CAJ | 학술논문

观察硫化氢(H2S)对肝硬化胶原蛋白形成的影响，探明其在肝硬化形成过程中的作用。方法采用四氯化碳(CCl4)复合因素法建立肝硬化大鼠模型。选取Wistar大鼠20只，按数字表法随机分成正常对照组6只、肝硬化遭模组(造模组)7只和肝硬化造模并加硫化氢钠(NaHS)组(观察组)7只，对观察组进行腹腔注射NaHS 1.4 μmol/kg，2次/d。4周后，取造模大鼠肝组织行胱硫醚-γ-裂解酶(CSE) Western 印迹检测和羟脯氨酸测定及H2S检测，分析H2S与羟脯氨酸的相关性。结果经过4周造模，造模组和观察组均有1只大鼠死亡。肝脏病理表现为造模组肝小叶破坏，假小叶形成，而观察组肝硬化程度较造模组轻。与正常对理相比，造模组肝硬化形成后，肝脏内源性H2S含量明显减少，两组的H2S含量分别为(344.54±33.19)和(166.11±50.54) μmol/L(t= 4.366，P＜0.01)，肝脏羟脯氨酸含量明显升高，分别为(0.25±0.12)和(2.11±0.86) mg/g(t=5.018，P＜0.01)；与观察组比较，造模组肝脏H2S含量明显增加，分别为(306.97±36.08)和(166.11±50.54) μmol/L(t=4.297，P＜0.01)；羟脯氨酸明显减少，分别为(1.03±0.41)和(2.11±0.86) mg/g(t =4.874，P＜0.01)。肝硬化过程中CSE含量逐渐降低，但观察组肝脏CSE表达却明显增加，表达水平与正常对照组相似。结论H2S在肝硬化形成过程中，能抑制肝脏胶原蛋白的合成，具有负向调整肝硬化进展的作用。
관찰류화경(H2S)대간경화효원단백형성적영향，탐명기재간경화형성과정중적작용。방법채용사록화탄(CCl4)복합인소법건립간경화대서모형。선취Wistar대서20지，안수자표법수궤분성정상대조조6지、간경화조모조(조모조)7지화간경화조모병가류화경납(NaHS)조(관찰조)7지，대관찰조진행복강주사NaHS 1.4 μmol/kg，2차/d。4주후，취조모대서간조직행광류미-γ-렬해매(CSE) Western 인적검측화간포안산측정급H2S검측，분석H2S여간포안산적상관성。결과경과4주조모，조모조화관찰조균유1지대서사망。간장병리표현위조모조간소협파배，가소협형성，이관찰조간경화정도교조모조경。여정상대리상비，조모조간경화형성후，간장내원성H2S함량명현감소，량조적H2S함량분별위(344.54±33.19)화(166.11±50.54) μmol/L(t= 4.366，P＜0.01)，간장간포안산함량명현승고，분별위(0.25±0.12)화(2.11±0.86) mg/g(t=5.018，P＜0.01)；여관찰조비교，조모조간장H2S함량명현증가，분별위(306.97±36.08)화(166.11±50.54) μmol/L(t=4.297，P＜0.01)；간포안산명현감소，분별위(1.03±0.41)화(2.11±0.86) mg/g(t =4.874，P＜0.01)。간경화과정중CSE함량축점강저，단관찰조간장CSE표체각명현증가，표체수평여정상대조조상사。결론H2S재간경화형성과정중，능억제간장효원단백적합성，구유부향조정간경화진전적작용。
Objective To observe the effect of the hydrogen sulfide on collagen formation in liver cirrhosis and to illustrate its role in the formation of cirrhosis of the liver. Methods The rat models of liver cirrhosis were induced by compound factors mainly CCl4. Twenty wistar rats were divided into normal control group with 6 rats, liver cirrhosis group (modeled group) with 7 rats, liver cirrhosis + NaHS group (survey group)with 7 rats, the survey group were injected NaHS intraperitoneally with 1.4 tmol/kg twice daily and were modeled for 4 weeks. Liver tissue was for the cystathionine-γ-lyase(CSE) detection by Western blot and hydroxyproline and hydrogen sulfide determination. The relations between hydroxyproline and H2S were analysed. Results After 4 weeks of modeling, modeled group and survey group all had one rat dead respectively. The hepatic lobules damaged and pseudlobes formatted in modeled group, while these alterations were slighter in survey group. After the formation of liver cirrhosis, the hydrogen sulfide in control group was significantly reduced significantly compared to modeled group, there were(344.54 ± 33.19) and( 166.11 ± 50.54)μnol/L respectively (t =4.366, P＜0.01); and liver hydroxyproline content increased, there were (0.25±0.12) and (2.11 ±0.86) mg/g respectively( t = 5.018, P ＜ 0.01 ). Compared to the survey group, the H2S content in modeled group were much higher. There were (306.97 ± 36.08) and (166.11 ±50.54) μmol/L (t =4.297 P＜0.01) respectively. The hydroxyproline in these two groups declined obviously, they were (1.03 ± 0.41 )and (2. 1 1 ± 0.86 ) mg/g respectively ( t = 4.874 P ＜ 0.01 ). The expression of CSE in modeled group decreased gradually, however, the expression of CSE increased significantly in survey group, the increased level was the same as the normal control group. Concluusions Hydrogen sulfide can negatively regulates the collagen synthesis in the liver and inhibits the liver cirrhosis progress.