Protection of Tanshinone IIA to Human Peritoneal Mesothelial Cells (HPMC) through Delaying Cellular Senescence Induced by High Glucose

Abstract

Background: Long-term peritoneal exposure to high glucose in the peritoneal dialysis (PD) solution may potentiate the development of peritoneal fibrosis in PD patients. The most important factor leading to peritoneal fibrosis may be injury of human peritoneal mesothelial cells (HPMC). Little is known about senescence of HPMC. It has been reported that Tanshinone IIA can ameliorate fibrosis. Whether Tanshinone IIA may delay senescence and protect HPMC against high glucose is not clear. The aim of this study is to investigate the protective role of Tanshinone IIA in senescence of HPMC induced by high glucose. Methods: HPMC were isolated and cultured with Roswell Park Memorial Institute 1640 medium containing high glucose concentrations (2.5%) and Tanshinone IIA (50 μmol/L and 100 μmol/L). The effects of high glucose and Tanshinone IIA on cellular senescence of HPMC were examined by observing cell generation, growth rate, cell cycle, positive rate of senescence-associated β-galactosidase (SA-β-gal) staining, telomere length, and expression of p16 and p21. Results: Compared with the control cells, HPMC cultured in high glucose showed decreased cell generations by four to five and suppression of growth rate, and the cell cycle was stopped at G1 phase. The positive rate of SA-β-gal staining was increased; the telomere length was shortened; and the expressions of p16 and p21 were increased. The characteristics in morphology of senescent cells appeared earlier. Tanshinone IIA may delay the process of senescence of HPMC induced by high glucose by increasing cell generations and growth rate, decreasing the rate of G1 phase and the positive rate of SA-β-gal staining, lengthening the telomere, and decreasing the expression of p16 and p21. Conclusions: Tanshinone IIA may protect HPMC through delaying cellular senescence induced by high glucose.

• Tanshinone IIA
• high glucose
• cellular senescence
• human peritoneal mesothelial cells
• peritoneal fibrosis

ACKNOWLEDGMENTS

This study was supported by the Key Science and Technology Development Program of Nanjing City of the People’s Republic of China (ZKX08026). I am grateful for my tutor, Xiangmei Chen (Department of Nephrology, General Hospital of PLA, Beijing, PR China).

Declaration of interest: The authors report no conflicts of interest. The author alone is responsible for the content and writing of the paper.