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Background: Sodium selenite and ginsenoside Rh2 (G-Rh2) are well known for their anticancer properties and have been exploited as a new therapeutic approach. In this study, we are interested to evaluate if sodium selenite and G-Rh2 combination results in a synergistic anticancer effect that could contribute to lower systemic toxicity. Methods: We observed the synergistic antitumor effect by combination of sodium selenite and G-Rh2 on HCT-116 human colorectal carcinoma cells in vitro. Cell growth, viability, cell cycle progression and cell apoptosis, Bax/Bcl2 ratio, caspase-3 expression, reactive oxygen species (ROS) production and autophagy were evaluated. Results: The results showed that sodium selenite and G-Rh2 combination have a synergistic effect on cell growth inhibition (57%) compared with sodium selenite (25%) and G-Rh2 alone (28%) after 24h of treatment. This combination also induced G1 and S phase arrest simultaneously and increased apoptosis rate. The results also indicated that Bax/Bcl2 ratio and caspase-3 expression, known as proapoptotic factors, were increased in the presence of sodium selenite and G-Rh2 alone. However, combined drug treatment results in a more significant increase in Bax/Bcl2 ratio and caspase-3 expression (P < 0.05). In addition, this combination significantly induces a depletion of ROS production and autophagy, compared to control, sodium selenite and G-Rh2 alone (P < 0.05). Conclusion: Sodium selenite and ginsenoside Rh2 combination may be a more effective treatment for human colorectal carcinoma and is a promising chemotherapeutic approach for malignant tumors. [ABSTRACT FROM AUTHOR]

Studies have shown that electroacupuncture (EA) ameliorates learning and memory after ischemic injury. However, there have been few studies elucidating the mechanisms of EA on learning and memory in cerebral hypoperfusion. In this study, we explored the cAMP response element-binding protein (CREB) signaling pathway-mediated antiapoptotic action involved in EA-induced improvement of learning and memory. EA at GV20 and GV14 acupoints was applied in cerebral hypoperfusion rats. A Morris water maze task was performed, and the immunoreactivities of pCREB, Bcl-2, and Bax in the hippocampal CA1 area were evaluated by the Western blotting technique. Our findings indicated that (1) EA ameliorated spatial learning and memory impairment in cerebral hypoperfusion rats; (2) EA increased the immunoreactivities of pCREB and Bcl-2 and decreased the immunoreactivity of Bax; (3) intracerebroventricular administration of H89 (the inhibitor of protein kinase A) blocked EA-induced, pCREB-mediated antiapoptotic action and improved learning and memory. These results suggest that EA can ameliorate learning and memory via activation of the CREB signaling pathway in the hippocampus to attenuate apoptosis after cerebral hypoperfusion. [ABSTRACT FROM AUTHOR]