Isorhamnetin inhibits IL‑1β‑induced expression of inflammatory mediators in human chondrocytes

Li,Jin; Wu,Ruishan; Qin,Xiaoping; Liu,Dongyang; Lin,Fenjie; Feng,Qinglu

doi:10.3892/mmr.2017.7041

Isorhamnetin inhibits IL‑1β‑induced expression of inflammatory mediators in human chondrocytes

Authors:
- Jin Li
- Ruishan Wu
- Xiaoping Qin
- Dongyang Liu
- Fenjie Lin
- Qinglu Feng
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Affiliations: Department of Pain Management, The First Affiliated Hospital of Jinan University, Guangzhou, Guangdong 510000, P.R. China, Department of Laboratory, Guangdong Provincial Family Planning Science and Technology Research Institute, Guangzhou, Guangdong 510000, P.R. China, Department of Urology, The First Affiliated Hospital of Jinan University, Guangzhou, Guangdong 510000, P.R. China, Department of Gynecology and Obstetrics, The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong 510000, P.R. China, Department of Pharmacy, The First Affiliated Hospital of Shenzhen University, Shenzhen, Guangdong 518000, P.R. China
Published online on: July 20, 2017 https://doi.org/10.3892/mmr.2017.7041
Pages: 4253-4258

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Abstract

Isorhamnetin (ISH) is a flavonoid primarily obtained from the fruit of Hippophae rhamnoides L., which possesses anti‑inflammatory properties. However, the effect of ISH on the expression of inflammatory mediators in response to interleukin (IL)‑1β stimulation has not been elucidated. The present study investigated the effects of ISH on the expression of inflammatory mediators in human chondrocytes, induced by IL‑1β. The results of the present study demonstrated that pretreatment with ISH inhibited the expression of stromelysin‑1 and collagenase 3 in chondrocytes, induced by IL‑1β. Pretreatment with ISH inhibited the IL‑1β‑stimulated synthesis of NO and prostaglandin E2 induced by IL‑1β, in addition to the expression of inducible nitric oxide synthase and prostaglandin G/H synthase 2 in chondrocytes. Additionally, ISH inhibited the expression of nuclear factor (NF)‑κB and transcription factor p65, and the degradation of NF‑κB inhibitor α induced by IL‑1β in chondrocytes. In conclusion, the results of the present study indicated that ISH exhibited anti‑inflammatory and chondroprotective effects in IL‑1β‑stimulated chondrocytes. The results of the present study suggest that ISH may be a potential agent in the future treatment of osteoarthritis.