-pinitol treatment not only decreased the tumor volume but also further examination revealed that tumors from animals that received D-pinitol reduced nuclear factor kappa B (NF-κB) activation which in turn results in modulation of its downstreaming p53 and proteins of caspase-3 family. Bcl-2 expression and caspase-3 activation were also decreased after D-pinitol supplementation leading to induction of apoptosis and finally cell death. Furthermore, the status of the inflammatory cytokines such as tumor necrosis factor-α (TNF-α), interleukin (IL)-2, IL-6, and tumor markers, lipid profile, and hormones was also significantly declined up on D-pinitol administration. Thus, it reveals the collective involvement of the above-mentioned parameters along with NF-κB signaling through which D-pinitol induces apoptosis and subsequently suppresses breast cancer during DMBA-induced rat breast carcinogenesis.