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Preventive effect of silymarin in cerebral ischemia-reperfusion-induced brain injury in rats possibly through impairing NF-κB and STAT-1 activation.
Phytomedicine 2010; 17(12):963-73P

Abstract

Silymarin and silibinin are bioactive components isolated from Silybum marianum. They have been reported to exhibit anti-oxidative and anti-inflammatory effects. Many studies revealed that drugs with potent anti-inflammatory potential can protect animals against inflammation-associated neurodegenerative disease, e.g., stroke. In this current work we established an animal model of acute ischemic stroke injury by inducing cerebral ischemic/reperfusion (CI/R) in rats to elucidate whether silymarin or silibinin can protect animals from CI/R injury. Pretreatment with silymarin, but not silibinin, dose-dependently (1-10μg/kg, i.v.) reduced CI/R-induced brain infarction by 16-40% and improved neurological deficits in rats with a stroke. Elevated pathophysiological biomarkers for CI/R-induced brain injury, including lipid peroxidation, protein nitrosylation, and oxidative stress, were all reduced by silymarin. In addition, expression of inflammation-associated proteins (e.g., inducible nitric oxide synthase, cyclooxygenase-2 and myeloperoxidase), and transcriptional factors (e.g., nuclear factor (NF)-kappa B and signal transducer and activator of transcription (STAT)-1), as well as production of proinflammatory cytokine (e.g., interleukin-1β and tumor necrosis factor-α) was all significantly prevented by silymarin. Furthermore, an in vitro study on microglial BV2 cells showed that silymarin could inhibit nitric oxide and superoxide anion production, possibly by interfering with NF-κB nuclear translocation/activation. Likewise, silymarin pretreatment also inhibited IκB-α degradation and NF-κB nuclear translocation in brain tissues of ischemic rats. Our results reveal that silymarin, but not its active component silibinin, protected rats against CI/R-induced stroke injury by amelioration of the oxidative and nitrosative stresses and inflammation-mediated tissue injury through impeding the activation of proinflammatory transcription factors (e.g., NF-κB and STAT-1) in the upregulation of proinflammatory proteins and cytokines in stroke-damaged sites. In conclusion, silymarin displays beneficial effects of preventing inflammation-related neurodegenerative disease, e.g., stroke, which needs further investigation and clinical evidences.

Authors+Show Affiliations

Department of Chinese Medicine, Taoyuan General Hospital, Department of Health, Department of Nursing, Yuanpei University, Hsinchu, Taiwan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

20833521

Citation

Hou, Yu-Chang, et al. "Preventive Effect of Silymarin in Cerebral Ischemia-reperfusion-induced Brain Injury in Rats Possibly Through Impairing NF-κB and STAT-1 Activation." Phytomedicine : International Journal of Phytotherapy and Phytopharmacology, vol. 17, no. 12, 2010, pp. 963-73.
Hou YC, Liou KT, Chern CM, et al. Preventive effect of silymarin in cerebral ischemia-reperfusion-induced brain injury in rats possibly through impairing NF-κB and STAT-1 activation. Phytomedicine. 2010;17(12):963-73.
Hou, Y. C., Liou, K. T., Chern, C. M., Wang, Y. H., Liao, J. F., Chang, S., ... Shen, Y. C. (2010). Preventive effect of silymarin in cerebral ischemia-reperfusion-induced brain injury in rats possibly through impairing NF-κB and STAT-1 activation. Phytomedicine : International Journal of Phytotherapy and Phytopharmacology, 17(12), pp. 963-73. doi:10.1016/j.phymed.2010.03.012.
Hou YC, et al. Preventive Effect of Silymarin in Cerebral Ischemia-reperfusion-induced Brain Injury in Rats Possibly Through Impairing NF-κB and STAT-1 Activation. Phytomedicine. 2010;17(12):963-73. PubMed PMID: 20833521.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Preventive effect of silymarin in cerebral ischemia-reperfusion-induced brain injury in rats possibly through impairing NF-κB and STAT-1 activation. AU - Hou,Yu-Chang, AU - Liou,Kuo-Tong, AU - Chern,Chang-Ming, AU - Wang,Yea-Hwey, AU - Liao,Jyh-Fei, AU - Chang,Shiou, AU - Chou,Yuan-Hwa, AU - Shen,Yuh-Chiang, PY - 2009/11/11/received PY - 2010/02/11/revised PY - 2010/03/13/accepted PY - 2010/9/14/entrez PY - 2010/9/14/pubmed PY - 2010/12/16/medline SP - 963 EP - 73 JF - Phytomedicine : international journal of phytotherapy and phytopharmacology JO - Phytomedicine VL - 17 IS - 12 N2 - Silymarin and silibinin are bioactive components isolated from Silybum marianum. They have been reported to exhibit anti-oxidative and anti-inflammatory effects. Many studies revealed that drugs with potent anti-inflammatory potential can protect animals against inflammation-associated neurodegenerative disease, e.g., stroke. In this current work we established an animal model of acute ischemic stroke injury by inducing cerebral ischemic/reperfusion (CI/R) in rats to elucidate whether silymarin or silibinin can protect animals from CI/R injury. Pretreatment with silymarin, but not silibinin, dose-dependently (1-10μg/kg, i.v.) reduced CI/R-induced brain infarction by 16-40% and improved neurological deficits in rats with a stroke. Elevated pathophysiological biomarkers for CI/R-induced brain injury, including lipid peroxidation, protein nitrosylation, and oxidative stress, were all reduced by silymarin. In addition, expression of inflammation-associated proteins (e.g., inducible nitric oxide synthase, cyclooxygenase-2 and myeloperoxidase), and transcriptional factors (e.g., nuclear factor (NF)-kappa B and signal transducer and activator of transcription (STAT)-1), as well as production of proinflammatory cytokine (e.g., interleukin-1β and tumor necrosis factor-α) was all significantly prevented by silymarin. Furthermore, an in vitro study on microglial BV2 cells showed that silymarin could inhibit nitric oxide and superoxide anion production, possibly by interfering with NF-κB nuclear translocation/activation. Likewise, silymarin pretreatment also inhibited IκB-α degradation and NF-κB nuclear translocation in brain tissues of ischemic rats. Our results reveal that silymarin, but not its active component silibinin, protected rats against CI/R-induced stroke injury by amelioration of the oxidative and nitrosative stresses and inflammation-mediated tissue injury through impeding the activation of proinflammatory transcription factors (e.g., NF-κB and STAT-1) in the upregulation of proinflammatory proteins and cytokines in stroke-damaged sites. In conclusion, silymarin displays beneficial effects of preventing inflammation-related neurodegenerative disease, e.g., stroke, which needs further investigation and clinical evidences. SN - 1618-095X UR - https://www.unboundmedicine.com/medline/citation/20833521/Preventive_effect_of_silymarin_in_cerebral_ischemia_reperfusion_induced_brain_injury_in_rats_possibly_through_impairing_NF_κB_and_STAT_1_activation_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0944-7113(10)00071-1 DB - PRIME DP - Unbound Medicine ER -