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Histidine protects human lens epithelial cells against H 2 O 2 ‐induced oxidative stress injury through the NF‐кB pathway
Author(s) -
Bai Jie,
Yu Nannan,
Mu Hua,
Dong Li,
Zhang Xiaomei
Publication year - 2018
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.26323
Subject(s) - oxidative stress , histidine , reactive oxygen species , glutathione , malondialdehyde , apoptosis , oxidative phosphorylation , biochemistry , chemistry , microbiology and biotechnology , biology , amino acid , enzyme
Histidine, an amino acid that is essential to humans, exerts favorable cytoprotective effects against oxidative stress in vivo and in vitro, but the effect of histidine on human lens epithelial cells (HLECs) and its regulatory mechanism have not previously been reported. The oxidative stress induced by H 2 O 2 plays an important role in the pathology of cataract. We know that HLECs are important for maintaining the transparency and integrity of the lens. In the present study, we investigated the possible molecular mechanisms underlying the cytoprotective effects of histidine against H 2 O 2 ‐induced oxidative stress in HLECs. The results showed that histidine reduced H 2 O 2 ‐induced cell apoptosis and reactive oxygen species (ROS) accumulation, protected HLECs from H 2 O 2 ‐induced oxidative damage, increased the expression levels of dismutase (SOD) and glutathione (GSH), and decreased the expression level of malondialdehyde (MDA), and the protective effect of histidine depended on the NF‐кB pathway. Together, these data suggest that histidine could be helpful in inhibiting oxidative stress in the lens and thus attenuating cataract formation.