Present investigation evaluates the anti tumor activity of stachydrine by inhibiting histone diacetylase enzyme in gastric cancer. Gastric cancer was induced by chronic administration of 1-Methyl-3-nitro-1- nitrosoguanidine (MNNG) for 40 weeks. Thereafter rats were treated with stachydrine (5 and 10 mg/kg, IP) for 8 week. Antitumor activity was assessed at the end of protocol by estimating lactate dehydrogenase (LDH) concentration in the serum and Cell cycle, apoptosis ratio, HDAC activity, expression of acetylated H3&4 proteins, markers of oxidative stress [superoxide dismutase (SOD) & glutathione peroxidase (GSH-Px)], cytokines and histopathological study of gastrointestinal tissues was also done in MNNG induced gastric cancerous rats. There were significantly (p<0.01) decreases the concentration of LDH in serum of stachydrine treated rats compared to MNNG induced gastric cancerous rats. It was observed that alteration in the cell cycle and apoptosis in the gastrointestinal tissues with the stachydrine treatment compared to cancerous rats. Moreover, activity of HDAC, markers of oxidative stress and level of cytokine significantly (p<0.01) decreases in the gastrointestinal tissues of stachydrine treated rats compared MNNG induced gastric cancerous rats. Histopathology of gastric tissue suggested that stachydrine treatment reverse the hyperplasia, metaplasia in MNNG induced gastric cancerous rat. Present study concludes that stachydrine ameliorates the gastric cancer induced MNNG in rats on the virtue of its HDAC inhibition activity.