PMID- 31336368
OWN - NLM
STAT- MEDLINE
DCOM- 20200122
LR  - 20200122
IS  - 1423-0313 (Electronic)
IS  - 0031-7012 (Linking)
VI  - 104
IP  - 3-4
DP  - 2019
TI  - The Protective Effect of Aesculus hippocastanum (Venoplant(R)) Against Concanavalin 
      A-Induced Liver Injury.
PG  - 196-206
LID - 10.1159/000501258 [doi]
AB  - AIM: The present study was performed to investigate the effect of Aesculus 
      hippocastanum (AH; Venoplant(R)) on concanavalin A (ConA)-induced acute liver 
      injury and explore the mechanism in mice. METHODS: ConA (20 mg/kg) was 
      administered via tail vein injection to induce hepatic damage. The groups of AH 
      (Venoplant(R)) were given at 65.8, 131.6, and 263.2 mg/kg by oral gavages for 20 
      days. The serum levels of aspartate transaminase (AST), alanine aminotransferase 
      (ALT), total protein (TP), and albumin (Alb) were determined by automatic 
      biochemical analyzer, and the Alb/globulin (A/G) ratio was calculated. Tumor 
      necrosis factor-alpha (TNF-alpha) and IFN-gamma levels were assayed by enzyme-linked 
      immunosorbent assay. The liver tissue was attained by hematoxylin and eosin, and 
      the histopathological changes were calculated. The cell apoptosis was assayed by 
      terminal dUTP nick-end labeling. The malondialdehyde (MDA), superoxide dismutase 
      (SOD), and glutathione (GSH) content of liver tissue were assayed by related 
      kits. The activity of caspase-3 was detected by spectrophotometry. The 
      expressions of cytochrome c, Bax, Bcl-2, c-Jun N-terminal kinase (JNK), and p-JNK 
      were detected by western blot. RESULTS: The results showed that the levels of 
      ALT, AST, IFN-gamma, and TNF-alpha in AH (Venoplant(R)) groups were significantly lower 
      than those in ConA-injured group, while the levels of TP, Alb, and A/G were 
      significantly higher. The SOD and GSH levels were significantly increased, and 
      the MDA level was decreased; liver histopathology was changed consistently with 
      the serological indicators, AH (Venoplant(R)) treatment significantly reduced the 
      pathological damage and cell apoptosis; while in AH (Venoplant(R)) group, the 
      expressions of cytochrome c, caspase-3, Bax/Bcl-2 ratio, and p-JNK were 
      significantly decreased. CONCLUSION: AH (Venoplant(R)) could significantly protect 
      the ConA-induced acute liver injury in mice via inhibition of reactive oxygen 
      species and JNK pathway.
CI  - (c) 2019 S. Karger AG, Basel.
FAU - Wu, Shujin
AU  - Wu S
AD  - Department of Pharmacy, Gan Su Province Hospital, Lan Zhou, China.
FAU - Sa, Rina
AU  - Sa R
AD  - Department of Pharmacy, Gan Su Province Hospital, Lan Zhou, China.
FAU - Gu, Zhirong
AU  - Gu Z
AD  - Department of Pharmacy, Gan Su Province Hospital, Lan Zhou, China.
FAU - Zhao, Pei
AU  - Zhao P
AD  - Department of Pharmacy, Gan Su Province Hospital, Lan Zhou, China.
FAU - Yu, Jing
AU  - Yu J
AD  - Department of Pharmacy, Gan Su Province Hospital, Lan Zhou, China.
FAU - Wang, Yanhong
AU  - Wang Y
AD  - Department of Pharmacy, Gan Su Province Hospital, Lan Zhou, China.
FAU - Ge, Bin
AU  - Ge B
AD  - Department of Pharmacy, Gan Su Province Hospital, Lan Zhou, China, 
      gjy0630@163.com.
LA  - eng
PT  - Journal Article
DEP - 20190723
PL  - Switzerland
TA  - Pharmacology
JT  - Pharmacology
JID - 0152016
RN  - 0 (Protective Agents)
RN  - 0 (Proto-Oncogene Proteins c-bcl-2)
RN  - 0 (Reactive Oxygen Species)
RN  - 11028-71-0 (Concanavalin A)
RN  - 4Y8F71G49Q (Malondialdehyde)
RN  - EC 1.15.1.1 (Superoxide Dismutase)
RN  - EC 2.6.1.1 (Aspartate Aminotransferases)
RN  - EC 2.6.1.2 (Alanine Transaminase)
RN  - EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases)
RN  - EC 3.4.22.- (Caspase 3)
RN  - GAN16C9B8O (Glutathione)
SB  - IM
MH  - Aesculus/*chemistry
MH  - Alanine Transaminase/metabolism
MH  - Animals
MH  - Apoptosis/drug effects
MH  - Aspartate Aminotransferases/metabolism
MH  - Caspase 3/metabolism
MH  - Chemical and Drug Induced Liver Injury/*drug therapy/metabolism
MH  - Concanavalin A/*pharmacology
MH  - Glutathione/metabolism
MH  - In Situ Nick-End Labeling/methods
MH  - JNK Mitogen-Activated Protein Kinases/metabolism
MH  - Liver/drug effects/metabolism
MH  - Male
MH  - Malondialdehyde/metabolism
MH  - Mice
MH  - Oxidative Stress/drug effects
MH  - Protective Agents/*pharmacology
MH  - Proto-Oncogene Proteins c-bcl-2/metabolism
MH  - Reactive Oxygen Species/metabolism
MH  - Superoxide Dismutase/metabolism
OTO - NOTNLM
OT  - Aesculus hippocastanum
OT  - Concanavalin A
OT  - Liver injury
OT  - c-Jun N-terminal kinase
EDAT- 2019/07/25 06:00
MHDA- 2020/01/23 06:00
CRDT- 2019/07/24 06:00
PHST- 2019/02/15 00:00 [received]
PHST- 2019/05/24 00:00 [accepted]
PHST- 2019/07/25 06:00 [pubmed]
PHST- 2020/01/23 06:00 [medline]
PHST- 2019/07/24 06:00 [entrez]
AID - 000501258 [pii]
AID - 10.1159/000501258 [doi]
PST - ppublish
SO  - Pharmacology. 2019;104(3-4):196-206. doi: 10.1159/000501258. Epub 2019 Jul 23.