Effect of ceramide on peritoneal mesothelial cells apoptosis induced by peritoneal dialysis solution
10.3760/cma.j.issn.1001-7097.2012.07.012
- VernacularTitle:神经酰胺在葡萄糖腹膜透析液诱导的腹膜间皮细胞凋亡中的作用
- Author:
Tianfeng TANG
;
Bin WANG
;
Miao ZHANG
;
Chunming JIANG
;
Cheng SUN
- Publication Type:Journal Article
- Keywords:
Peritoneal dialysis;
Apoptosis;
Ceramides;
Peritoneal mesothelium cells
- From:
Chinese Journal of Nephrology
2012;28(7):553-557
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveToexploretheeffectof ceremideonprocess of peritoneal mesothelial cells(PMCs) apoptosis induced by peritoneal dialysis solution(PDS).Methods PMCs were cultured with normal DMEM,1.5％ PDS and 4.25％ PDS.4.25％ mannitol was used as high osmotic pressure control.Ceremide were detected by LC-MS-MS.Flow cytometry was used in apoptosis analysis.Bax,p53 and bcl-2 protein expressions were detected by Western blotting.Results (1) PDS caused the increase of intracellular ceremide in PMCs,and normal and high osmotic pressure controls had no such effect.As the acidic sphigomyelinase inhibitor,desipramine significantly inhibited the production of ceramide induced by 4.25％ PDS [(56.08±12.24) μg/L vs (91.25:t:15.89) μg/L,P＜0.01]. (2) Compared with 1.5％ PDS,4.25％ PDS stimulated PMCs apoptosis (26.65％±6.21％ vs 4.04％±1.86％,P＜0.01),up-regulated bax and p53 proteins expression (P＜0.01),and down-regulated bcl-2 protein exprssion(P＜0.05).Desipramine obviously inhibited the apoptosis induced by 4.25％ PDS,decreased bax and p53 proteins expression,increased bcl-2 protein expression(P＜0.05).Exogenous C2-ceremide reversed the effect of desipramine(P＜0.05).Conclusion The increase of intracellular ceremide may play an important role in the PMCs apoptosis induced by high glucose PDS.
