PMID- 25769560
OWN - NLM
STAT- MEDLINE
DCOM- 20150921
LR  - 20211203
IS  - 1873-2623 (Electronic)
IS  - 0041-1345 (Linking)
VI  - 47
IP  - 2
DP  - 2015 Mar
TI  - Protective effect of Berberine pretreatment in hepatic ischemia/reperfusion 
      injury of rat.
PG  - 275-82
LID - S0041-1345(15)00086-X [pii]
LID - 10.1016/j.transproceed.2015.01.010 [doi]
AB  - BACKGROUND: Berberine (BBR) has been demonstrated to protect against hepatic 
      ischemia/reperfusion (I/R) injury. However, the exact mechanism is largely 
      unknown. In the present study, we examined the role of phosphatidylinositol 
      3-kinase/protein kinase B (PI3K/Akt) and mammalian target of rapamycin (mTOR) in 
      the protective effect of BBR on hepatic I/R-mediated apoptosis in rats. METHODS: 
      Adult male Sprague-Dawley rats were assigned randomly to groups of sham, 
      ischemia/reperfusion (I/R), I/R+DMSO (vehicle) and I/R+BBR (100 mg/kg/d, 2 
      weeks). The hepatic cold ischemia model was established by perfusing the liver 
      with heparinized cold saline through the portal vein for 20 minutes. The liver 
      function and oxidative stress level were measured by biochemical and 
      histopathologic examinations. The apoptotic rate was determined by terminal 
      deoxynucleotidyl transferase biotin-dUTP nick end labeling (TUNEL) assay. The 
      expression of Bcl-2, Bax, caspase-3, and the phosphorylation of Akt and mTOR were 
      assayed by Western blot analysis and immunohistochemistry. RESULTS: Compared with 
      the I/R group, BBR dramatically attenuated the histopathologic damage, restored 
      the liver function, and decreased the oxidative stress level. Simultaneously, BBR 
      significantly ameliorated apoptosis by decreasing the apoptotic rate, increasing 
      the Bcl-2/Bax ratio and inhibiting cleaved caspase-3 expression in rats subjected 
      to hepatic I/R. The expression of p-Akt were effectively upregulated with the 
      inhibited expression of p-mTOR. CONCLUSION: Our study reveals that BBR 
      preconditioning protects against hepatic I/R partly by reducing apoptosis, which 
      is possibly involved with the modulation of the PI3K/Akt/mTOR signaling pathway.
CI  - Copyright (c) 2015. Published by Elsevier Inc.
FAU - Sheng, M
AU  - Sheng M
AD  - Department of Anesthesiology, Tianjin First Center Hospital, Tianjin, China.
FAU - Zhou, Y
AU  - Zhou Y
AD  - Department of Anesthesiology, Xiangyang No.1 People's Hospital, Hubei, China.
FAU - Yu, W
AU  - Yu W
AD  - Department of Anesthesiology, Tianjin First Center Hospital, Tianjin, China.
FAU - Weng, Y
AU  - Weng Y
AD  - Department of Anesthesiology, Tianjin First Center Hospital, Tianjin, China.
FAU - Xu, R
AU  - Xu R
AD  - Department of Anesthesiology, Tianjin First Center Hospital, Tianjin, China.
FAU - Du, H
AU  - Du H
AD  - Department of Anesthesiology, Tianjin First Center Hospital, Tianjin, China. 
      Electronic address: duhongyin999@sina.com.
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Transplant Proc
JT  - Transplantation proceedings
JID - 0243532
RN  - 0I8Y3P32UF (Berberine)
RN  - EC 2.7.1.1 (mTOR protein, rat)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
RN  - EC 3.4.22.- (Caspase 3)
SB  - IM
MH  - Animals
MH  - Apoptosis/drug effects
MH  - Berberine/*pharmacology
MH  - Caspase 3/metabolism
MH  - In Situ Nick-End Labeling
MH  - Liver/*blood supply/pathology
MH  - Male
MH  - Oxidative Stress/drug effects
MH  - Phosphatidylinositol 3-Kinases/*physiology
MH  - Phosphorylation
MH  - Proto-Oncogene Proteins c-akt/metabolism
MH  - Random Allocation
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Reperfusion Injury/chemically induced/*prevention & control
MH  - Signal Transduction/drug effects
MH  - TOR Serine-Threonine Kinases/*physiology
EDAT- 2015/03/15 06:00
MHDA- 2015/09/22 06:00
CRDT- 2015/03/15 06:00
PHST- 2014/10/12 00:00 [received]
PHST- 2015/01/14 00:00 [accepted]
PHST- 2015/03/15 06:00 [entrez]
PHST- 2015/03/15 06:00 [pubmed]
PHST- 2015/09/22 06:00 [medline]
AID - S0041-1345(15)00086-X [pii]
AID - 10.1016/j.transproceed.2015.01.010 [doi]
PST - ppublish
SO  - Transplant Proc. 2015 Mar;47(2):275-82. doi: 10.1016/j.transproceed.2015.01.010.