BACKGROUND： HOW to control the effect of oxygen-derived free radicals on development of cerebral injury and cerebral edema is a key factor for treating cerebral ischemia-reperfusion injury. OBJECTIVE： To observe and...BACKGROUND： HOW to control the effect of oxygen-derived free radicals on development of cerebral injury and cerebral edema is a key factor for treating cerebral ischemia-reperfusion injury. OBJECTIVE： To observe and compare the protective effects, synergistic action and mechanisms of ultrashortwave （USW） and radix salviae miltiorrhizae （RSM） on the focal cerebral ischemia-reperfusion injuries in rats. DESIGN： Randomized controlled animal study SEI-FING： Department of Rehabilitation Medicine, First Hospital affiliated to China Medical University MATERIALS： A total of 160 healthy Wistar rats of both genders and aged 18-20 weeks weighing 250-300 g of clean grade were selected in this study. 5 mL/ampoule RSM injection fluid was produced by the First Pharmaceutical Corporation of Shanghai （batch number： 011019, 0.01 mug）. The USW therapeutic device was produced by Shanghai Electronic Device Factory with the frequency of 40.68 MHz and the maximal export power of 40 W. The first channel of power after modulation was 11 W. METHODS： The experiment was carried out in the Rehabilitation Medicine Department of the First Hospital affiliated to China Medical University from May 2002 to January 2003. Focal ischemia-reperfusion model was established in rats by reversible right middle cerebral artery occlusion with filament. Right cerebral ischemia was for 2 hours and then with 24 hours reperfusion. The scores of neurological deficits were evaluated by 0 to 4 scales. After surgery, 64 successful rats models were divided into four groups according to digital table： control group, USW group, RSM group and RSM ＋ USW group with 16 cases in each group. Rats in control group were intraperitoneally injected with the same volume of saline （0.1 mL/g）; rats in USW group were given small dosage of USW on head for 10 minutes at 6 hours after reperfusion; rats in RSM group were intraperitoneally injected with 0.01 mL/g RSM solution at 30 minutes before reperfusion; rats in RSM ＋ USW group were intraperitoneally injected with 0.01 mL/g RSM parenteral solution at 30 minutes before reperfusion and given small dosage of USW on head for 10 minutes once at 6 hours after reperfusion; sixteen rats in sham operation group did not receive any treatment. All 80 rats were taken brains at 24 hours after reperfusion to measure wet and dry weights to calculate water content： Cerebral water content （%） = （1-dry/wet weight） × 100%. Superoxide dismutase （SOD） activity was measured by hydroxylamine method and malondialdehyde （MDA） content was measured by TBA photometric method. MAIN OUTCOME MEASURES ： Cerebral water content, SOD activity and MDA content RESULTS： All 160 rats except 80 failing in modeling were involved in the final analysis. （① The cerebral water content of left hemisphere made no significant difference （P 〉 0.05）. The cerebral water content of right hemisphere in the control group and the three treatment groups was obviously higher than that of the sham operation group [（81.26±0.77）%, （79.74±0.68）%, （79.76±0.81）%, （79.61±0.79）%, （77.43±0.61）%, P 〈 0.05]. The cerebral water content of right hemisphere in the three treatment groups was obviously lower than that of the control group （P〈 0.05）. There was no significant difference among the three treatment groups （P 〉 0.05）. ② Compared with the control group, SOD activity （right） of the control group decreased obviously （P 〈 0.05）, while MDA content increased obviously （P 〈 0.05）. SOD activity in the three therapeutic groups increased obviously, while MDA content decreased obviously （P 〈 0.05）; there was no significant difference among the three treatment groups （P 〉 0.05）. CONCLUSION： ① USW and RSM therapy have neuroprotective effects against focal cerebral ischemia-reperfusion injuries by means of decreasing cerebral water content and MDA and increasing the activity of SOD. ② Synergistic action was not observed between these two therapeutic methods.展开更多
