![](/Jwk_zgyyyx/develop/static/common/images/pdf.png)
虎杖苷通过TLR4/NF-κB信号通路调控糖尿病肾病大鼠肾脏炎症作用的研究
Polydatin protects diabetic nephropathy rats from renal inflammation by regulating the TLR4/NF-κB signal pathway
目的:研究虎杖苷通过TLR4/NF-κB信号通路调控糖尿病肾病大鼠肾脏炎症作用的影响。方法:通过尾静脉注射链脲佐菌素,高脂饲料喂养建立糖尿病肾病大鼠模型。将成模的大鼠随机分为模型组、缬沙坦组(20 mg·kg-1)、虎杖苷组(75 mg·kg-1)、虎杖苷组(150 mg·kg-1),每组10只,日常进行高脂饮食喂养,连续灌胃给药90 d,每日1次。于第90天采集尿液,测量尿量及终点法测24 h尿白蛋白(UP)含量。通过HE染色观察大鼠肾脏组织的病理学变化。采用ELISA法检测肾组织中TGF-β1、FN纤维化指标表达及肾脏组织中炎症因子肿瘤坏死因子(TNF-α)、白介素-1β(IL-1β)、白介素-6(IL-6)的含量。Western blot法检测肾组织中Toll样受体4(TLR4)、髓样分化因子(Myd88)、核转录因子kappa B(NF-κB)的表达。结果:与模型组相比,虎杖苷组大鼠Scr、BUN、UP含量显著降低(P<0.05)。TGF-β1、FN纤维化指标明及炎症因子TNF-α、IL-1β、IL-6含量显减少(P<0.05),TLR4、Myd88、NF-κB蛋白表达显著降低(P<0.05)。结论:虎杖苷对糖尿病肾病所引起的肾脏炎症有一定的保护作用,其作用机制可能与调节TLR4/NF-κB信号通路,降低肾脏组织的炎症因子含量,而起到抗炎的保护作用有关。
OBJECTIVE To investigate the effect of polydatin on renal inflammation of diabetic nephropathy rats by regulating the TLR4/NF-κB signal pathway.METHODS Diabetic nephropathy rats were established by tail vein injection of streptozotocin and high fat diet. The model rats were randomly divided into following groups:model control group, valsartan group (20 mg·kg-1), polydatin group (75 mg·kg-1), polydatin group (150 mg·kg-1), 10 rats per group. The rats were given high fat diet and drugs once a day for 90 days. Urine was collected on the 90th day for 24 hours urinary albumin (UP) detection. HE staining was used to observe the pathological changes of kidney tissues. The levels of fibrosis index TGF-β1, FN and inflammatory factor tumor necrosis factor (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6) were assessed by ELISA. Western blot was used to determine the expressions of Toll-like receptor 4 (TLR4), myeloid differentiation factor (Myd88) and nuclear transcription factor kappa B (NF-κB).RESULTS Compared with model control group, the contents of Scr, BUN and UP were significantly decreased (P<0.05). And the levels of fibrosis index TGF-β1, FN inflammatory factor TNF-α, IL-1β, IL-6 were also decreased (P<0.05). In addition, the expressions of TLR4, Myd88 and NF-κB were markedly decreased (P<0.05).CONCLUSION The protective effect of polydatin on renal inflammation of diabetic nephropathy rats may be related to regulation of the TLR4/NF-κB signal pathway, reduction of the contents of inflammatory factor of kidney tissues, which plays protective effects against inflammation.
虎杖苷 / 糖尿病肾病 / TLR4/NF-κB / 大鼠 {{custom_keyword}} /
polydatin / diabetic nephropathy / TLR4/NF-κB / rats {{custom_keyword}} /
[1] Mo ML, Duan MX, Wang TW,et al. Establishment and evaluation of a behavior intervention model for diabetes in community population based on the information platform[J]. Journal of Third Military Medical University, 2017, 39(10):1056-1062.
[2] Li ZS, Huang GC. Combined detection of multiple indexes in the early diagnosis of diabetic nephropathy Clinical application[J]. Chinese Journal of Modern Drug Application, 2016(4):19-20.
[3] Wu H, Sun ZL. Research Progress in the Pathogenesis and Drug Intervention of Diabetic Nephropathy[J]. Progress in Pharmaceutical Sciences, 2016(5):337-343.
[4] Meng QH, Liu HB, Wang JB. Protective effects of polydatin on HK-2 cells against oxygen-glucose deprivation/re-oxygenation-induced injury by regulating Sonic hedgehog through PI3K/Akt signaling pathway[J]. Chinese Journal of Cellular and Molecular Immunology, 2015, 31(11):1452-1457.
[5] Wang YY, Zhang Q. Research Progress of Polydatin Pharmacologic Actions[J]. Medical Recapitulate, 2017, 23(5):989-991.
[6] Xu XH, Zheng N, Chen ZN, et al. Puerarin, isolated from Pueraria lobata (Willd.), protects against diabetic nephropathy by attenuating oxidative stress[J]. Gene, 2016, 591(2):411-416.
[7] Brancato SK, Thomay AA, Daley JM, et al. Toll-like receptor 4 signaling regulates the acute local inflammatory response to injury and the fibrosis/neovascularization of sterile wounds[J]. Wound Repair & Regeneration, 2013, 21(4):624-633.
[8] Mukherjee S, Karmakar S, Babu SP. TLR2 and TLR4 mediated host immune responses in major infectious diseases:a review[J]. Brazilian Journal of Infectious Diseases, 2016, 20(2):193-204.
[9] Ma J, Chadban SJ, Zhao CY, et al. TLR4 activation promotes podocyte injury and interstitial fibrosis in diabetic nephropathy[J]. PloS one, 2014, 9(5):97985-97989.
[10] Liu P, Li F, Qiu M, et al. Expression and cellular distribution of TLR4, MyD88, and NF-κB in diabetic renal tubulointerstitial fibrosis, in vitro, and in vivo[J]. Diabetes Research & Clinical Practice, 2014, 105(2):206-216.
[11] Lin M, Yiu WH, Li RX, et al. The TLR4 antagonist CRX-526 protects against advanced diabetic nephropathy[J]. Kidney international, 2013, 83(5):887-900.
[12] Zhao PM, Wang JQ, Liang YJ. Role of endothelial cells injury in the pathogenesis of diabetic nephropathy[J]. Chinese Journal of Diabetes, 2016, 24(2):169-172.
[13] Wang S, Chen TH, Peng H,et al. Relationship between inflammatory markers and serum Vaspin level in patients with diabetic nephropathy[J]. Guangdong Medical Journal, 2017, 38(1):111-114.
[14] Zeng QY, Xiao J, Zhang JP,et al. Inhibiting effects of Apelin-13 against high glucose induced inflammation in mesangial cells[J]. Chinese Journal of Hospital Pharmacy, 2016, 36(3):168-171.
[15] FanWeir, Xu CX, Cui Y. The Association between Urinary Inflammatory Factors and the Stage of Diabetic Nephropathy[J]. Chinese General Practice, 2017, 20(S1):21-23.
国家自然科学青年基金(编号:81500633);福建省卫生系统中青年骨干人才培养重点项目(编号:2013-ZQN-ZD-21)
/
〈 |
|
〉 |