Original Article4-Guanidino-n-butyl Syringate (Leonurine, SCM 198) Protects H9c2 Rat Ventricular Cells From Hypoxia-induced ApoptosisLiu, Xin-hua PhD*; Chen, Pei-fang BS†; Pan, Li-long PhD*; Silva, Ranil De§; Zhu, Yi-zhun MD, PhD*‡Author Information From the *Departments of Pharmacology and †Biochemistry, School of Pharmacy and Institute of Biomedical Sciences, Fudan University, Shanghai, China; ‡Department of Pharmacology, National University of Singapore, Singapore; and §Department of Anatomy, University of Sri Jayewardenepua, Sri Lanka. Received for publication February 23, 2009; accepted July 20, 2009. Supported by a grant from the Major Subject (No. 06DZ19709) and PuJiang Talent Project (No. 06PJ14018) of the Science and Technology Commission of Shanghai Municipality in China. The authors report no conflict of interest. Reprints: Prof Yi-Zhun Zhu, PhD, School of Pharmacy, Fudan University, Shanghai, China (e-mail: firstname.lastname@example.org). Journal of Cardiovascular Pharmacology: November 2009 - Volume 54 - Issue 5 - p 437-444 doi: 10.1097/FJC.0b013e3181bae160 Buy Metrics Abstract In the present study, we examined the ability of a chemically synthesized compound based on the structure of leonurine, a phytochemical component of Herba leonuri, to protect H9c2 rat ventricular cells from apoptosis induced by hypoxia and serum deprivation, as a model of ischemia. The results revealed a concentration-dependent increase in cell viability associated with leonurine treatment, accompanied by a consistent decline in lactate dehydrogenase leakage into the culture medium. The fraction of annexin V-fluorescein isothiocyanate-positive cells was increased by hypoxia but reduced by leonurine. These changes were associated with increased expression of the antiapoptotic gene, Bcl-2, and reduced expression of the proapoptotic gene, Bax. Leonurine also reduced the cytosolic Ca2+ overload induced by hypoxia. These results suggest that leonurine elicits potent cardioprotective effects in H9c2 cells, and these effects may be mediated by inhibition of intracellular Ca2+ overload and apoptosis during hypoxia. © 2009 Lippincott Williams & Wilkins, Inc.