Aim Reduction of Sheng-Nao-Kang decoction （RSNK）, is a modified traditional Chinese medicinal formula of Sheng-Nao-Kang pill preparation, which is protective in rats against focal cerebral ischemia/reperfusion （I/R...Aim Reduction of Sheng-Nao-Kang decoction （RSNK）, is a modified traditional Chinese medicinal formula of Sheng-Nao-Kang pill preparation, which is protective in rats against focal cerebral ischemia/reperfusion （I/R） injury. In the current study, we investigate the protective effect of RSNK against apoptosis and oxidative damage induced by cerebral I/R and explore the underlying mechanisms. Cerebral I/R injury was induced by in- traluminal middle cerebral artery occlusion （MCAO） for 2 h followed by reperfusion for 24 h in adult male Sprague- Dawley rats. Rats were randomized into seven groups （n- 8）： Sham group, I/R group, RSNK-treated groups （ 0.7 g · kg ^- 1, 1 . 4 g · kg ^- 1 and 2. 8 g · kg^ - 1 ） , nimodipine （NMP） -treated group and Whitmania pigra Whitman （WW）-treated group. Neurological deficit scores, cerebral humidity content and cerebral infarction volume were measured after the 24 h reperfusion. Malondialdehyde （ MDA）, superoxide dismutase （ SOD）, catalase （ CAT）, inducible nitric oxide synthase （iNOS） and total nitric oxide synthase （TNOS） in serum were measured by assay kits for biochemical analysis. Histological structures of the cortex of the ipsilateral ischemic cerebral hemisphere in rats were observed by Nissl staining. The caspase-3 protein content in the hippocampus and cortex was detected by immunohistochemistry. Additionally, Bax and Bcl-2 protein expressions in the injured brain were evaluated by Western blot. RSNK administration not only markedly improved neurological deficit scores, but also reduced cere- bral humidity content and cerebral infarction volume, lowered MDA content, up-regulated SOD and CAT levels, down-regulated iNOS and TNOS levels, restrained the expression of caspase-3 positive protein and alleviated the Bax and Bcl-2 protein expressions.展开更多
Objective: To study the protective effect of extract of Folium Ginkgo (FGE) on repeated cerebral ischemia-reperfusion injury. Methods: The model in waking mice induced by repeated cerebral ischemia-reperfusion were us...Objective: To study the protective effect of extract of Folium Ginkgo (FGE) on repeated cerebral ischemia-reperfusion injury. Methods: The model in waking mice induced by repeated cerebral ischemia-reperfusion were used in the experiment to observe the effect of FGE on behavior, oxygen free radical metabolism and prostaglandin E2 (PGE2) content by step-through experiment, diving stand and colorimetric method. Results: FGE could obviously improve the learning ability and memory of model animals, and could lower obviously the content of malonyldialdehyde, nitric oxide and PGE2, restore the lowered activity of superoxide dismutase and catalase in cerebral tissue. Conclusion: FGE has highly protective effect against repeated ischemia-reperfusion injury, the mechanism might be related with its action on anti-lipid oxidatin, improve the activity of antioxidase and inhibit the producing of PGE2.展开更多
基金Liaoning Province Social Development Fund Sustentation Item, No. 99225003
文摘BACKGROUND： HOW to control the effect of oxygen-derived free radicals on development of cerebral injury and cerebral edema is a key factor for treating cerebral ischemia-reperfusion injury. OBJECTIVE： To observe and compare the protective effects, synergistic action and mechanisms of ultrashortwave （USW） and radix salviae miltiorrhizae （RSM） on the focal cerebral ischemia-reperfusion injuries in rats. DESIGN： Randomized controlled animal study SEI-FING： Department of Rehabilitation Medicine, First Hospital affiliated to China Medical University MATERIALS： A total of 160 healthy Wistar rats of both genders and aged 18-20 weeks weighing 250-300 g of clean grade were selected in this study. 5 mL/ampoule RSM injection fluid was produced by the First Pharmaceutical Corporation of Shanghai （batch number： 011019, 0.01 mug）. The USW therapeutic device was produced by Shanghai Electronic Device Factory with the frequency of 40.68 MHz and the maximal export power of 40 W. The first channel of power after modulation was 11 W. METHODS： The experiment was carried out in the Rehabilitation Medicine Department of the First Hospital affiliated to China Medical University from May 2002 to January 2003. Focal ischemia-reperfusion model was established in rats by reversible right middle cerebral artery occlusion with filament. Right cerebral ischemia was for 2 hours and then with 24 hours reperfusion. The scores of neurological deficits were evaluated by 0 to 4 scales. After surgery, 64 successful rats models were divided into four groups according to digital table： control group, USW group, RSM group and RSM ＋ USW group with 16 cases in each group. Rats in control group were intraperitoneally injected with the same volume of saline （0.1 mL/g）; rats in USW group were given small dosage of USW on head for 10 minutes at 6 hours after reperfusion; rats in RSM group were intraperitoneally injected with 0.01 mL/g RSM solution at 30 minutes before reperfusion; rats