CAJ | 학술논문

目的探讨慢性间歇低氧(CIH)对大鼠颏舌肌细胞线粒体功能的影响及脂联素干预作用.方法健康雄性Wistar大鼠39只,采用随机数字表法分成健康对照(NC)组、CIH组、CIH脂联素干预组(CIH+Ad组),每组13只.NC组大鼠呼吸正常空气,CIH组与CIH+Ad组均接受CIH环境(CIH 8 h/d,共5周),CIH+Ad组加用经静脉脂联素注射10 μg/次,2次/周,共5周.于实验终止(第35天)时测定并比较各组大鼠血清脂联素浓度、颏舌肌线粒体膜电位、线粒体复合物Ⅰ活性、线粒体复合物Ⅳ活性.结果 CIH组血清脂联素浓度明显低于NC组[(1108±112)ng/ml,(2241±121)ng/ml,P＜0.01];CIH+Ad组高于CIH组[(1889±119)ng/ml]但低于NC组[(2241±121)ng/ml,均P＜0.01].CIH组颏舌肌线粒体膜电位相对值(1.82±0.11)明显低于NC组(2.09±0.14,P＜0.01),CIH+Ad组(1.98±0.09)较CIH组略高但低于NC组,差异均有统计学差异(均P＜0.05).CIH组线粒体复合物Ⅰ、Ⅳ浓度[(35.68±1.73)μmol·min-1·mg-1,(2.37±0.11)nmol·min-1·mg-1]最低,CIH+Ad组[(37.18±1.95)μmol·min-1·mg-1,(2.49±0.09)nmol·min-1·mg-1]及NC组[(39.02±1.38)μmol·min-1·mg-1,(2.81±0.12)nmol·min-1·mg-1]依次增高.NC组与CIH组比较差异有统计学意义(P＜0.01),CIH+Ad组与CIH组和NC组比较差异有统计学意义(均P＜0.05).结论 CIH可致大鼠血清脂联素水平降低,并能显著损伤颏舌肌细胞线粒体功能,补充外源性脂联素能部分改善CIH对大鼠颏舌肌细胞线粒体功能的损伤,提示低脂联素血症可能参与CIH导致的颏舌肌能量代谢障碍.
목적 탐토만성간헐저양(CIH)대대서해설기세포선립체공능적영향급지련소간예작용.방법 건강웅성Wistar대서39지,채용수궤수자표법분성건강대조(NC)조、CIH조、CIH지련소간예조(CIH+Ad조),매조13지.NC조대서호흡정상공기,CIH조여CIH+Ad조균접수CIH배경(CIH 8 h/d,공5주),CIH+Ad조가용경정맥지련소주사10 μg/차,2차/주,공5주.우실험종지(제35천)시측정병비교각조대서혈청지련소농도、해설기선립체막전위、선립체복합물Ⅰ활성、선립체복합물Ⅳ활성.결과 CIH조혈청지련소농도명현저우NC조[(1108±112)ng/ml,(2241±121)ng/ml,P＜0.01];CIH+Ad조고우CIH조[(1889±119)ng/ml]단저우NC조[(2241±121)ng/ml,균P＜0.01].CIH조해설기선립체막전위상대치(1.82±0.11)명현저우NC조(2.09±0.14,P＜0.01),CIH+Ad조(1.98±0.09)교CIH조략고단저우NC조,차이균유통계학차이(균P＜0.05).CIH조선립체복합물Ⅰ、Ⅳ농도[(35.68±1.73)μmol·min-1·mg-1,(2.37±0.11)nmol·min-1·mg-1]최저,CIH+Ad조[(37.18±1.95)μmol·min-1·mg-1,(2.49±0.09)nmol·min-1·mg-1]급NC조[(39.02±1.38)μmol·min-1·mg-1,(2.81±0.12)nmol·min-1·mg-1]의차증고.NC조여CIH조비교차이유통계학의의(P＜0.01),CIH+Ad조여CIH조화NC조비교차이유통계학의의(균P＜0.05).결론 CIH가치대서혈청지련소수평강저,병능현저손상해설기세포선립체공능,보충외원성지련소능부분개선CIH대대서해설기세포선립체공능적손상,제시저지련소혈증가능삼여CIH도치적해설기능량대사장애.
Objective To investigate the effect of chronic intermittent hypoxia (CIH) on mitochondrial function in genioglossus cells of rats and intervention role of adiponectin (Ad). Methods Thirty-nine healthy male Wistar rats were randomly divided into 3 groups, normal control (NC) group, CIH group and CIH + Ad group with 13 rats in each. Rats in NC group were kept breathing normal air, while rats in both CIH and CIH + Ad groups experienced the same CIH environment ( CIH 8 h/day for successive 5 weeks). However, rats in CIH + Ad group was given intravenous Ad supplement at the dosage of 10 μg,twice a week for sucessive 5 weeks. At the end of experiment ( day 35 ), the levels of plasma adiponectin,mitochondrial membrane potential activities of respiratory chain complexes Ⅰ and Ⅳ in mitochondrion of genioglossus cells were compared among different groups. Results Serum Ad level was significantly lower in CIH group than that in NC group [(1108 ± 112) ng/ml vs (2241 ± 121) ng/ml, P＜0.01 ]. Serum Ad level in CIH + Ad group [ ( 1889 ± 119) ng/ml] was significantly higher than that in NC group but lower than that in CIH group ( all P ＜ 0. 01 ). Mitochondrial membrane potential was significantly lower in CIH group than that in NC group [ ( 1.82 ± 0. 11 ) vs (2. 09 ± 0. 14), P ＜ 0. 01 ]. Mitochondrial membrane potential in CIH + Ad group ( 1.98 ± 0. 09) was higher than that in CIH group but lower than that in NC group ( all P ＜ 0. 05 ). The concentrations of mitochondrial respiratory chain complexes Ⅰ and Ⅳ in CIH group ( 35.68 ± 1.73 ) μmol · min - 1 · mg- 1 and (2. 37 ± 0. 11 ) nmol · min - 1 ·mg - 1, respectively) were the lowest but became higher from CIH + Ad group [ (37. 18 ± 1.95) μ mol· min-1 · mg-1 and (2. 49 ±0.09) nmol · min-1 ·mg-1 ,respectively] to NC group (39.02 ± 1.38) μmol · min-1 · mg-1 and (2. 81±0. 12) nmol · min-1 ·mg-1 ,respectively), with a significant difference between NC and CIH groups ( P ＜ 0. 01 ), between CIH + Ad and CIH groups ( P ＜ 0. 05 ), as well as between CIH + Ad and NC groups (P ＜ 0. 05 ). Conclusion CIH could lead to hypoadiponectinemia and impaired mitochondrial function in genioglossus cells of rats. Since such changes could be partially improved by supplement of adiponectin, it was suggested that hypoadiponectinemia might be involved in CIH-induced impairment of genioglossus energy metabolism.