Hydrogen relieves neuropathic pain in diabetic rats by inhibiting mcp1 and ccr2 expressions

Abstract

We aimed to explore the mechanism for hydrogen in the treatment of neuropathic pain in diabetic rats. Eight-week-old male SD rats were randomly divided into control, model and hydrogen treatment groups. Th e hydrogen treatment group was intraperitoneally injected with hydrogen-rich saline daily in 7th and 8th weeks aft er modeling. Before and 2, 4, 6 and 8 weeks aft er modeling, the neurological function, behavioral changes and levels of infl ammatory factors TNF-α and IL-6 in the sciatic nerve were detected, and MCP1 and CCR2 protein expressions were measured by Western blotting. Compared with the model group, the hydrogen treatment group had signifi cantly increased motor nerve conduction velocity, thermal withdrawal latency and mechanical withdrawal threshold (P<0.05). Th e signifi cantly higher levels of TNF-α and IL-6 in the sciatic nerve of the model group than those of the control group decreased in the hydrogen treatment group (P<0.05). Th e protein expressions of MCP1 and CCR2 in the sciatic nerve of the model group signifi cantly exceeded those of the control group. Such expressions of the hydrogen treatment group were lower than those of the model group. Hydrogen alleviated the inflammatory response of peripheral nerves in diabetic rats by inhibiting the MCP1-CCR2 signaling pathway, thus mitigating neuropathic pain.

Keywords

• diabetic neuropathy
• hydrogen
• mcp1
• ccr2
• tnf-α
• il-6