FOLLOWUS
1. College of Pharmacy, Chengdu University of Traditional Chinese Medicine,Chengdu,China
2. Department of Pharmacy, Hospital of People’s Liberation Army,Beijing,China,302
3. Department of Integrative Medical Center, Hospital of People’s Liberation Army,Beijing,China,302
4. China Military Institute of Chinese Medicine, Hospital of People’s Liberation Army,Beijing,China,302
5. Animal Laboratory Center, Hospital of People’s Liberation Army,Beijing,China,302
6. Chongqing Academy of Chinese Traditional Materia Medica, Key Laboratory of Chongqing Traditional Chinese Medicine Resources,Chongqing,China
纸质出版日期:2018,
网络出版日期:2015-12-19,
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Wei, Sz., Luo, Sq., Wang, J. et al. San-Cao Granule (三草颗粒) Ameliorates Hepatic Fibrosis through High Mobility Group Box-1 Protein/Smad Signaling Pathway., Chin. J. Integr. Med. 24, 502–511 (2018). https://doi.org/10.1007/s11655-015-2127-0
Shi-zhang Wei, Sheng-qiang Luo, Jian Wang, et al. San-Cao Granule (三草颗粒) Ameliorates Hepatic Fibrosis through High Mobility Group Box-1 Protein/Smad Signaling Pathway[J]. Chinese Journal of Integrative Medicine, 2018,24(7):502-511.
Wei, Sz., Luo, Sq., Wang, J. et al. San-Cao Granule (三草颗粒) Ameliorates Hepatic Fibrosis through High Mobility Group Box-1 Protein/Smad Signaling Pathway., Chin. J. Integr. Med. 24, 502–511 (2018). https://doi.org/10.1007/s11655-015-2127-0 DOI:
Shi-zhang Wei, Sheng-qiang Luo, Jian Wang, et al. San-Cao Granule (三草颗粒) Ameliorates Hepatic Fibrosis through High Mobility Group Box-1 Protein/Smad Signaling Pathway[J]. Chinese Journal of Integrative Medicine, 2018,24(7):502-511. DOI: 10.1007/s11655-015-2127-0.
To investigate the possible mechanism of San-Cao Granule (SCG
三草颗粒) mediating antiliver fibrosis. A total of 60 male Sprague-Dawley rats were randomly divided into the normal control group
porcine serum-treated group
ursodesoxycholic acid (UDCA
60 mg/kg)
SCG (3.6 g/kg) group
SCG (1.8 g/kg) group and SCG (0.9 g/kg) group
with 10 rats in each group. Liver fibrosis was induced with porcine serum by intraperitoneal injection for 8 weeks
except for the normal control group. Then
the rats in the three SCG-treated groups and UDCA group were administered SCG and UDCA respectively for 4 weeks. The serum levels of alanine transaminase (ALT)
aspartate transaminase (AST)
albumin (ALB)
total bilirubin (TBIL)
hyaluronic acid (HA)
laminin (LN)
and type IV collagen (IVC) were examined using commercial kits and hepatic histopathology was examined with hematoxylin and eosin and Masson staining. Moreover
the protein expression levels of high mobility group box-1 protein (HMGB1)
transforming growth factor β1 (TGF-β1)
phosphorylated mothers against decapentaplegic homolog 3 (p-Smad3)
Smad7
toll-like receptor 4 (TLR4)
myeloid differentiation factor 88 (MyD88)
nuclear factor-kappa B (NF-κB) and α-smooth muscle actin (α-SMA) were determined by western blot
immunohistochemistry and real time quantitative-reverse transcription polymerase. Both SCG (3.6 and 1.8 g/kg) and UDCA significantly ameliorated the liver fibrosis induced by porcine serum as indicated by retarding the serum levels increasing of ALT
AST
TBIL
HA
LN and IVC and preventing the serum level reducing of ALB compared with the model group (all P<0.01). Meanwhile
the collagen deposition was attenuated by SCG and UDCA treatment. Furthermore
SCG markedly reduced the expressions of HMGB1
TGF-β1
p-Smad3
TLR4
MyD88
NF-κB and α-SMA
and enhanced the expression of the Smad7 compared with the model group (all P<0.01). SCG ameliorates hepatic fibrosis possibly through inhibiting HMGB1
TLR4/NF-κB and TGF-β1/Smad signaling pathway.
To investigate the possible mechanism of San-Cao Granule (SCG
三草颗粒) mediating antiliver fibrosis. A total of 60 male Sprague-Dawley rats were randomly divided into the normal control group
porcine serum-treated group
ursodesoxycholic acid (UDCA
60 mg/kg)
SCG (3.6 g/kg) group
SCG (1.8 g/kg) group and SCG (0.9 g/kg) group
with 10 rats in each group. Liver fibrosis was induced with porcine serum by intraperitoneal injection for 8 weeks
except for the normal control group. Then
the rats in the three SCG-treated groups and UDCA group were administered SCG and UDCA respectively for 4 weeks. The serum levels of alanine transaminase (ALT)
aspartate transaminase (AST)
albumin (ALB)
total bilirubin (TBIL)
hyaluronic acid (HA)
laminin (LN)
and type IV collagen (IVC) were examined using commercial kits and hepatic histopathology was examined with hematoxylin and eosin and Masson staining. Moreover
the protein expression levels of high mobility group box-1 protein (HMGB1)
transforming growth factor β1 (TGF-β1)
phosphorylated mothers against decapentaplegic homolog 3 (p-Smad3)
Smad7
toll-like receptor 4 (TLR4)
myeloid differentiation factor 88 (MyD88)
nuclear factor-kappa B (NF-κB) and α-smooth muscle actin (α-SMA) were determined by western blot
immunohistochemistry and real time quantitative-reverse transcription polymerase. Both SCG (3.6 and 1.8 g/kg) and UDCA significantly ameliorated the liver fibrosis induced by porcine serum as indicated by retarding the serum levels increasing of ALT
AST
TBIL
HA
LN and IVC and preventing the serum level reducing of ALB compared with the model group (all P<0.01). Meanwhile
the collagen deposition was attenuated by SCG and UDCA treatment. Furthermore
SCG markedly reduced the expressions of HMGB1
TGF-β1
p-Smad3
TLR4
MyD88
NF-κB and α-SMA
and enhanced the expression of the Smad7 compared with the model group (all P<0.01). SCG ameliorates hepatic fibrosis possibly through inhibiting HMGB1
TLR4/NF-κB and TGF-β1/Smad signaling pathway.
San-Cao GranuleLiver Fibrosishigh mobility group box-1 proteintoll-like receptor 4/nuclear factor-kappa Btransforming growth factor β1/mothers against decapentaplegic homolog
San-Cao GranuleLiver Fibrosishigh mobility group box-1 proteintoll-like receptor 4/nuclear factor-kappa Btransforming growth factor β1/mothers against decapentaplegic homolog
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