【Abstract】ObjectiveTo evaluate the relationships between the transporters BSEP， MRP2， MDR3 and cholesterol calculus formation.
MethodsTwenty hepatic tissue specimens were taken from consented patients with cholesterol calculus during intraoperative liver biopsy, of which ten were taken from patients without cholesterol calculus. RNA of liver tissue from all the samples was extracted and ultraviolet spectrophotometry was used to measure the content and purity of it. The mRNA and protein expressions of BSEP, MRP2 and MDR3 were determined by reverse transcriptionpolymerase chain reaction (RTPCR) and Western blot analysis, respectively.
ResultsRTPCR showed that the mRNA expressions of BSEP, MRP2 and MDR3 in liver were significantly lower in patients with cholesterol calculus （0.47±0.18, 1.12±0.39 and 1.02±0.24） than those in the liver of patients without calculus （0.90±0.42, 2.48±0.89 and 1.94±0.80）,P＜0.01. And Western blot also showed the protein expressions of these transporters were significantly lower in patients with cholesterol calculus （90.16±18.82, 45.43±22.77 and 61.08±14.77） than those in the liver of patients without calculus (186.17±4.34, 160.47±30.19 and 100.84±15.44).
ConclusionThe decreased expression of BSEP, MRP2 and MDR3 may correlate with the formation of cholesterol calculus.
Citation：
KONG Fanmin,SUI Chunyang,LI Hangyu,LI Yuji,SUN Hongzhi,GUO Renxuan,GUO Kejian,TIAN Yulin.. Study about the Relationships Between the Formation of Cholesterol Calculus and the Transporters of BSEP， MRP2 and MDR3. CHINESE JOURNAL OF BASES AND CLINICS IN GENERAL SURGERY, 2006, 13(3): 314-316. doi:
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刘君， 龙厚勇， 明晗昕， 等. 肝细胞MDR1基因表达与胆囊胆固醇结石相关性研究 [Ｊ]. 中国普外基础与临床杂志， 2005； 12（4）∶346.
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- 1. [Ｊ]. Scand J Gastroenterol, 2004； 241（Suppl）∶ 60.
- 2. van BergeHenegouwen GP, Venneman NG, Portincasa P, et al. Relevance of hereditary defects in lipid transport proteins for the pathogenesis of cholesterol gallstone disease.
- 3. Trauner M, Boyer JL. Bile salt transporters: molecular characterization, function, and regulation [Ｊ]. Physiol Rev, 2003; 83(2)∶633.
- 4. Hoda F, Green RM. Hepatic canalicular membrane transport of bile salt in C57L/J and AKR/J mice: implications for cholesterol gallstone formation [Ｊ]. J Membr Biol， 2003; 196(1)∶9.
- 5. Huang L, Zhao A, Lew JL, et al. Farnesoid X receptor activates transcription of the phospholipid pump MDR3 [Ｊ]. J Biol Chem, 2003; 278(51)∶51085.
- 6. Meier PJ, Stieger B. Bile salt transporters [Ｊ]. Annu Rev Physiol， 2002; 64(2)∶635.
- 7. Plass JR, Mol O, Heegsma J, et al. A progressive familial intrahepatic cholestasis type 2 mutation causes an unstable, temperaturesensitive bile salt export pump [Ｊ]. J Hepatol， 2004; 40(1)∶24.
- 8. Fickert P, Fuchsbichler A, Wagner M, et al. Regurgitation of bile acids from leaky bile ducts causes sclerosing cholangitis in Mdr2 (Abcb4) knockout mice [Ｊ]. Gastroenterology, 2004; 127(1)∶261.
- 9. Shoda J, Oda K, Suzuki H, et al. Etiologic significance of defects in cholesterol, phospholipid, and bile acid metabolism in the liver of patients with intrahepatic calculi [Ｊ]. Hepatology, 2001; 33(5)∶1194.
- 10. Smit JJ, Schinkel AH, Oude Elferink RP, et al. Homozygous disruption of the murine mdr2 Pglycoprotein gene leads to a complete absence of phospholipid from bile and to liver disease [Ｊ]. Cell, 1993; 75(3)∶451.
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