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Calcitriol prevents peripheral RSC96 Schwann neural cells from high glucose & methylglyoxal-induced injury through restoration of CBS/H2S expression.
Neurochem Int 2016; 92:49-57NI

Abstract

A meta-analysis has suggested that vitamin D deficiency is involved in diabetic peripheral neuropathy (DPN) and the levels of hydrogen sulfide (H2S) are also decreased in type 2 diabetes. The injection of vitamin D induces cystathionine-β-synthase (CBS) expression and H2S generation. However, it remains unclear whether the supplementation of vitamin D prevents DPN through improvement of CBS/H2S 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 (O2(-)) 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 O2(-) 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 O2(-) 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 H2S 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 H2S system, which may provide a basal support for the treatment of DPN with vitamin D clinically.

Authors+Show Affiliations

Department of Physiology, Guangzhou Medical University, Guangzhou 511436, China; Quality Control Section of Academic Affairs, Guangzhou Medical University, Guangzhou 511436, China.Department of Cardiology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou 510080, China.Department of Physiology, Guangzhou Medical University, Guangzhou 511436, China.Department of Physiology, Guangzhou Medical University, Guangzhou 511436, China.Department of Cardiology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou 510080, China.Department of Physiology, Guangzhou Medical University, Guangzhou 511436, China.Department of Physiology, Guangzhou Medical University, Guangzhou 511436, China; Quality Control Section of Academic Affairs, Guangzhou Medical University, Guangzhou 511436, China.Department of Physiology, Guangzhou Medical University, Guangzhou 511436, China.Department of Physiology, Guangzhou Medical University, Guangzhou 511436, China.Department of Physiology, Guangzhou Medical University, Guangzhou 511436, China. Electronic address: yang-chuntao@163.com.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

26707812

Citation

Zhang, Hui, et al. "Calcitriol Prevents Peripheral RSC96 Schwann Neural Cells From High Glucose & Methylglyoxal-induced Injury Through Restoration of CBS/H2S Expression." Neurochemistry International, vol. 92, 2016, pp. 49-57.
Zhang H, Zhuang XD, Meng FH, et al. Calcitriol prevents peripheral RSC96 Schwann neural cells from high glucose & methylglyoxal-induced injury through restoration of CBS/H2S expression. Neurochem Int. 2016;92:49-57.
Zhang, H., Zhuang, X. D., Meng, F. H., Chen, L., Dong, X. B., Liu, G. H., ... Yang, C. T. (2016). Calcitriol prevents peripheral RSC96 Schwann neural cells from high glucose & methylglyoxal-induced injury through restoration of CBS/H2S expression. Neurochemistry International, 92, pp. 49-57. doi:10.1016/j.neuint.2015.12.005.
Zhang H, et al. Calcitriol Prevents Peripheral RSC96 Schwann Neural Cells From High Glucose & Methylglyoxal-induced Injury Through Restoration of CBS/H2S Expression. Neurochem Int. 2016;92:49-57. PubMed PMID: 26707812.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Calcitriol prevents peripheral RSC96 Schwann neural cells from high glucose & methylglyoxal-induced injury through restoration of CBS/H2S expression. AU - Zhang,Hui, AU - Zhuang,Xiao-dong, AU - Meng,Fu-hui, AU - Chen,Li, AU - Dong,Xiao-bian, AU - Liu,Guo-Hui, AU - Li,Jian-hua, AU - Dong,Qi, AU - Xu,Ji-de, AU - Yang,Chun-tao, Y1 - 2015/12/17/ PY - 2015/08/14/received PY - 2015/12/04/revised PY - 2015/12/09/accepted PY - 2015/12/29/entrez PY - 2015/12/29/pubmed PY - 2016/10/19/medline KW - Diabetic peripheral neuropathy KW - Hydrogen sulfide KW - Inducible nitric oxide synthase KW - Methylglyoxal KW - Mitochondrial function KW - Vitamin D SP - 49 EP - 57 JF - Neurochemistry international JO - Neurochem. Int. VL - 92 N2 - A meta-analysis has suggested that vitamin D deficiency is involved in diabetic peripheral neuropathy (DPN) and the levels of hydrogen sulfide (H2S) are also decreased in type 2 diabetes. The injection of vitamin D induces cystathionine-β-synthase (CBS) expression and H2S generation. However, it remains unclear whether the supplementation of vitamin D prevents DPN through improvement of CBS/H2S 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 (O2(-)) 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 O2(-) 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 O2(-) 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 H2S 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 H2S system, which may provide a basal support for the treatment of DPN with vitamin D clinically. SN - 1872-9754 UR - https://www.unboundmedicine.com/medline/citation/26707812/Calcitriol_prevents_peripheral_RSC96_Schwann_neural_cells_from_high_glucose_&_methylglyoxal_induced_injury_through_restoration_of_CBS/H2S_expression_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0197-0186(15)30074-7 DB - PRIME DP - Unbound Medicine ER -