ABSTRACT
Aim To study the mechanisms of protective effects of extract of astragalus against focal cerebral ischemia/reperfusion injury in rats. Methods Focal cerebral ischemia was induced by intraluminal thread occlusion of middle cerebral artery. Immunohistochemistry was used to determine expression of TNF-?,IL-1? was measured by radioimmunity, and the apoptosis was observed by TUNEL. Results EA(20、40、80 mg?kg -1,ig)could decrease the expression of TNF-? and the level of IL-1? and reduce cell apoptosis. Conclusion EA has inhibitory action on the increase in the expression of TNF-?,the level of IL-1? and the apoptosis of neurons induced by focal cerebral ischemia/reperfusion.
ABSTRACT
Aim To study the effects of total extract of astragalus(TEA) on activating the primary cultured hepatic stellate cells(HSC) and synthesizing collagen. Methods Livers of adult rats were perfused by pronase E and collagenase in situ, HSC and Kupffer cell (KC) were isolated by centrifugation with 18% Nycodenz. The subcultured HSC were induced by Kupffer cell conditioned medium(KCCM) and were incubated with 5～ 80 mg?L -1 TEA for 6 days. The proliferation of the cells was measured by 3H TdR and the production of collagen by 3H Proline.Results TEA (10～ 40 mg?L -1 ) could suppress the proliferation of hepatic stellate cells and TEA(40～ 80 mg?L -1 ) could suppress the production of collagen. Conlusion The suppression of hepatic stellate cell proliferation and the collagen's production by the TEA may be one of the mechanisms for depressing the hepatic fibrosis by the TEA.
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Aim To study the protective effect of total extract of astragalus(TEA) on primary rat hepatocytes injured by CCl4 or H2O2 and its mechanism.Methods The primary hepatocytes were isolated by Ⅳ collaganase and injured by CCl4 or H2O2.The contents of malondialdehyde(MDA) and glutathion(GSH),glutathion peroxidase(GSHpx) activity of hepatocytes and the AST and /or ALT level in cultural supernatant were determined by general methods. Results (1) The elevation of MDA content of hepatocytes and AST level in supernatant of cultural hepatocytes,and the loss of GSH content and GSHpx activity induced by CCl4 were restored remarkably by TEA(5～80 mg?L-1);(2)The elevation of ALT level in the supernatant of hepatocytes and MDA content of hepatocytes, and the loss of GSH content and GSHpx activity induced by H2O2 were improved significantly by TEA(5～80 mg?L-1) treatment.Conclusion The results suggest that TEA possess direct protective action on primary hepatocyte in vitro injured by CCl4 or H2O2. These might be associated with its anti-oxidative activity.
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Aim To study the anti-oxidative and mitochondria-protective effects of estract of astragalus (EA ) on focal cerebral ischemia-reperfusion injury and its mechanism in rats.Methods Middle cerebral artery occlusion(MACO) was used to induce focal cerebral ischemia-reperfusion model. After 24 h reperfusion,MDA, LD content and SOD activity of brain homogenate were tested. MDA content,SOD and ATPase activity in mitochondrion were also tested.Transmission electron microscopy was used to assess the ultrastructure dstruction. Results EA(20, 40, 80 mg?kg -1) significantly inhibited the increase of MDA, LD after cerebral ischemia-reperfusion. EA (40, 80 mg?kg -1) also inhibited the decrease of activit of SOD in rats. EA(20, 40, 80 mg?kg -1) inhibited the increase of MDA and inhibited the decrease of activities of SOD, Na+,K+-ATPase, Ca 2+,Mg 2+-ATPase in mitochondrion. The examination by transmission electron microscopy showed that EA (20, 40 mg?kg -1) protected the ultrastructure destruction. Conclusion EA had protective effects against focal cerebral ischemia reperfusion injuries via attenuating cerebral oxygen free radical(OFR)lipid peroxidation and protecting mitochondria.
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AIMTo study the protective effects of EA against cer ebral ischemia-reperfusion injury. METHODSAcute cerebral ischemia w as produced by the occlusion of bilateral common carotid arteries of mice .The s urvival time in 12 h of the mice was observed, and the mortalities in 2 h, 6 h, 12 h were recorded. Pulsinelli four-vessel occlusion method was used to make ce rebral ischemia-reperfusion model of rats. The EEG and the reappearing time of righting reflex were recorded and the activity of GSH-Px,LDH,NOS in the brain w as tested. Researching the iNOS expression in hippocampiwith immunocytochemistry method and measure the mean optical density. RESULTSEA can decrease the mortalities and prolong the survival t ime in 12 h of the mice. EA can promote the recovery of the EEG and the RR after cerebral ischemia-reperfusion operation in rats and enhance the activities of the GSH-Px LDH, reduce the activity of the NOS. EA also inhibits the expression of iNOS and reduce it's value of mean optical density in hippocampi of the rat s. CONCLUSIONEA has protective effects against cerebral ischemai-r eperfusion injury.
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Aim To study the effects of extract of astragalus on hippocampal delayed neuronal death of totalcerebral ischemia and 7 days reperfusion in rats.Methods Global ischemia was made by four-vessel occlusion. Electron microscope was used to observe the ultramicrostructure of dorsal hippocampal neurons.Light microscope was used to survey the structure of hippocampal neurons and to count the number of normal neurons in CA1 sector. Glial fibrillary acidic protein(GFAP) was detected by immune histochemistry.Results Compared with ischemia and reperfusion group(I/R),EA improved the ultrastructure of hippocampal neurons, suppressed the decrease of normal neurons in CA1 and degraded the expression of GFAP .The number of normal neurons in I/R group was 38?11.5,and in EA(20,40 mg?kg -1) groups,63?12.8(P