PMID- 18167242 OWN - NLM STAT- MEDLINE DCOM- 20080630 LR - 20181201 IS - 0376-2491 (Print) IS - 0376-2491 (Linking) VI - 87 IP - 38 DP - 2007 Oct 16 TI - [Influence of atorvastatin on the expression of monocyte chemoattractant protein-1 in peritoneal mesothelial cells by high glucose]. PG - 2677-80 AB - OBJECTIVE: To investigate the influence of atorvastatin (ATOR) on the expression of monocyte chemoattractant protein-1 (MCP-1) induced by high concentration glucose in peritoneal mesothelial cells (PMCs) and the possible mechanism thereof. METHODS: Rt PMCs were isolated, cultured, passaged, and divided into 3 groups: (1) treated with glucose of the concentrations of 0.1, 1.5, 2.5, 4.25% respectively, (2) treated with 1.5% glucose for 0, 0.5, 1, 3, 12, 24, and 48 h respectively, (3) pretreated with ammonium pyrrolidinedithiocarbomate (PDTC) of the concentrations of 5, 10, 25, or 50 micromol/L for 2 h, and then treated with 1.5% glucose for 3 h; and (4) pretreated with ATOR of the concentrations of 0.1, 1, or 10 mmol/L for 24 h, and then treated with 1.5% glucose for 3 h. Western blotting was used to measure the expression of MCP-1, p65, and inhibitor of nuclear factor-kappaBalpha (IkappaBalpha). RT-PCR was used to measure the expression of MCP-1 mRNA. RESULTS: PMCs expressed MCP-1 in the normal condition. Glucose dose- and time-dependently reduced the protein expression of IkappaBalpha in the PMCs and increased the p65 expression in the nucleus, and accelerated the PMCs to express MCP-1 mRNA and protein (P < 0.05 and P < 0.01). PDTC dose-dependently inhibited the acceleration of expression of MCP-1 mRNA and protein in the PMCs induced by high concentration glucose (P < 0.05 or P < 0.01). ATOR dose-dependently increased the IkappaBalpha expression, decreased the p65 expression in nucleus, and decreased the expression of MCP-1 mRNA and protein (P < 0.05 or P < 0.01). CONCLUSION: High concentration glucose induces PMCs to express MCP-1 in a time- and dose-dependent manner. Nuclear factor- kappaB (NF-kappaB) takes part in this regulation. ATOR inhibits PMCs to express MCP-1 through inhibiting NF-kappaB pathway. FAU - Li, Zhi-ming AU - Li ZM AD - Department of Nephrology, First Affiliated Hospital of China Medical University, Shenyang 110001, China. FAU - Ma, Jian-fei AU - Ma JF FAU - Wang, Li-ning AU - Wang LN LA - chi PT - Journal Article PL - China TA - Zhonghua Yi Xue Za Zhi JT - Zhonghua yi xue za zhi JID - 7511141 RN - 0 (Chemokine CCL2) RN - 0 (Heptanoic Acids) RN - 0 (I-kappa B Proteins) RN - 0 (Nfkbia protein, rat) RN - 0 (Pyrroles) RN - 0 (RNA, Messenger) RN - 0 (Transcription Factor RelA) RN - 139874-52-5 (NF-KappaB Inhibitor alpha) RN - A0JWA85V8F (Atorvastatin) RN - IY9XDZ35W2 (Glucose) SB - IM MH - Animals MH - Atorvastatin MH - Blotting, Western MH - Cells, Cultured MH - Chemokine CCL2/*biosynthesis/genetics MH - Dose-Response Relationship, Drug MH - Epithelial Cells/cytology/*drug effects/metabolism MH - Gene Expression/drug effects MH - Glucose/*pharmacology MH - Heptanoic Acids/*pharmacology MH - I-kappa B Proteins/biosynthesis MH - Male MH - NF-KappaB Inhibitor alpha MH - Peritoneum/cytology MH - Pyrroles/*pharmacology MH - RNA, Messenger/genetics/metabolism MH - Rats MH - Rats, Sprague-Dawley MH - Reverse Transcriptase Polymerase Chain Reaction MH - Time Factors MH - Transcription Factor RelA/biosynthesis EDAT- 2008/01/03 09:00 MHDA- 2008/07/01 09:00 CRDT- 2008/01/03 09:00 PHST- 2008/01/03 09:00 [pubmed] PHST- 2008/07/01 09:00 [medline] PHST- 2008/01/03 09:00 [entrez] PST - ppublish SO - Zhonghua Yi Xue Za Zhi. 2007 Oct 16;87(38):2677-80.