[Protective effect of shenfu injection against ischemia-reperfusion injury due to pancreas transplantation in rats].
OBJECTIVE
To investigate the protective effect of Shenfu Injection against ischemia-reperfusion (I/R) injury due to pancreas transplantation in rats, and explore its possible mechanism.


METHODS
Six normal SD rats with sham operation were taken as the normal control group, 24 steptozozin-induced diabetic SD rats were randomly divided into 4 groups, with 6 in each group. Except I/R group, the rats in the other groups were intravenous injected with Shenfu Injection (SF,10 mg/kg), Hongshen Injection (HS, 9 mg/kg) and Fuzi Injection (FZ 1 mg/kg) respectively at the day and 30 minutes before pancreas transplantation performed in the SF group, HS group and FZ group, respectively. At the same time, rats in the normal control group and in the I/R group were intravenously injected the same volume of normal saline. The blood glucose was detected before and after reperfusion, and 2 hours later after reperfusion, the contents of serum nitric oxide (NO) and tumor necrosis factor-alpha (TNF-alpha), the concentrations of malondialdehyde (MDA) , superoxide dismutase (SOD) , and myeloperoxidase (MPO) in the transplanted pancreas tissues were detected. The cell apoptosis of the transplanted pancreas tissue was determined by TUNEL, and the bcl-2 and Bax protein expression was determined by Western blot.


RESULTS
After reperfusion, the levels of blood glucose and TNF-alpha decreased and the concentration of NO increased in the SF group, HS group and FZ group, compared with those in the I/R group. The activity of SOD, bcl-2 expression and the ratio of bcl-2 and Bax were higher, while the content of MDA, the activity of MPO, apoptotic indexes, and Bax expression were lower in the SF group, HS group and FZ group than those in the I/R group.


CONCLUSIONS
Shenfu Injection can protect L/R injury due to pancreas transplantation in rats, the possible mechanism may be related to promoting activity of SOD, increasing synthesis of endogenous NO, decreasing the excretion of TNF-alpha, alleviating conglutination and aggregation of polymorphonuclear neutrophils (PMNs) in pancreas, as well as up-regulating Bcl-2 gene expression and down-regulating the Bax gene expression.
Liu
Xiao-nan
XN
The Fourth Military Medical University, Xi' an. liuxnys@yahoo.com.cn
Huo
Ting-ting
TT
Wang
Wei-zhong
WZ
D000818:Animals; D002449:Cell Aggregation / Q000187:drug effects; D003921:Diabetes Mellitus, Experimental / Q000201:enzymology / Q000378:metabolism; D004365:Drugs, Chinese Herbal / Q000627:therapeutic use*; D007267:Injections; D008315:Malondialdehyde / Q000378:metabolism; D009569:Nitric Oxide / Q000097:blood; D010179:Pancreas / Q000187:drug effects* / Q000378:metabolism; D016035:Pancreas Transplantation / Q000009:adverse effects*; D020011:Protective Agents / Q000627:therapeutic use*; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000209:etiology / Q000517:prevention & control*; D013482:Superoxide Dismutase / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D004365:Drugs, Chinese Herbal; D020011:Protective Agents; C492793:Shen-Fu; D014409:Tumor Necrosis Factor-alpha; D009569:Nitric Oxide; D008315:Malondialdehyde; D013482:Superoxide Dismutase