Development and evaluation of a novel herbal formula for tobacco cessation in nicotine addicted rat model

381-388Tobacco addiction is a major cause of disabilities and premature death. Numerous therapies for de-addiction are available; however, nicotine dependence and withdrawal symptoms pose problems for addicts. Here, we developed novel herbal formulations using natural plant parts and evaluated for de-addiction of nicotine. Parts of Withania somnifera (L.) Dunal, Avena sativa L., Cinnamomum cassia Blume, Acacia catechu (L.f.)Willd., Ocimum tenuiflorum L. and Glycyrrhiza glabra L. were formulated in three formulations containing alcohol extracts (AELF), aqueous extracts (WELF) and powdered herbs (PHLF). Swiss albino Wistar rats were addicted with nicotine 10 mg/kg/day for first five days and 20 mg/kg/day for next 10 days subcutaneously. Control rats were administered with 0.9% NaCl (Group VII) and addicted animals were treated with bupropion, 40 mg/kg, p.o. (Group I), rid-tobak, 200 mg/kg, p.o. (Group II), AELF, 200 mg/kg, p.o. (Group III), WELF, 200 mg/kg, p.o. (Group IV), PHLF, 200 mg/kg, p.o. (Group V), 0.5% sodium carboxymethyl cellulose, p.o. (Group VI) for 15 days. The animals were subjected to Y-maze test, swimming endurance test, behavioural studies on Day 0, 1, 6, 11 and on Day 16 after withdrawal of nicotine. On Day16, brain dopamine and serum cortisol levels were measured. Rats treated with AELF and PHLF showed significant improvement in behavioural parameters, increased brain dopamine level and decreased serum cortisol levels thus being a promising choice for tobacco cessation

Semaphorin 3A Suppresses Tumor Growth and Metastasis in Mice Melanoma Model

<div><h3>Background</h3><p>Recent understanding on cancer therapy indicated that targeting metastatic signature or angiogenic switch could be a promising and rational approach to combat cancer. Advancement in cancer research has demonstrated the potential role of various tumor suppressor proteins in inhibition of cancer progression. Current studies have shown that axonal sprouting inhibitor, semaphorin 3A (Sema 3A) acts as a potent suppressor of tumor angiogenesis in various cancer models. However, the function of Sema 3A in regulation of melanoma progression is not well studied, and yet to be the subject of intense investigation.</p> <h3>Methodology/Principal Findings</h3><p>In this study, using multiple <em>in vitro</em> and <em>in vivo</em> approaches we have demonstrated that Sema 3A acts as a potent tumor suppressor <em>in vitro</em> and <em>in vivo</em> mice (C57BL/6) models. Mouse melanoma (B16F10) cells overexpressed with Sema 3A resulted in significant inhibition of cell motility, invasiveness and proliferation as well as suppression of <em>in vivo</em> tumor growth, angiogenesis and metastasis in mice models. Moreover, we have observed that Sema 3A overexpressed melanoma clone showed increased sensitivity towards curcumin and Dacarbazine, anti-cancer agents.</p> <h3>Conclusions</h3><p>Our results demonstrate, at least in part, the functional approach underlying Sema 3A mediated inhibition of tumorigenesis and angiogenesis and a clear understanding of such a process may facilitate the development of novel therapeutic strategy for the treatment of cancer.</p> </div