穿心莲内酯
细胞凋亡
化学
免疫印迹
p38丝裂原活化蛋白激酶
细胞生物学
活性氧
活力测定
MAPK/ERK通路
椎间盘
血红素加氧酶
染色
分子生物学
信号转导
血红素
生物化学
生物
解剖
病理
酶
医学
基因
作者
Cunxin Zhang,Ziang Lu,Chaoliang Lyu,Shanshan Zhang,Dechun Wang
摘要
To explore the molecular mechanism by which andrographolide (ADR) inhibits static mechanical pressure-induced apoptosis in nucleus pulposus cells (NPCs) and to assess the role of ADR in inhibiting IDD.Hematoxylin-eosin (HE), toluidine blue, and immunofluorescence staining were used to identify NPCs. An NPC apoptosis model was constructed using a homemade cell pressurization device. The proliferation activity, reactive oxygen species (ROS) content, and apoptosis rate were detected using kits. The expression of related proteins was detected using Western blot. A rat tailbone IDD model was constructed using a homemade tailbone stress device. HE staining and safranine O-fast green FCF cartilage staining were used to observe the degeneration degree of the intervertebral disk.ADR inhibits static mechanical pressure-induced apoptosis and ROS accumulation in NPCs and improves cell viability. ADR can promote the expression of Heme oxygenase-1 (HO-1), p-Nrf2, p-p38, p-Erk1/2, p-JNK, and other proteins, and its effects can be blocked by inhibitors of the above proteins.ADR can inhibit IDD by activating the MAPK/Nrf2/HO-1 signaling pathway and suppressing static mechanical pressure-induced ROS accumulation in the NPCs.
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