Heijiangdan Ointment(黑绛丹膏)Relieves Oxidative Stress from Radiation Dermatitis Induced by ~(60)Co γ-R

来源 :Chinese Journal of Integrative Medicine | 被引量 : 0次 | 上传用户:qianchen912009
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Objective:To investigate the effects of Heijiangdan Ointment(黑绛丹膏,HJD) on oxidative stress in ~(60)Co γ-ray radiation-induced dermatitis in mice.Methods:Female Wistar mice with grade 4 radiation dermatitis induced by ~(60)Co γ-rays were randomly divided into four groups(n=12 per group);the HJD-treated,recombinant human epidermal growth factor(rhEGF)-treated,Trolox-treated,and untreated groups,along with a negative control group.On the 11 th and 21 st days after treatment,6 mice in each group were chosen for evaluation.The levels of superoxide dismutase(SOD),malondialdehyde(MDA),and lactate dehydrogenase(LDH) were detected using spectrophotometric methods.The fibroblast mitochondria were observed by transmission electron microscopy(TEM).The expressions of fibroblast growth factor 2(FGF-2) and transforming growth factor β1(TGF-β1) were analyzed by western blot.Results:Compared with the untreated group,the levels of SOD,MDA and LDH,on the 11 th and 21 st days after treatment showed significant difference(P<0.05).TEM analysis indicated that fibroblast mitochondria in the untreated group exhibited swelling and the cristae appeared fractured,while in the HJD group,the swelling of mitochondria was limited and the rough endoplasmic reticulum appeared more relaxed.The expressions of FGF-2 and TGF-β1 increased in the untreated group compared with the negative control group(P<0.05).After treatment,the expression of FGF-2,rhEGF and Trolox in the HJD group were significantly increased compared with the untreated group(P<0.05),or compared with the negative control group(P<0.05).The expression of TGF-β1 showed significant difference between untreated and negative control groups(P<0.05).HJD and Trolox increased the level of TGF-β1 and the difference was marked as compared with the untreated and negative control groups(P<0.05).Conclusion:HJD relieves oxidative stress-induced injury,increases the antioxidant activity,mitigates the fibroblast mitochondrial damage,up-regulates the expression of growth factor,and promotes mitochondrial repair in mice. Objective: To investigate the effects of Heijiangdan Ointment on oxidative stress in ~ (60) Co γ-ray radiation-induced dermatitis in mice. Methods: Female Wistar mice with grade 4 radiation dermatitis induced by ~ ( HJD-treated, recombinant human epidermal growth factor (rhEGF) -treated, Trolox-treated, and untreated groups, along with a negative control group .On the 11th and 21 st days after treatment, 6 mice in each group were chosen for evaluating the levels of superoxide dismutase (SOD), malondialdehyde (MDA), and lactate dehydrogenase (LDH) were detected using spectrophotometric methods. The fibroblast Mitochondria were observed by transmission electron microscopy (TEM). The expressions of fibroblast growth factor 2 (FGF-2) and transforming growth factor β1 (TGF-β1) were analyzed by western blot. Results: Compared with the untreated group, the levels of SOD, MDA and LDH, on the 11 th and 21 st days after treatment s The analysis of that fibroblast mitochondria in the untreated group showed swelling and the cristae were fractured, while in the HJD group, the swelling of mitochondria was limited and the rough endoplasmic reticulum had more relaxed.The expressions of FGF-2 and TGF-β1 increased in the untreated group compared with the negative control group (P <0.05). After treatment, the expression of FGF-2, rhEGF and Trolox in the HJD group were significantly increased compared with the untreated group (P <0.05). The expression of TGF-β1 showed significant difference between untreated and negative control groups (P <0.05) .HJD and Trolox increased the level of TGF-β1 and the difference was marked as compared with the untreated and negative control groups (P <0.05) .Conclusion: HJD relieves oxidative stress-induced injury, increases the antioxidant activity, mitigates the fibroblast mitochondrial damage, up-reg ulates the exprsession of growth factor, and promotes mitochondrial repair in mice.
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