Effects of Upregulation of TNFAIP3 on Diabetic Neuropathic Pain in Mice

Abstract

Globally, diabetes has assumed epidemic proportions with the neuropathic complications attributed to the malady emerging as a substantial burden on patients and society. DNP has greatly affected the daily life of patients, the effect of traditional treatment methods is not ideal, and it is easy to produce drug resistance. This work is aimed at scrutinizing the effect of upregulating the expression of TNFAIP3 on diabetic neuralgia in mice. This work entailed ascertaining the effects of TNFAIP3 on a murine DNP system. This inspired us to observe the analgesic effect via high expression of lentivirus-mediated TNFAIP3 by intrathecal injection in the animal model to explore its regulatory impacts, symptom relief, and mechanistic role in pain. The results displayed an attenuation of hind paw pain hypersensitivity by LV-TNFAIP3 in the animals. The spinal cord and dorsal root ganglion of mice with neuropathic pain displayed an evident dip in TNFAIP3. Inhibition of the ERK/NF-κB signaling pathway employing LV-TNFAIP3 conspicuously suppressed this pathway while the diabetic pain hypersensitivity was quelled. This effect was also seen with insulin treatment evidently. In conclusion, according to the above analyses, the interaction between DNP and extracellular signal-regulated kinase signal transduction pathway is one of the key factors of pathogenesis.

A meta-analysis of genome-wide gene expression differences identifies promising targets for type 2 diabetes mellitus

“…The literature has also confirmed their role in the progression of type 2 diabetes mellitus; hence, these genes can further be used as potential targets to treat diabetes mellitus by formulating drugs that would specifically target these genes. The secondary genes TNFAIP , MMP9 , and CXCL showing interaction with PTX3 have a potential role in diabetes mellitus ( 22 , 30 , 31 ). Several lines of evidence have also supported the role of the secondary genes FMO1 and ALOX1 having interaction with CYP3A4 and PTGS1 in diabetes mellitus ( 31 , 32 ).…”