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Zhongguo Zhongyao Zazhi 2005-Mar

[Clinical efficacy and T-lymphocyte subset, serum interferon-gamma (IFN-gamma), tumor necrosis factor-alpha (TNF-alpha), interleukin-2(IL-2) levels on treatment of chronic aplastic anemia patients by shenfu injection combined with stanozol and cyclosporin A].

Només els usuaris registrats poden traduir articles
Inicieu sessió / registreu-vos
L'enllaç es desa al porta-retalls
Su-yun Wang
Ying-fei Wei
Hui-lan Du
Li-li Ren
Shi-hui Li

Paraules clau

Resum

OBJECTIVE

To observe the effect of Shenfu injection (SFI) and influence on T-lymphocyte subset, serum level of interferon-gamma(IFN-gamma), tumor necrosis factor-alpha(TNF-alpha), interleukin-2(IL-2) in patients with chronic aplastic anemia (CAA) based on treating with stanozol and cyclosporin A.

METHODS

60 patients with CAA were randomly divided into two groups, 30 patients in the SFI group were treated with SFI (100 mL which contains Ginsenoside 0.8 mg x mL(-1) and aconitine 1.8 microg x mL(-1) by adding it in 500 mL of 5% glucose every day) plus stanozol and cyclosporin A and 30 patients in the control group treated with slanozol and cyclosporin A alone for 2 months. The clinical efficacy was observed. The change of T-lymphocyte subset analyzed by flow cytometry and the levels of serum IFN-gamma, TNF-alpha, IL-2 measured with ELISA method were also observed before and after treatment.

RESULTS

After treatment, the total effective rate of the SFI group was higher than that in the control group, but it did not showing significant difference. The CD4/CD8 levels were significantly increased (1.76+/-0.49, P< 0.01) and CD8 levels were significantly lowered (22.57+/-6.30, P < 0.01) in the SFI group after treatment. Serum levels of lFN-gamma, TNF-alpha and IL-2 were lower in both groups, and the level of TNF-alpha and IL-2 in the SFI group (0.710+/-0.213) ng x L(-1) and (0.639+/-0.247) ng x L(-1) was significantly lowered than that in the control group (P < 0.05, P < 0.01).

CONCLUSIONS

SFI might believe the hemopoietic inhibition so as to promote the recovery of hemopoietic function through improving the T-lymphocyte subset and reducing the release of hemopoietic negative regulatory factors such as IFN-gamma, TNF-alpha and IL-2.

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