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目的观察长链脂肪酸对脂肪细胞GPR120的作用及对脂肪细胞炎症、内质网应激及胰岛素信号分子的影响。方法体外培养3T3-L1前脂肪细胞,采用1μM地塞米松、1μg/ml胰岛素和10%加强型小牛血清的DMEM培养基诱导为分化3T3-L1脂肪细胞,采用100Μm PA刺激2 h后,采用Western blot方法检测GPR120、XBP1S、PERK、P-PERK、IRE-1α、P-IRE-1α、IKKβ、p-IKKβ、JNK1、P-JNK1、JNK2和P-JNK2蛋白表达水平。加入含有100ng/ml胰岛素的DMEM培养基,孵育15 min,采用Western blot方法检测IR、P-IR、IRS-1、p-IRS、Akt和P-Akt蛋白表达水平。结果在PA的刺激下,GPR120、XBP1S、PERK、P-PERK、IRE-1α、P-IRE-1α、IKKβ、p-IKKβ、JNK1、PJNK1、JNK2和P-JNK2表达显著提高(P<0.05),IR、P-IR、IRS-1、p-IRS-1、Akt和P-Akt蛋白表达水平显著下降(P<0.05),而使用GPR120阻滞剂LGW9508可以抑制该过程。结论长链饱和脂肪酸PA可通过上调GPR120蛋白的表达,诱导脂肪内质网应激反应、炎症反应和胰岛素抵抗。
Objective To observe the effect of long chain fatty acids (GPFAs) on GPs of adipocytes and their effects on adipocyte inflammation, endoplasmic reticulum stress and insulin signaling molecules. Methods 3T3-L1 preadipocytes were cultured in vitro and differentiated into 3T3-L1 adipocytes using DMEM medium supplemented with 1μM dexamethasone, 1μg / ml insulin and 10% booster calf serum. After stimulated with 100μM PA for 2 hours, The protein expression of GPR120, XBP1S, PERK, P-PERK, IRE-1α, P-IRE-1α, IKKβ, p-IKKβ, JNK1, P-JNK1, JNK2 and P-JNK2 were detected by Western blot. The DMEM medium containing 100ng / ml insulin was added and incubated for 15 min. The protein expression of IR, P-IR, IRS-1, p-IRS, Akt and P-Akt were detected by Western blot. Results The expression of GPR120, XBP1S, PERK, P-PERK, IRE-1α, P-IRE-1α, IKKβ, p-IKKβ, JNK1, PJNK1, JNK2 and P-JNK2 were significantly increased (P < IR, P-IR, IRS-1, p-IRS-1, Akt and P-Akt protein expression were significantly decreased (P <0.05), while the use of GPR120 blocker LGW9508 can inhibit the process. Conclusion Long-chain saturated fatty acid PA can induce fat ER reaction, inflammatory reaction and insulin resistance by up-regulating GPR120 protein expression.