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Berberine Ameliorates MCAO Induced Cerebral Ischemia/Reperfusion Injury via Activation of the BDNF-TrkB-PI3K/Akt Signaling Pathway.
Neurochem Res. 2018 Mar; 43(3):702-710.NR

Abstract

Cerebral ischemic injury remains associated with high mortality rates and lacks effective therapeutic intervention. Berberine (BBR) possesses anti-oxidant, anti-inflammatory, and anti-tumor activities, as well as potent neuroprotective effects. Although recent studies have examined the neuroprotective effects of berberine, little is known regarding its usefulness in treating cerebral ischemia. Thus, the aim of this study is to investigate the possible effect and the mechanism of berberine against cerebral ischemic injury using the middle cerebral artery occlusion (MCAO) model. Rats were randomly divided into three groups: control group, MCAO group, and MCAO + BBR group. Modified neurological severity score tests (mNSS) and infarct volumes were measured to determine the neuroprotective effects of berberine. Neuronal survival in striatum was examined by TUNEL staining and immunohistochemistry. Western blotting measured the expression of BDNF, TrkB, p-Akt and cleaved caspase-3. The results demonstrated that BBR could significantly protect against MCAO. Berberine also increased the expression of BDNF, TrkB, and p-Akt, which were reduced after MCAO. Furthermore, treatment with BBR declined the apoptosis-related proteins induced by MCAO. However, treatment with LY294002 (PI3K inhibitor) reversed the BBR-induced increases in BDNF and p-Akt proteins and decreased cleaved caspase-3 protein expression in focal cerebral ischemic rats. In summary, our results demonstrated that BBR could exert neuroprotective effects through reduction of striatum apoptosis via the BDNF-TrkB-PI3K/Akt signaling pathway.

Authors+Show Affiliations

Department of Neurology, Affiliated Hospital of Jining Medical University, 89 guhuai Road, Jining, 272000, Shandong, People's Republic of China.Department of Neurology, Affiliated Hospital of Jining Medical University, 89 guhuai Road, Jining, 272000, Shandong, People's Republic of China.Department of Neurology, Affiliated Hospital of Jining Medical University, 89 guhuai Road, Jining, 272000, Shandong, People's Republic of China.Department of Neurology, Affiliated Hospital of Jining Medical University, 89 guhuai Road, Jining, 272000, Shandong, People's Republic of China. sdmzhangming@126.com.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

29357017

Citation

Yang, Jun, et al. "Berberine Ameliorates MCAO Induced Cerebral Ischemia/Reperfusion Injury Via Activation of the BDNF-TrkB-PI3K/Akt Signaling Pathway." Neurochemical Research, vol. 43, no. 3, 2018, pp. 702-710.
Yang J, Yan H, Li S, et al. Berberine Ameliorates MCAO Induced Cerebral Ischemia/Reperfusion Injury via Activation of the BDNF-TrkB-PI3K/Akt Signaling Pathway. Neurochem Res. 2018;43(3):702-710.
Yang, J., Yan, H., Li, S., & Zhang, M. (2018). Berberine Ameliorates MCAO Induced Cerebral Ischemia/Reperfusion Injury via Activation of the BDNF-TrkB-PI3K/Akt Signaling Pathway. Neurochemical Research, 43(3), 702-710. https://doi.org/10.1007/s11064-018-2472-4
Yang J, et al. Berberine Ameliorates MCAO Induced Cerebral Ischemia/Reperfusion Injury Via Activation of the BDNF-TrkB-PI3K/Akt Signaling Pathway. Neurochem Res. 2018;43(3):702-710. PubMed PMID: 29357017.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Berberine Ameliorates MCAO Induced Cerebral Ischemia/Reperfusion Injury via Activation of the BDNF-TrkB-PI3K/Akt Signaling Pathway. AU - Yang,Jun, AU - Yan,Hui, AU - Li,Sumei, AU - Zhang,Min, Y1 - 2018/01/22/ PY - 2017/09/18/received PY - 2018/01/09/accepted PY - 2017/12/25/revised PY - 2018/1/23/pubmed PY - 2018/8/31/medline PY - 2018/1/23/entrez KW - Apoptosis KW - BDNF KW - Berberine KW - MCAO KW - PI3K/Akt KW - TrkB SP - 702 EP - 710 JF - Neurochemical research JO - Neurochem. Res. VL - 43 IS - 3 N2 - Cerebral ischemic injury remains associated with high mortality rates and lacks effective therapeutic intervention. Berberine (BBR) possesses anti-oxidant, anti-inflammatory, and anti-tumor activities, as well as potent neuroprotective effects. Although recent studies have examined the neuroprotective effects of berberine, little is known regarding its usefulness in treating cerebral ischemia. Thus, the aim of this study is to investigate the possible effect and the mechanism of berberine against cerebral ischemic injury using the middle cerebral artery occlusion (MCAO) model. Rats were randomly divided into three groups: control group, MCAO group, and MCAO + BBR group. Modified neurological severity score tests (mNSS) and infarct volumes were measured to determine the neuroprotective effects of berberine. Neuronal survival in striatum was examined by TUNEL staining and immunohistochemistry. Western blotting measured the expression of BDNF, TrkB, p-Akt and cleaved caspase-3. The results demonstrated that BBR could significantly protect against MCAO. Berberine also increased the expression of BDNF, TrkB, and p-Akt, which were reduced after MCAO. Furthermore, treatment with BBR declined the apoptosis-related proteins induced by MCAO. However, treatment with LY294002 (PI3K inhibitor) reversed the BBR-induced increases in BDNF and p-Akt proteins and decreased cleaved caspase-3 protein expression in focal cerebral ischemic rats. In summary, our results demonstrated that BBR could exert neuroprotective effects through reduction of striatum apoptosis via the BDNF-TrkB-PI3K/Akt signaling pathway. SN - 1573-6903 UR - https://www.unboundmedicine.com/medline/citation/29357017/Berberine_Ameliorates_MCAO_Induced_Cerebral_Ischemia/Reperfusion_Injury_via_Activation_of_the_BDNF_TrkB_PI3K/Akt_Signaling_Pathway_ L2 - https://doi.org/10.1007/s11064-018-2472-4 DB - PRIME DP - Unbound Medicine ER -