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盐酸青藤碱对碘乙酸钠诱导的大鼠膝髋损伤的骨保护作用:炎症通路。

Bone protective effect of sinomenine against monosodium iodoacetate induced knee and hip injury in rat model: an inflammatory pathway.

机构信息

Affiliated Hospital of Yunnan University, Bone and Traumatic Surgery, Kunming, China.

出版信息

Acta Cir Bras. 2024 Feb 5;39:e390924. doi: 10.1590/acb390924. eCollection 2024.

Abstract

PURPOSE

Osteoarthritis (OA) is a degenerative joint disease which is categorized via destruction of joint cartilage and it also affects the various joints, especially knees and hips. Sinomenine active phytoconstituents isolated from the stem of Sinomenium acutum and already proof anti-inflammatory effect against the arthritis model of rodent. In this experimental protocol, we scrutinized the anti-osteoarthritis effect of sinomenine against monosodium iodoacetate (MIA) induced OA in rats.

METHODS

MIA (3 mg/50 μL) was used for inducing the OA in the rats, and rats received the oral administration of sinomenine (2.5, 5 and 7.5 mg/kg body weight) up to the end of the experimental study (four weeks). The body and organs weight were estimated. Aggrecan, C-terminal cross-linked telopeptide of type II collagen (CTX-II), glycosaminoglycans (GCGs), monocyte chemoattractant protein-1 (MCP-1), Interferon gamma (IFN-γ), antioxidant, inflammatory cytokines, inflammatory mediators and matrix metalloproteinases (MMP) were analyzed.

RESULTS

Sinomenine significantly (P < 0.001) boosted the body weight and reduced the heart weight, but the weight of spleen and kidney remain unchanged. Sinomenine significantly (P < 0.001) reduced the level of nitric oxide, MCP-1 and improved the level of aggrecan, IFN-γ and GCGs. Sinomenine remarkably upregulated the level of glutathione, superoxide dismutase and suppressed the level of malonaldehyde. It effectually modulated the level of inflammatory cytokines and inflammatory mediators and significantly (P < 0.001) reduced the level of MMPs, like MMP-1, 2, 3, 9 and 13.

CONCLUSIONS

Sinomenine is a beneficial active agent for the treatment of OA disease.

摘要

目的

骨关节炎(OA)是一种退行性关节疾病,其特征为关节软骨破坏,还会影响到各种关节,尤其是膝盖和臀部。从青风藤的茎中分离得到的青藤碱是一种具有活性的植物成分,已经证明对啮齿动物关节炎模型具有抗炎作用。在本实验方案中,我们研究了青藤碱对 MIA 诱导的大鼠骨关节炎的抗骨关节炎作用。

方法

MIA(3mg/50μL)用于诱导大鼠 OA,大鼠接受青藤碱(2.5、5 和 7.5mg/kg 体重)的口服治疗,直至实验研究结束(四周)。估计体重和器官重量。分析聚集蛋白聚糖、Ⅱ型胶原 C 末端交联肽(CTX-II)、糖胺聚糖(GCGs)、单核细胞趋化蛋白-1(MCP-1)、干扰素γ(IFN-γ)、抗氧化剂、炎症细胞因子、炎症介质和基质金属蛋白酶(MMP)。

结果

青藤碱显著(P<0.001)增加体重,降低心脏重量,但脾重和肾重不变。青藤碱显著(P<0.001)降低一氧化氮、MCP-1 水平,提高聚集蛋白聚糖、IFN-γ 和 GCGs 水平。青藤碱显著上调谷胱甘肽、超氧化物歧化酶水平,抑制丙二醛水平。它有效地调节了炎症细胞因子和炎症介质的水平,并显著(P<0.001)降低了 MMPs(如 MMP-1、2、3、9 和 13)的水平。

结论

青藤碱是治疗 OA 疾病的有益活性药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d31c/10852535/9f584fbcd2a8/1678-2674-acb-39-e390924-gf01.jpg

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