Details

Autor(en) / Beteiligte

• Zhang, Hui
• Zhuang, Xiao-dong
• Meng, Fu-hui
• Chen, Li
• Dong, Xiao-bian
• Liu, Guo-hui
• Li, Jian-hua
• Dong, Qi
• Xu, Ji-de
• Yang, Chun-tao

Titel

Calcitriol prevents peripheral RSC96 Schwann neural cells from high glucose & methylglyoxal-induced injury through restoration of CBS/H sub(2)S expression

Ist Teil von

• Neurochemistry international, 2016-01, Vol.92, p.49-57

Erscheinungsjahr

2016

Quelle

Alma/SFX Local Collection

Beschreibungen/Notizen

• A meta-analysis has suggested that vitamin D deficiency is involved in diabetic peripheral neuropathy (DPN) and the levels of hydrogen sulfide (H sub(2)S) are also decreased in type 2 diabetes. The injection of vitamin D induces cystathionine- beta -synthase (CBS) expression and H sub(2)S generation. However, it remains unclear whether the supplementation of vitamin D prevents DPN through improvement of CBS/H sub(2)S expression. In the present study, RSC96 cells, a rat Schwann cell line, were exposed to high glucose and methylglyoxal (HG&MG) to simulate diabetic peripheral nerve injury in vivo. Before the exposure to HG&MG, the cells were preconditioned with calcitriol (CCT), an active form of vitamin D, and then CCT-mediated neuroprotection was investigated in respect of cellular viability, superoxide anion (O sub(2) super(-)) generation, inducible nitric oxide (NO) synthase (iNOS)/NO expression, mitochondrial membrane potential (MMP), as well as CBS expression and activity. It was found that both high glucose and MGO decreased cell viability and co-treatment with the two induced a more serious injury in RSC96 cells. Therefore, the exposure to HG&MG was used in the present study. The exposure to HG&MG markedly induced iNOS expression, NO and O sub(2) super(-) generation, as well as MMP loss. In addition, the exposure to HG&MG depressed CBS expression and activity in RSC96 cells. However, the preconditioning with CCT significantly antagonized HG&MG-induced cell injury including the decreased viability, iNOS overexpression, NO and O sub(2) super(-) accumulation, as well as MMP loss. CCT also partially restored the decreased CBS expression and activity triggered by HG&MG, while the inhibition of CBS with hydroxylamine attenuated CCT-mediated neuroprotection. Moreover, the exogenous donation of H sub(2)S produced similar cellular protective effects to CCT. The data indicate that the supplementation of vitamin D prevents HG&MG-induced peripheral nerve injury involving the restoration of endogenous H sub(2)S system, which may provide a basal support for the treatment of DPN with vitamin D clinically.