中华临床医师杂志（电子版）
中華臨床醫師雜誌（電子版）
중화림상의사잡지（전자판）
CHINESE JOURNAL OF CLINICIANS(ELECTRONIC VERSION)
2013年
15期
7064-7067
,共4页
曹艳丽%暴素青%范雨鑫%白淑亭%单忠艳
曹豔麗%暴素青%範雨鑫%白淑亭%單忠豔
조염려%폭소청%범우흠%백숙정%단충염
Toll样受体4%肿瘤坏死因子α%炎症%高脂饮食%胰岛素敏感性
Toll樣受體4%腫瘤壞死因子α%炎癥%高脂飲食%胰島素敏感性
Toll양수체4%종류배사인자α%염증%고지음식%이도소민감성
Toll-like receptor 4%Tumor necrosis factor-alpha%Inflammation%Diet,high-fat%Insulin sensitivity
目的：探讨高脂饮食喂养对肥胖大鼠脂肪组织中 TLR4炎症信号通路的影响。方法将20只SPF级雄性4周龄SD大鼠随机分为正常饮食组（NC，n=10）和高脂饮食组（HFD，n=10）。检测每组大鼠空腹血糖及胰岛素水平，并计算HOMA-IR；应用Real-time PCR及Western blot方法检测脂肪组织中炎症信号通路TLR4、TRAF6、IKKβ、TNF-α、IL-6的表达。结果（1）与NC组相比，HFD组空腹胰岛素水平显著升高[分别为（14.64±0.66）mIU/L vs.（31.71±3.61）mIU/L，P=0.005]；HOMA-IR值升高（分别为3.40±0.15 vs.7.59±0.99，P=0.008）；两组大鼠空腹血糖水平无明显统计学差异。（2）Real time PCR结果显示，HFD组脂肪组织中TLR4、TRAF6、TNF-α及IL-6 mRNA水平均明显升高，分别为NC组的1.85倍（P=0.002）、1.72倍（P=0.031）、3.82倍（P=0.045）及3.17倍（P=0.003）。（3）HFD 组大鼠炎症因子TLR4、IKKβ及TNF-α蛋白水平亦明显升高，分别为NC组的1.62倍（P=0.000）、1.77倍（P=0.003）及3.02倍（P=0.002）。结论高脂饮食可通过介导TLR4炎症信号通路活化，使脂肪组织中炎症因子TNF-α、IL-6表达升高，进而导致胰岛素抵抗的发生。
目的：探討高脂飲食餵養對肥胖大鼠脂肪組織中 TLR4炎癥信號通路的影響。方法將20隻SPF級雄性4週齡SD大鼠隨機分為正常飲食組（NC，n=10）和高脂飲食組（HFD，n=10）。檢測每組大鼠空腹血糖及胰島素水平，併計算HOMA-IR；應用Real-time PCR及Western blot方法檢測脂肪組織中炎癥信號通路TLR4、TRAF6、IKKβ、TNF-α、IL-6的錶達。結果（1）與NC組相比，HFD組空腹胰島素水平顯著升高[分彆為（14.64±0.66）mIU/L vs.（31.71±3.61）mIU/L，P=0.005]；HOMA-IR值升高（分彆為3.40±0.15 vs.7.59±0.99，P=0.008）；兩組大鼠空腹血糖水平無明顯統計學差異。（2）Real time PCR結果顯示，HFD組脂肪組織中TLR4、TRAF6、TNF-α及IL-6 mRNA水平均明顯升高，分彆為NC組的1.85倍（P=0.002）、1.72倍（P=0.031）、3.82倍（P=0.045）及3.17倍（P=0.003）。（3）HFD 組大鼠炎癥因子TLR4、IKKβ及TNF-α蛋白水平亦明顯升高，分彆為NC組的1.62倍（P=0.000）、1.77倍（P=0.003）及3.02倍（P=0.002）。結論高脂飲食可通過介導TLR4炎癥信號通路活化，使脂肪組織中炎癥因子TNF-α、IL-6錶達升高，進而導緻胰島素牴抗的髮生。
목적：탐토고지음식위양대비반대서지방조직중 TLR4염증신호통로적영향。방법장20지SPF급웅성4주령SD대서수궤분위정상음식조（NC，n=10）화고지음식조（HFD，n=10）。검측매조대서공복혈당급이도소수평，병계산HOMA-IR；응용Real-time PCR급Western blot방법검측지방조직중염증신호통로TLR4、TRAF6、IKKβ、TNF-α、IL-6적표체。결과（1）여NC조상비，HFD조공복이도소수평현저승고[분별위（14.64±0.66）mIU/L vs.（31.71±3.61）mIU/L，P=0.005]；HOMA-IR치승고（분별위3.40±0.15 vs.7.59±0.99，P=0.008）；량조대서공복혈당수평무명현통계학차이。（2）Real time PCR결과현시，HFD조지방조직중TLR4、TRAF6、TNF-α급IL-6 mRNA수평균명현승고，분별위NC조적1.85배（P=0.002）、1.72배（P=0.031）、3.82배（P=0.045）급3.17배（P=0.003）。（3）HFD 조대서염증인자TLR4、IKKβ급TNF-α단백수평역명현승고，분별위NC조적1.62배（P=0.000）、1.77배（P=0.003）급3.02배（P=0.002）。결론고지음식가통과개도TLR4염증신호통로활화，사지방조직중염증인자TNF-α、IL-6표체승고，진이도치이도소저항적발생。
Objective To explore toll-like receptor 4(TLR4) inflammatory pathway in adipose tissue of rats induced by high-fat diet. Methods 20 male Sprague-Dawley rats were divided into two groups:the standard diet(NC, n=10) group and the high-fat diet(HFD, n=10) group. Plasma glucose and fasting plasma insulin(FINS) levels were assessed. Insulin resistance was calculated by the homeostasis model assessment-insulin resistance index (HOMA-IR index). The levels of inflammation signaling pathway TLR4, TRAF6,IKKβ,TNF-α,IL-6 were examined in adipose tissue. Results (1) In HFD group, there were significant increases in FINS [(14.64±0.66) mIU/L vs.(31.71±3.61) mIU/L, separately, P=0.005], HOMA-IR(3.40±0.15 vs. 7.59±0.99, separately, P=0.008), compared to the NC group. (2) The levels of mRNA expression results of real-time PCR of TLR4 (1.85 fold, P=0.002), TRAF6 (1.72 fold, P=0.031), TNF-α (3.82 fold, P=0.045) and IL-6 (3.17 fold, P=0.003) levels were higher in HFD group than the NC group. (3) The protein levels of inflammation-related substances such as TLR4 (1.62 fold, P=0.000), IKKβ (1.77 fold, P=0.003) as well as TNF-α (3.02 fold, P=0.002) examined in the HFD group were all higher than the NC group, and the differences were significant. Conclusion TLR4 signaling pathway increasing the degree of inflammatory cytokines TNF-αand IL-6, and thus attenuated insulin sensitivity in adipose tissue of high-fat diet rats.
