CAJ | 학술논문

目的：探讨慢性间歇性低氧（chronic intermittent hypoxia，CIH）对心肌重塑的影响及脂联素（adiponectin， Ad）的干预作用。方法将45只Wistar大鼠随机分为3组：正常对照组（NC），CIH组和CIH+Ad组。CIH 35d后，使用马松染色分析方法检测左室纤维化程度及使用Western blot方法来衡量Ⅰ型胶原蛋白、Ⅲ型胶原蛋白和TGF-β/smad2/3通路蛋白的表达。通过RT-PCR方法来研究基质金属蛋白酶-2（MMP2）/基质金属蛋白酶的组织抑制剂-2（TIMP-2）的mRNA表达比值情况。结果慢性间歇性低氧处理后，CIH组左心室的纤维化程度显著高于NC组和CIH＋Ad组（P＜0.05），但NC组和CIH＋Ad组之间差异具有统计学意义（P＜0.05）。CIH组Ⅰ型胶原蛋白和Ⅲ型胶原蛋白和MMP2/TIMP-2的mRNA比值表达最高，NC组表达最低，CIH＋Ad组居中，3组之间均差异具有统计学意义（P＜0.05）。TGF-β/smad通路蛋白在CIH组中表达显著高于NC组和CIH组（P＜0.05），且NC组和CIH＋Ad组差异具有统计学意义（P＜0.05）。结论慢性间歇性低氧可引起左室重构，而Ad可能通过抑制TGF-β/smad2/3通路改善此损害。
목적：탐토만성간헐성저양（chronic intermittent hypoxia，CIH）대심기중소적영향급지련소（adiponectin， Ad）적간예작용。방법장45지Wistar대서수궤분위3조：정상대조조（NC），CIH조화CIH+Ad조。CIH 35d후，사용마송염색분석방법검측좌실섬유화정도급사용Western blot방법래형량Ⅰ형효원단백、Ⅲ형효원단백화TGF-β/smad2/3통로단백적표체。통과RT-PCR방법래연구기질금속단백매-2（MMP2）/기질금속단백매적조직억제제-2（TIMP-2）적mRNA표체비치정황。결과만성간헐성저양처리후，CIH조좌심실적섬유화정도현저고우NC조화CIH＋Ad조（P＜0.05），단NC조화CIH＋Ad조지간차이구유통계학의의（P＜0.05）。CIH조Ⅰ형효원단백화Ⅲ형효원단백화MMP2/TIMP-2적mRNA비치표체최고，NC조표체최저，CIH＋Ad조거중，3조지간균차이구유통계학의의（P＜0.05）。TGF-β/smad통로단백재CIH조중표체현저고우NC조화CIH조（P＜0.05），차NC조화CIH＋Ad조차이구유통계학의의（P＜0.05）。결론만성간헐성저양가인기좌실중구，이Ad가능통과억제TGF-β/smad2/3통로개선차손해。
ObjectiveTo investigate the effects of chronic intermittent hypoxia (CIH) on myocardiac remodeling and intervention role of adiponectin(Ad) in the process.Methods A total of 45 Wistarrats were randomly divided into3 groups: normal control (NC) group, CIH group and CIH+Ad group (10μg Ad injection through caudal vein twice per week, for 5 weeks). After 35 days’ CIH exposure (in a chamber with 60 s nitrogen infusion to reduce theoxygen concentration to 5% followed by another 60 s oxygen infusion to increase theconcentration to 20% for totally 8 h of each day),Masson analysis was used to detect the left ventricular fibrosis, and Western blot was used to measure the protein expression of collagenⅠ, collagenⅢ and pathway proteins TGF-β/smad2/3. RT-PCR was used to study the expression of matrix metalloproteinase-2 (MMP-2) and tissue inhibitor of metalloproteinase-2 (TIMP-2).Results After CIH exposure, the left ventricular fibrosis was significantly more severe in CIH group than in NC groupand CIH+Ad group (P<0.05), and there was statistical difference between the 2 latter groups (P<0.05). In addition, the protein expression of collagenⅠ and collagenⅢ and the mRNA expression of MMP-2 and TIMP-2 were the highest in CIH group, the lowest in NC group, and CIH+Ad group in the middle. There was a significant difference among 3 groups (all P<0.05). The pathway proteins TGF-β/smad2/3 were most significantly expressed in CIH group (P<0.05) , but there was still significant difference in their expression between NC group and CIH+Ad group (P<0.05).Conclusion CIHmay cause may left ventricular remodeling, while Ad supplementmay ameliorate the impairmentvia inhibiting TGF-β/smad2/3 pathway.