Protective effect of polydatin against lipopolysaccharide-induced myocardial injury.

Objective: To observe the effect of lipopolysaccharide (LPS) on actin cytoskeleton of rat cardiac myocytes and the intervention effect of polydatin against this effect.

Methods: Rat cardiac myocytes were isolated from newborn SD rats (3 days old) and cultured in vitro, which were then divided into control group (treated with D-Hank's solution for 30 min), polydatin group (with 0.2 mmol/L polydatin treatment for 10 min), LPS group (with 100 ng/ml LPS stimulation for 30 min), and LPS/polydatin group (with 100 ng/ml LPS stimulation for 30 min followed by incubation with 0.2 mmol/L polydatin for 10 min). When the treatments were completed, the cells were analyzed for myocardial F-actin by immunofluorescent staining.

Results: In the control group, F-actin was localized in the cortex of cardiac myocytes and the cells were filled with F-actin organized into reticular structures. After LPS stimulation, the staining for F-actin was faint or even invisible in the cortex, with the formation of stress fibers observed in the cells, which disappeared upon the 10-min polydatin treatment and the F-actin resumed normal arrangement. No obvious difference was found between the control and polydatin groups.

Conclusion: LPS may directly induce stress fiber formation, therefore cause damages to rat cardiac myocytes, which can be reverted by polydatin through the mechanism of participating in the F-actin organization.