论文部分内容阅读
目的检测肥胖大鼠网膜脂肪组织KLF4及KLF7 m RNA表达水平,分析其与炎症的相关性。方法 Wistar健康雄性大鼠高脂喂养,诱导肥胖模型。高脂喂养后第4、10周检测大鼠血脂、血糖水平;ELISA法测定血浆中TNF-α、LPT、APN水平;10周后,q RT-PCR法检测网膜脂肪组织KLF4、KLF7及NF-κB炎症信号通路关键因子m RNA表达水平。结果高脂喂养4周后,实验组大鼠体质量开始显著高于对照组,第10周实验组大鼠体质量进入平台期,但仍高于对照组(P<0.05)。高脂喂养第4及第10周,实验组大鼠血浆FFA、Glu、TG、TC、LDL、TNF-α水平高于对照组,LPT、APN水平低于对照组(P<0.05)。网膜脂肪组织中,实验组TLR9、KLF4 m RNA表达水平低于对照组,KLF7、SRC和IL-6 m RNA表达水平高于对照组;TLR9与血浆FFA负相关,与KLF4正相关;KLF4与SRC、NF-κB负相关;KLF7与TLR4、SRC、NF-κB和IL-6正相关,与KLF4负相关(P<0.05)。结论肥胖状态下,高水平的FFA一方面可与TLR4结合上调KLF7表达,促进炎症因子表达,导致释放组织发生炎症;同时,可抑制TLR9水平而下调KLF4表达,减弱KLF4对炎症信号通路关键因子的抑制作用,从而促进炎症反应。
Objective To detect the expression of KLF4 and KLF7 mRNA in omental adipose tissue of obese rats and analyze their correlation with inflammation. Methods Wistar healthy male rats were fed with high fat diet and induced with obesity model. Serum lipids and blood glucose levels were measured at 4 and 10 weeks after high-fat diet; TNF-α, LPT and APN levels in plasma were measured by ELISA. After 10 weeks, the expression of KLF4, KLF7 and NF κB inflammatory signal pathway key factor m RNA expression level. Results After 4 weeks of high-fat diet, the body weight of rats in the experimental group began to be significantly higher than that of the control group. The body weight of the rats in the experimental group reached the plateau in the 10th week, but still higher than that of the control group (P <0.05). The levels of plasma FFA, Glu, TG, TC, LDL and TNF-α in the experimental group were higher than those in the control group at 4 and 10 weeks of high-fat diet, while the levels of LPT and APN were lower in the experimental group than those in the control group (P <0.05). In omental adipose tissue, the expression of TLR9 and KLF4 mRNA in the experimental group was lower than that in the control group, the expression levels of KLF7, SRC and IL-6 m RNA were higher than those in the control group; TLR9 was negatively correlated with plasma FFA and positively correlated with KLF4; SRC and NF-κB. KLF7 was positively correlated with TLR4, SRC, NF-κB and IL-6, and negatively correlated with KLF4 (P <0.05). Conclusions In the obese state, high levels of FFA can combine with TLR4 to up-regulate the expression of KLF7 and promote the expression of inflammatory cytokines, leading to the inflammation of the released tissues. At the same time, it can inhibit the level of TLR9 and down-regulate the expression of KLF4, and attenuate the effect of KLF4 on the key factors of inflammatory signaling pathway Inhibition, thereby promoting the inflammatory response.