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Saeng-Kankunbi-Tang (生肝健脾汤) protects liver against oxidative damage through activation of ERK/Nrf2 pathway
Saeng-Kankunbi-Tang (生肝健脾汤) protects liver against oxidative damage through activation of ERK/Nrf2 pathway
- 中国结合医学杂志（英文版） 2016年22卷第8期 页码：619-628
- Affiliations：
1. Department of Internal Oriental Medicine of Hepatology, College of Oriental Medicine, Daegu Haany University,Daegu,Korea
2. Medical Research Center for Globalization of Herbal Formulation, College of Oriental Medicine, Daegu Haany University,Daegu,Korea
3. College of Oriental Medicine, Dongguk University,Gyeongju,Korea
4. School of Mental Health, Jining Medical University,Shandong Province,Jining,China
- Author bio：
- Funds：Supported by the National Research Foundation of Korea Grant funded by the Korea government (No. 2014R1A2A2A01007375, No. 2012R1A5A2A42671316)
DOI：10.1007/s11655-016-2466-5
中图分类号：纸质出版日期：2016，
网络出版日期：2016-6-14，
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Lee, I.W., Choi, H.Y., Lee, JH. et al. Saeng-Kankunbi-Tang (生肝健脾汤) protects liver against oxidative damage through activation of ERK/Nrf2 pathway., Chin. J. Integr. Med. 22, 619–628 (2016). https://doi.org/10.1007/s11655-016-2466-5
In Woo Lee, Hee Yoon Choi, Ju-Hee Lee, et al. Saeng-Kankunbi-Tang (生肝健脾汤) protects liver against oxidative damage through activation of ERK/Nrf2 pathway[J]. Chinese Journal of Integrative Medicine, 2016,22(8):619-628.
Lee, I.W., Choi, H.Y., Lee, JH. et al. Saeng-Kankunbi-Tang (生肝健脾汤) protects liver against oxidative damage through activation of ERK/Nrf2 pathway., Chin. J. Integr. Med. 22, 619–628 (2016). https://doi.org/10.1007/s11655-016-2466-5 DOI：
In Woo Lee, Hee Yoon Choi, Ju-Hee Lee, et al. Saeng-Kankunbi-Tang (生肝健脾汤) protects liver against oxidative damage through activation of ERK/Nrf2 pathway[J]. Chinese Journal of Integrative Medicine, 2016,22(8):619-628. DOI： 10.1007/s11655-016-2466-5.
摘要
To investigate the cytoprotective effects of Saeng-kankunbi-tang (生肝健脾汤
SKT)
a herbal prescription consisting of Artemisia capillaris and Alisma canaliculatum
and its underlying mechanism involved. In mice
blood biochemistry and histopathology were assessed in carbon tetrachloride (CCl4)-induced oxidative hepatic injury in vivo. The animal groups included vehicle-treated control
CCl4
SKT 500 mg/(kg day) CCl4+SKT 200 or 500 mg/(kg day). In HepG2 cell
tert-butyl hydroperoxide (tBHP) induced severe oxidative stress and mitochondrial dysfunction in vitro. The cyto-protective effects of SKT were determined by 3-(4
5-dimethylthiazol)-2
5-diphenyltetrazolium bromide (MTT) assay
flfluorescence activated cell sorting analysis and western blotting. The administration of SKT prevented liver damage induced by CCl4 in mice
by inhibition of hepatocyte degeneration and inflflammatory cell infifiltration as well as plasma parameters such as alanine aminotransferase (P<0.01). Moreover
treatment with tBHP induced hepatocyte death and cellular reactive oxygen species production in hepatocyte cell line. However
SKT pretreatment (30–300 μg/mL) reduced this cell death and oxidative stress (P<0.01). More importantly
SKT inhibited the ability of tBHP to induce changes in mitochondrial membrane transition in cell stained with rhodamine 123 P<0.01). Furthermore
treatment with SKT induced extracellular signal-regulated kinases-mediated nuclear factor erythroid-2-related factor 2 (Nrf2) activation as well as the expressions of heme oxygenase 1 and glutamate- cystein ligase catalytic
Nrf2 target genes. SKT has the ability to protect hepatocyte against oxidative stress and mitochondrial damage mediated by Nrf2 activation.
Abstract
To investigate the cytoprotective effects of Saeng-kankunbi-tang (生肝健脾汤
SKT)
a herbal prescription consisting of Artemisia capillaris and Alisma canaliculatum
and its underlying mechanism involved. In mice
blood biochemistry and histopathology were assessed in carbon tetrachloride (CCl4)-induced oxidative hepatic injury in vivo. The animal groups included vehicle-treated control
CCl4
SKT 500 mg/(kg day) CCl4+SKT 200 or 500 mg/(kg day). In HepG2 cell
tert-butyl hydroperoxide (tBHP) induced severe oxidative stress and mitochondrial dysfunction in vitro. The cyto-protective effects of SKT were determined by 3-(4
5-dimethylthiazol)-2
5-diphenyltetrazolium bromide (MTT) assay
flfluorescence activated cell sorting analysis and western blotting. The administration of SKT prevented liver damage induced by CCl4 in mice
by inhibition of hepatocyte degeneration and inflflammatory cell infifiltration as well as plasma parameters such as alanine aminotransferase (P<0.01). Moreover
treatment with tBHP induced hepatocyte death and cellular reactive oxygen species production in hepatocyte cell line. However
SKT pretreatment (30–300 μg/mL) reduced this cell death and oxidative stress (P<0.01). More importantly
SKT inhibited the ability of tBHP to induce changes in mitochondrial membrane transition in cell stained with rhodamine 123 P<0.01). Furthermore
treatment with SKT induced extracellular signal-regulated kinases-mediated nuclear factor erythroid-2-related factor 2 (Nrf2) activation as well as the expressions of heme oxygenase 1 and glutamate- cystein ligase catalytic
Nrf2 target genes. SKT has the ability to protect hepatocyte against oxidative stress and mitochondrial damage mediated by Nrf2 activation.
关键词
aeng-kankunbi-tangmitochondrianuclear factor erythroid-2-related factor 2oxidative stresslivermouse
Keywords
aeng-kankunbi-tangmitochondrianuclear factor erythroid-2-related factor 2oxidative stresslivermouse
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