in RSM ＋ USW group were intraperitoneally injected with 0.01 mL/g RSM parenteral solution at 30 minutes before reperfusion and given small dosage of USW on head for 10 minutes once at 6 hours after reperfusion; sixteen rats in sham operation group did not receive any treatment. All 80 rats were taken brains at 24 hours after reperfusion to measure wet and dry weights to calculate water content： Cerebral water content （%） = （1-dry/wet weight） × 100%. Superoxide dismutase （SOD） activity was measured by hydroxylamine method and malondialdehyde （MDA） content was measured by TBA photometric method. MAIN OUTCOME MEASURES ： Cerebral water content, SOD activity and MDA content RESULTS： All 160 rats except 80 failing in modeling were involved in the final analysis. （① The cerebral water content of left hemisphere made no significant difference （P 〉 0.05）. The cerebral water content of right hemisphere in the control group and the three treatment groups was obviously higher than that of the sham operation group [（81.26±0.77）%, （79.74±0.68）%, （79.76±0.81）%, （79.61±0.79）%, （77.43±0.61）%, P 〈 0.05]. The cerebral water content of right hemisphere in the three treatment groups was obviously lower than that of the control group （P〈 0.05）. There was no significant difference among the three treatment groups （P 〉 0.05）. ② Compared with the control group, SOD activity （right） of the control group decreased obviously （P 〈 0.05）, while MDA content increased obviously （P 〈 0.05）. SOD activity in the three therapeutic groups increased obviously, while MDA content decreased obviously （P 〈 0.05）; there was no significant difference among the three treatment groups （P 〉 0.05）. CONCLUSION： ① USW and RSM therapy have neuroprotective effects against focal cerebral ischemia-reperfusion injuries by means of decreasing cerebral water content and MDA and increasing the activity of SOD. ② Synergistic action was not observed between these two therapeutic methods.
文摘Aim Reduction of Sheng-Nao-Kang decoction （RSNK）, is a modified traditional Chinese medicinal formula of Sheng-Nao-Kang pill preparation, which is protective in rats against focal cerebral ischemia/reperfusion （I/R） injury. In the current study, we investigate the protective effect of RSNK against apoptosis and oxidative damage induced by cerebral I/R and explore the underlying mechanisms. Cerebral I/R injury was induced by in- traluminal middle cerebral artery occlusion （MCAO） for 2 h followed by reperfusion for 24 h in adult male Sprague- Dawley rats. Rats were randomized into seven groups （n- 8）： Sham group, I/R group, RSNK-treated groups （ 0.7 g · kg ^- 1, 1 . 4 g · kg ^- 1 and 2. 8 g · kg^ - 1 ） , nimodipine （NMP） -treated group and Whitmania pigra Whitman （WW）-treated group. Neurological deficit scores, cerebral humidity content and cerebral infarction volume were measured after the 24 h reperfusion. Malondialdehyde （ MDA）, superoxide dismutase （ SOD）, catalase （ CAT）, inducible nitric oxide synthase （iNOS） and total nitric oxide synthase （TNOS） in serum were measured by assay kits for biochemical analysis. Histological structures of the cortex of the ipsilateral ischemic cerebral hemisphere in rats were observed by Nissl staining. The caspase-3 protein content in the hippocampus and cortex was detected by immunohistochemistry. Additionally, Bax and Bcl-2 protein expressions in the injured brain were evaluated by Western blot. RSNK administration not only markedly improved neurological deficit scores, but also reduced cere- bral humidity content and cerebral infarction volume, lowered MDA content, up-regulated SOD and CAT levels, down-regulated iNOS and TNOS levels, restrained the expression of caspase-3 positive protein and alleviated the Bax and Bcl-2 protein expressions.
文摘Objective: To study the protective effect of extract of Folium Ginkgo (FGE) on repeated cerebral ischemia-reperfusion injury. Methods: The model in waking mice induced by repeated cerebral ischemia-reperfusion were used in the experiment to observe the effect of FGE on behavior, oxygen free radical metabolism and prostaglandin E2 (PGE2) content by step-through experiment, diving stand and colorimetric method. Results: FGE could obviously improve the learning ability and memory of model animals, and could lower obviously the content of malonyldialdehyde, nitric oxide and PGE2, restore the lowered activity of superoxide dismutase and catalase in cerebral tissue. Conclusion: FGE has highly protective effect against repeated ischemia-reperfusion injury, the mechanism might be related with its action on anti-lipid oxidatin, improve the activity of antioxidase and inhibit the producing of PGE2.
