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Pravastatin activates PPARα/PPARγexpression in the liver and gallbladder epithelium of hamsters

Hepatobiliary & Pancreatic Diseases International 2011年第2期10卷 185-190页

作者： Seok Ho Dong Jin Lee Dong Hee Koh Min Ho Choi Hyun Joo Jang sea hyub kae Division of Gastroenterology Department of Internal MedicineKyung Hee University College of Medicine Division of Gastroenterology Department of Internal MedicineHallym University College of Medicine

BACKGROUND:Our earlier study with cultured gallbladder epithelial cells demonstrated that statins(HMG-CoA reductase inhibitors)activate the expression of PPARαand PPARγ, consequently blocking the production of pro-inflmmatory *** present study used hamsters to investigate the effects of pavastatin on PPARα/PPARγexpression in the liver and gallbladder epithelium,and to determine whether pravastatin suppresses cholesterol crystal formation in the gallbladder. METHODS:A total of 40 Golden Syrian male hamsters(4 weeks old)were randomly assigned to four groups(basal diet control; basal diet+pavastatin;high cholesterol diet;high cholesterol diet+pravastatin).All hamsters were 11 weeks old at the end of the *** liver,gallbladder and bile were harvested. Immunohistochemical staining and Western blotting for PPARαand PPARγwere performed in the liver and gallbladder. A drop of fresh bile was examined for cholesterol crystals under a microscope. RESULTS:In the gallbladder and liver of the hamsters, pravastatin activated the PPARαand PPARγexpression of gallbladder epithelial cells and hepatocytes,and particularly the response of PPARγwas much stronger than that of PPARα. Pravastatin suppressed the formation of cholesterol gallstones or crystals in the gallbladder. CONCLUSION:Pravastatin is an effective medication to activate PPARs(especially PPARγ)in the liver and the gallbladder epithelium of hamsters,and contributes to the prevention of gallstone formation.

关键词： pravastatin PPARα PPARγ hamster gallstone

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Pravastatin activates the expression of farnesoid X receptor and liver X receptor alpha in Hep3B cells

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Hepatobiliary & Pancreatic Diseases International 2014年第1期13卷 65-73页

作者： Hyun Woo Byun Eun Mi Hong Soo Hee Park Dong Hee Koh Min Ho Choi Hyun Joo Jang sea hyub kae Jin Lee Division of Gastroenterology Department of Internal Medicine Hallym University College of Medicine Dongtan Sacred Heart Hospital

BACKGROUND: Statins are suggested to preserve gallbladder function by suppressing pro-inflammatory cytokines and preventing cholesterol accumulation in gallbladder epithelial cells. They also affect cross-talk among the nuclear hormone receptors that regulate cholesterol-bile acid metabolism in the nuclei of hepatocytes. However, there is controversy over whether or how statins change the expression of peroxisome proliferator-activated receptor(PPAR)α, PPARγ, liver X receptor α(LXRα), farnesoid X receptor(FXR), ABCG5, ABCG8, and 7α-hydroxylase(CYP7A1) which are directly involved in the cholesterol saturation index in bile. METHODS: Human Hep3B cells were cultured on dishes. MTT assays were performed to determine the appropriate concentrations of reagents to be used. The protein expression of PPARα and PPARγ was measured by Western blotting analysis, and the mRNA expression of LXRα, FXR, ABCG5, ABCG8 and CYP7A1 was estimated by RT-PCR. RESULTS: In cultured Hep3B cells, pravastatin activated PPARα and PPARγ protein expression, induced stronger expression of PPARγ than that of PPARα, increased LXRα mRNA expression, activated ABCG5 and ABCG8 mRNA expression mediated by FXR as well as LXRα, enhanced FXR mRNA expression, and increased CYP7A1 mRNA expression mediated by the PPARγ and LXRα pathways, together or independently. CONCLUSION: Our data suggested that pravastatin prevents cholesterol gallstone diseases via the increase of FXR, LXRαand CYP7A1 in human hepatocytes.

关键词： pravastatin PPARγ liver X receptor α farnesoid X receptor gallstone disease

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Endoscopic submucosal dissection for early gastric cancer with undifferentiated-type histology:A meta-analysis

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World Journal of Gastroenterology 2015年第19期21卷 6032-6043页

作者： Chang Seok Bang Gwang Ho Baik In Soo Shin Jing Bong Kim Ki Tae Suk Jai Hoon Yoon Yeon Soo Kim Dong Joon Kim Woon Geon Shin Kyung Ho Kim Hak Yang Kim Hyun Lim Ho Seok Kang Jong Hyeok Kim Jin Bae Kim Sung Won Jung sea hyub kae Hyun Joo Jang Min Ho Choi Department of Internal Medicine Hallym University College of Medicine College of Education Jeonju University

AIM: To evaluate the efficacy and safety of endoscopicsubmucosal dissection(ESD) for early gastric cancer(EGC) with undifferentiated-type ***: A systematic literature review was conducted using the core databases. Complete resection,curative resection, en bloc resection, recurrence and adverse event rate were extracted and analyzed. A random effect model was applied. The methodological quality of the enrolled studies was assessed using the Newcastle-Ottawa Scale. Publication bias was evaluated using a funnel plot, the trim and fill method, Egger's test,and a rank correlation ***: Fourteen retrospective studies between2009 and 2014 were identified(972 EGC lesions with undifferentiated-type histology). The total en bloc and complete resection rates were estimated as92.1%(95%CI: 87.4%-95.2%) and 77.5%(95%CI:69.3%-84%), respectively. The total curative resection rate was 61.4%(95%CI: 44.5%-75.9%). The overall recurrence rate was 7.6%(95%CI: 3.4%-16%).Limited to histologically diagnosed expanded-criteria lesions, the en bloc and complete resection rates were91.2% and 85.6%, respectively. The curative resection rate was 79.8%.CONCLUSION: In this analysis, ESD is a technically feasible treatment modality for EGC with undifferentiatedtype histology. Long-term studies are needed to confirm these therapeutic outcomes.

关键词： Carcinoma Endoscopic submucosal dissection Endoscopy Gastric cancer Meta-analysis

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