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Isosteviol Sodium Protects Against Permanent Cerebral Ischemia Injury in Mice via Inhibition of NF-κB-Mediated Inflammatory and Apoptotic Responses.
J Stroke Cerebrovasc Dis. 2017 Nov; 26(11):2603-2614.JS

Abstract

BACKGROUND

Isosteviol sodium (STVNa) has been reported to have neuroprotective effects against ischemia/reperfusion (I/R) injury in rats. Furthermore, recanalization treatments, including thrombolytic therapy, have several limitations. Excessive inflammation and apoptosis contribute to the pathogenesis of ischemic brain damage. Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) is critical to these processes and is associated with cerebral ischemia. Therefore, we studied the potential therapeutic effects and mechanisms of STVNa on permanent cerebral ischemia in mice.

METHODS

Permanent middle cerebral artery occlusion (pMCAO) was established via the suture method, followed by intravenous STVNa (7.5, 15, 30, 45, and 60 mg/kg). Neurobehavioral deficits, infarct volume, and histology were examined 24 hours after cerebral ischemia. In addition, the messenger RNA (mRNA) expression of NF-κB-related genes was detected using real-time quantitative polymerase chain reaction (qPCR).

RESULTS

STVNa (30 mg/kg) had significant neuroprotective effects 24 hours after pMCAO, including the reduction of the infarct volume and the improvement of the neurological severity score. Immunohistochemistry demonstrated that STVNa significantly increased the number of restored neurons and decreased the number of astrocytes. qPCR also demonstrated that the mRNA expression of inhibitor of nuclear factor kappa-B kinase-α, inhibitor of nuclear factor kappa-B kinase-β, NF-κB, inhibitor of NF-κB-α, tumor necrosis factor-α, interleukin-1 beta, Bcl2-associated X protein, and caspase-3 were significantly downregulated, whereas B-cell CLL/lymphoma 2 mRNA was upregulated with STVNa treatment compared with vehicle.

CONCLUSIONS

These findings demonstrate a neuroprotective role of STVNa during cerebral ischemia, which may result from interactions with the NF-κB signaling pathway and the associated inflammatory and apoptotic responses.

Authors+Show Affiliations

School of Bioscience and Bioengineering, South China University of Technology, Guangzhou 510006, China.School of Bioscience and Bioengineering, South China University of Technology, Guangzhou 510006, China; Institute of Biomedical and Pharmaceutical Sciences, Guangdong University of Technology, Guangzhou 510005, China.School of Bioscience and Bioengineering, South China University of Technology, Guangzhou 510006, China.Institute of Biomedical and Pharmaceutical Sciences, Guangdong University of Technology, Guangzhou 510005, China.School of Bioscience and Bioengineering, South China University of Technology, Guangzhou 510006, China; Institute of Biomedical and Pharmaceutical Sciences, Guangdong University of Technology, Guangzhou 510005, China. Electronic address: went@gdut.edu.cn.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

28784277

Citation

Zhang, Hao, et al. "Isosteviol Sodium Protects Against Permanent Cerebral Ischemia Injury in Mice Via Inhibition of NF-κB-Mediated Inflammatory and Apoptotic Responses." Journal of Stroke and Cerebrovascular Diseases : the Official Journal of National Stroke Association, vol. 26, no. 11, 2017, pp. 2603-2614.
Zhang H, Sun X, Xie Y, et al. Isosteviol Sodium Protects Against Permanent Cerebral Ischemia Injury in Mice via Inhibition of NF-κB-Mediated Inflammatory and Apoptotic Responses. J Stroke Cerebrovasc Dis. 2017;26(11):2603-2614.
Zhang, H., Sun, X., Xie, Y., Zan, J., & Tan, W. (2017). Isosteviol Sodium Protects Against Permanent Cerebral Ischemia Injury in Mice via Inhibition of NF-κB-Mediated Inflammatory and Apoptotic Responses. Journal of Stroke and Cerebrovascular Diseases : the Official Journal of National Stroke Association, 26(11), 2603-2614. https://doi.org/10.1016/j.jstrokecerebrovasdis.2017.06.023
Zhang H, et al. Isosteviol Sodium Protects Against Permanent Cerebral Ischemia Injury in Mice Via Inhibition of NF-κB-Mediated Inflammatory and Apoptotic Responses. J Stroke Cerebrovasc Dis. 2017;26(11):2603-2614. PubMed PMID: 28784277.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Isosteviol Sodium Protects Against Permanent Cerebral Ischemia Injury in Mice via Inhibition of NF-κB-Mediated Inflammatory and Apoptotic Responses. AU - Zhang,Hao, AU - Sun,Xiaoou, AU - Xie,Yanxiang, AU - Zan,Jie, AU - Tan,Wen, Y1 - 2017/08/04/ PY - 2017/04/08/received PY - 2017/06/01/revised PY - 2017/06/09/accepted PY - 2017/8/9/pubmed PY - 2018/5/25/medline PY - 2017/8/9/entrez KW - NF-κB KW - Permanent cerebral ischemia KW - STVNa KW - apoptosis KW - inflammatory SP - 2603 EP - 2614 JF - Journal of stroke and cerebrovascular diseases : the official journal of National Stroke Association JO - J Stroke Cerebrovasc Dis VL - 26 IS - 11 N2 - BACKGROUND: Isosteviol sodium (STVNa) has been reported to have neuroprotective effects against ischemia/reperfusion (I/R) injury in rats. Furthermore, recanalization treatments, including thrombolytic therapy, have several limitations. Excessive inflammation and apoptosis contribute to the pathogenesis of ischemic brain damage. Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) is critical to these processes and is associated with cerebral ischemia. Therefore, we studied the potential therapeutic effects and mechanisms of STVNa on permanent cerebral ischemia in mice. METHODS: Permanent middle cerebral artery occlusion (pMCAO) was established via the suture method, followed by intravenous STVNa (7.5, 15, 30, 45, and 60 mg/kg). Neurobehavioral deficits, infarct volume, and histology were examined 24 hours after cerebral ischemia. In addition, the messenger RNA (mRNA) expression of NF-κB-related genes was detected using real-time quantitative polymerase chain reaction (qPCR). RESULTS: STVNa (30 mg/kg) had significant neuroprotective effects 24 hours after pMCAO, including the reduction of the infarct volume and the improvement of the neurological severity score. Immunohistochemistry demonstrated that STVNa significantly increased the number of restored neurons and decreased the number of astrocytes. qPCR also demonstrated that the mRNA expression of inhibitor of nuclear factor kappa-B kinase-α, inhibitor of nuclear factor kappa-B kinase-β, NF-κB, inhibitor of NF-κB-α, tumor necrosis factor-α, interleukin-1 beta, Bcl2-associated X protein, and caspase-3 were significantly downregulated, whereas B-cell CLL/lymphoma 2 mRNA was upregulated with STVNa treatment compared with vehicle. CONCLUSIONS: These findings demonstrate a neuroprotective role of STVNa during cerebral ischemia, which may result from interactions with the NF-κB signaling pathway and the associated inflammatory and apoptotic responses. SN - 1532-8511 UR - https://www.unboundmedicine.com/medline/citation/28784277/Isosteviol_Sodium_Protects_Against_Permanent_Cerebral_Ischemia_Injury_in_Mice_via_Inhibition_of_NF_κB_Mediated_Inflammatory_and_Apoptotic_Responses_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1052-3057(17)30306-3 DB - PRIME DP - Unbound Medicine ER -