Intrathecal Injection of SIRT1-modified Human Mesenchymal Stem Cells Alleviates Neuropathic Pain in Rat.

Accumulating evidence has elucidated that human mesenchymal stem cells (hMSCs) exert profound analgesic effects on numerous animal models of neuropathic pain, including drug-induced peripheral nerves, diabetes-induced neuropathy, and chronic constriction injury. We aimed to address whether forcing expression of sirtuin 1 (SIRT1) can enhance the efficacy of hMSCs on alleviation of pain sensation. A rat model of chronic constriction injury (CCI) mimicking peripheral nerve injury was incorporated in the study.

lncRNA MALAT1 contributes to neuropathic pain development through regulating miR-129-5p/HMGB1 axis in a rat model of chronic constriction injury.

Mounting studies pay attention to the functional roles of long non-coding RNAs (lncRNAs) in many human diseases including neuropathic pain. LncRNA MALAT1 has been indicated to serve as a critical mediator in neuropathic pain with unclear mechanisms. The present study aims to explore the functional roles of MALAT1 in neuropathic pain progression and the related mechanisms.

miR-129-5p Alleviates Neuropathic Pain Through Regulating HMGB1 Expression in CCI Rat Models.

Recently, microRNAs are reported to be participated in the development of pain and persistence of neuropathic and inflammatory pain in animal models. Here, we characterized the functional role of miR-129-5p in pain processing in chronic constriction injury (CCI) rat models. Bilateral CCI operation was used to generate neuropathic pain rat model.

TRPM2 participates the transformation of acute pain to chronic pain during injury-induced neuropathic pain.

Transient receptor melastatin 2 (TRPM2) is a nonselective Ca -permeable cation channel highly expressed in brain and other tissues. Studies showed that TRPM2 contributed to the induction of inflammatory cytokine and chemokine of immune cells, resulted in neuropathic pain. However, how TRPM2 regulates neuropathic pain is not clear.

Thalidomide alleviates bone cancer pain by down-regulating expressions of NF-κB and GFAP in spinal astrocytes in a mouse model.

Thalidomide is one of the first line therapies in cancer pain management. Previous study has shown that thalidomide decreases the expression of tumor necrosis factor alpha in the mouse spinal cord. However, the exact cellular and molecular mechanism underlying the effect of thalidomide remains unclear.