Neuroprotective effects of leonurine against oxygen-glucose deprivation by targeting Cx36/CaMKII in PC12 cells.

Leonurine has been reported to play an important role in ameliorating cognitive dysfunction, inhibiting ischemic stroke, and attenuating perihematomal edema and neuroinflammation in intracerebral hemorrhage. However, the exact mechanism and potential molecular targets of this effect remain unclear....

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Main Authors: Jiao Li, Shuang Zhang, Xiaoxi Liu, Deping Han, Jianqin Xu, Yunfei Ma
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2018-01-01
Series:PLoS ONE
Online Access:http://europepmc.org/articles/PMC6049927?pdf=render
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author Jiao Li
Shuang Zhang
Xiaoxi Liu
Deping Han
Jianqin Xu
Yunfei Ma
author_facet Jiao Li
Shuang Zhang
Xiaoxi Liu
Deping Han
Jianqin Xu
Yunfei Ma
author_sort Jiao Li
collection DOAJ
description Leonurine has been reported to play an important role in ameliorating cognitive dysfunction, inhibiting ischemic stroke, and attenuating perihematomal edema and neuroinflammation in intracerebral hemorrhage. However, the exact mechanism and potential molecular targets of this effect remain unclear. Thus, in this study we investigated the neuroprotective effects of leonurine on hypoxia ischemia injury and explored the underlying mechanisms. An in vitro model of oxygen-glucose deprivation (OGD)-induced PC12 cells was established to mimic ischemic-like conditions. Cell viability, apoptosis, Cx36 and pCaMKII/CaMKII expression levels were evaluated after treatment with leonurine. The Cx36-selective antagonist mefloquine and CaMKII Inhibitor KN-93 were used to investigate the neuroprotective effect of leonurine on and the involvement of Cx36/CaMKII in this process. The results revealed that cell viability decreased and cell apoptosis and the protein expression of Cx36 and pCaMKII/CaMKII increased in the OGD-induced PC12 cells. Leonurine significantly increased cell viability and decreased cell apoptosis and the protein expression of Cx36 and pCaMKII/CaMKII in the OGD-induced PC12 cells. The specific inhibitor of Cx36 and CaMKII displayed similar protective effects. Moreover, the inhibition of Cx36 reduced pCaMKII levels and the ratio of pCaMKII/CaMKII in the OGD-induced PC12 cells, and vice versa. Taken together, these results suggest that leonurine might have a protective effect on OGD-induced PC12 cells through targeting the Cx36/CaMKII pathway. Thus, leonurine appears to have potential as a preventive or therapeutic drug against ischemic-induced neuronal injury.
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spelling doaj.art-4e44f78fe95b41248a8cb314f1e7e55a2022-12-22T02:43:10ZengPublic Library of Science (PLoS)PLoS ONE1932-62032018-01-01137e020070510.1371/journal.pone.0200705Neuroprotective effects of leonurine against oxygen-glucose deprivation by targeting Cx36/CaMKII in PC12 cells.Jiao LiShuang ZhangXiaoxi LiuDeping HanJianqin XuYunfei MaLeonurine has been reported to play an important role in ameliorating cognitive dysfunction, inhibiting ischemic stroke, and attenuating perihematomal edema and neuroinflammation in intracerebral hemorrhage. However, the exact mechanism and potential molecular targets of this effect remain unclear. Thus, in this study we investigated the neuroprotective effects of leonurine on hypoxia ischemia injury and explored the underlying mechanisms. An in vitro model of oxygen-glucose deprivation (OGD)-induced PC12 cells was established to mimic ischemic-like conditions. Cell viability, apoptosis, Cx36 and pCaMKII/CaMKII expression levels were evaluated after treatment with leonurine. The Cx36-selective antagonist mefloquine and CaMKII Inhibitor KN-93 were used to investigate the neuroprotective effect of leonurine on and the involvement of Cx36/CaMKII in this process. The results revealed that cell viability decreased and cell apoptosis and the protein expression of Cx36 and pCaMKII/CaMKII increased in the OGD-induced PC12 cells. Leonurine significantly increased cell viability and decreased cell apoptosis and the protein expression of Cx36 and pCaMKII/CaMKII in the OGD-induced PC12 cells. The specific inhibitor of Cx36 and CaMKII displayed similar protective effects. Moreover, the inhibition of Cx36 reduced pCaMKII levels and the ratio of pCaMKII/CaMKII in the OGD-induced PC12 cells, and vice versa. Taken together, these results suggest that leonurine might have a protective effect on OGD-induced PC12 cells through targeting the Cx36/CaMKII pathway. Thus, leonurine appears to have potential as a preventive or therapeutic drug against ischemic-induced neuronal injury.http://europepmc.org/articles/PMC6049927?pdf=render
spellingShingle Jiao Li
Shuang Zhang
Xiaoxi Liu
Deping Han
Jianqin Xu
Yunfei Ma
Neuroprotective effects of leonurine against oxygen-glucose deprivation by targeting Cx36/CaMKII in PC12 cells.
PLoS ONE
title Neuroprotective effects of leonurine against oxygen-glucose deprivation by targeting Cx36/CaMKII in PC12 cells.
title_full Neuroprotective effects of leonurine against oxygen-glucose deprivation by targeting Cx36/CaMKII in PC12 cells.
title_fullStr Neuroprotective effects of leonurine against oxygen-glucose deprivation by targeting Cx36/CaMKII in PC12 cells.
title_full_unstemmed Neuroprotective effects of leonurine against oxygen-glucose deprivation by targeting Cx36/CaMKII in PC12 cells.
title_short Neuroprotective effects of leonurine against oxygen-glucose deprivation by targeting Cx36/CaMKII in PC12 cells.
title_sort neuroprotective effects of leonurine against oxygen glucose deprivation by targeting cx36 camkii in pc12 cells
url http://europepmc.org/articles/PMC6049927?pdf=render
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