Andrographolide Inhibits Static Mechanical Pressure-Induced Intervertebral Disc Degeneration via the MAPK/Nrf2/HO-1 Pathway

Purpose: 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.

Methods: 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.

Results: 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.

Conclusion: ADR can inhibit IDD by activating the MAPK/Nrf2/HO-1 signaling pathway and suppressing static mechanical pressure-induced ROS accumulation in the NPCs.

HO-1; andrographolide; apoptosis; intervertebral disc degeneration; nucleus pulposus cells; reactive oxygen species.