Wang Ming, Xiu Liangchang, Diao Jianxin, Wei Lianbo, Sun Jia
Nephrology center of integrated traditional Chinese Medicine and Western Medicine, ZhuJiang Hospital, Southern Medical University, Guangzhou, 510280, China.
Department of Epidemiology and Medical Statistics, School of Public Health, Guangdong Medical College, Dongguan, Guangdong 523808, China.
Eur J Pharmacol. 2015 Dec 15;769:79-85. doi: 10.1016/j.ejphar.2015.10.050. Epub 2015 Oct 30.
Sparstolonin B (SsnB), an isocoumarin compound isolated from the tubers of both Sparganium stoloniferum and Scirpus yagara, has been reported to have anti-inflammatory effects. However, whether SsnB has anti-inflammatory effects on LPS-stimulated 3T3-L1 adipocytes remains unclear. In this study, we investigated the effects of SsnB on adipocyte inflammation in 3T3-L1 adipocytes and anti-obesity properties in high fat diet (HFD)-induced obese rats. 3T3-L1 adipocytes were pretreated with SsnB 1h before LPS treatment. The expression of MCP-1, IL-6, TNF-α, and IL-10 were measured by qRT-PCR and ELISA. The expression of PPAR-γ, TLR4 and NF-κB were detected by western blotting. SsnB was administered to HFD-induced obese rats to confirm its effects in vivo. Our results showed that SsnB dose-dependently inhibited LPS-induced MCP-1, IL-6, and TNF-α production. SsnB was found to inhibit LPS-induced TLR4 expression and NF-κB activition. Furthermore, SsnB was found to activate PPAR-γ and the inhibitory effects of SsnB on MCP-1, IL-6, and TNF-α production can be reversed by PPAR-γ antagonist GW9662. In vivo, SsnB was found to reduce the body weight of rats fed with HFD. SsnB also inhibited the levels of serum triglyceride (TG) and cholesterol (TC) induced by HFD. In conclusion, the results suggested that SsnB could reduce HFD-induced obesity in rats and inhibited LPS-induced cytokines production in 3T3-L1 adipocytes by activating PPAR-γ.
水菖蒲宁B（SsnB）是一种从黑三棱和萤蔺块茎中分离出的异香豆素化合物，据报道具有抗炎作用。然而，SsnB对脂多糖刺激的3T3-L1脂肪细胞是否具有抗炎作用仍不清楚。在本研究中，我们研究了SsnB对3T3-L1脂肪细胞中脂肪细胞炎症的影响以及对高脂饮食（HFD）诱导的肥胖大鼠的抗肥胖特性。在脂多糖处理前1小时用SsnB预处理3T3-L1脂肪细胞。通过qRT-PCR和ELISA检测MCP-1、IL-6、TNF-α和IL-10的表达。通过蛋白质印迹法检测PPAR-γ、TLR4和NF-κB的表达。将SsnB给予HFD诱导的肥胖大鼠以确认其体内作用。我们的结果表明，SsnB剂量依赖性地抑制脂多糖诱导的MCP-1、IL-6和TNF-α的产生。发现SsnB抑制脂多糖诱导的TLR4表达和NF-κB激活。此外，发现SsnB激活PPAR-γ，并且SsnB对MCP-1、IL-6和TNF-α产生的抑制作用可被PPAR-γ拮抗剂GW9662逆转。在体内，发现SsnB可降低喂食HFD大鼠的体重。SsnB还抑制HFD诱导的血清甘油三酯（TG）和胆固醇（TC）水平。总之，结果表明SsnB可减轻HFD诱导的大鼠肥胖，并通过激活PPAR-γ抑制3T3-L1脂肪细胞中脂多糖诱导的细胞因子产生。
