Department of Tea Science, College of Agriculture and Biotechnology, Zhejiang University, Hangzhou, 310058, People's Republic of China.
Key Laboratory of Tea Science of Ministry of Education, Hunan Agricultural University, Changsha, 410128, People's Republic of China.
Plant Foods Hum Nutr. 2022 Mar;77(1):105-111. doi: 10.1007/s11130-021-00937-0. Epub 2022 Feb 9.
Obesity is a worldwide epidemic and increases the risk of metabolic syndrome through chronic inflammation. Tea polyphenols (TP), the major functional component of tea, has shown preventive effects on obesity and obesity-related disease, but the underlying mechanism is complicated and remains obscure. The present study was aimed to elucidate the anti-inflammation effect of TP in high-fat-diet (HFD)-induced obese mice. Results showed that TP reduced obesity-induced inflammation and systemic lipopolysaccharides (LPS) level. The decrease of LPS level in circulation was followed by the downregulation of LPS specific receptor, toll-like receptor 4 (TLR4), and its co-receptor cluster of differentiation 14 (CD14) and adaptor protein differentiation factor 88 (MyD88) in hepatic and adipose tissues. That further inhibited the activation of nuclear factor κB (NF-κB). The serum levels of tumor necrosis factor-alpha (TNF-α), interleukin-1-beta (IL-1β) and interleukin-6 (IL-6) were significantly decreased by TP in HFD-fed mice. TP also maintained the intestinal barrier integrity by increasing intestinal tight junction proteins and reversed gut dysbiosis in obese mice. These results suggested that TP attenuated obesity-induced inflammation by reducing systemic LPS level and inhibiting LPS-activated TLR4/NF-κB pathway.
肥胖是一种全球性的流行病，通过慢性炎症增加代谢综合征的风险。茶多酚（TP）是茶叶的主要功能成分，已显示出对肥胖和肥胖相关疾病的预防作用，但潜在机制复杂且仍不清楚。本研究旨在阐明 TP 在高脂肪饮食（HFD）诱导肥胖小鼠中的抗炎作用。结果表明，TP 可减轻肥胖引起的炎症和全身内毒素（LPS）水平。循环中 LPS 水平的降低伴随着肝脏和脂肪组织中 LPS 特异性受体、 toll 样受体 4（TLR4）及其共受体 CD14 和衔接蛋白分化因子 88（MyD88）的下调，从而进一步抑制核因子 κB（NF-κB）的激活。TP 还通过增加肠道紧密连接蛋白来维持肠道屏障的完整性，并逆转肥胖小鼠的肠道菌群失调。这些结果表明，TP 通过降低全身 LPS 水平和抑制 LPS 激活的 TLR4/NF-κB 通路来减轻肥胖引起的炎症。
