ABSTRACT
Autophagy is a process of degrading the damaged organelles and macromolecules by lysosomes in cells, which belongs to the programmed cell death. Cerebral ischemia is one of the important reasons for activation of autophagy. Studies have showed that autophagy plays a protective role in neuronal death induced by ischemia. However, it has also been found that excessive activation of autophagy could aggravate cerebral ischemia injury. In recent years, more and more Chinese medicine has been proved to regulate the autophagy level of brain neurons and reduce cerebral ischemia injury. In this paper, the main molecular mechanism of autophagy in the process of cerebral ischemic injury and the intervention effects of Chinese herbs on autophagy arereviewed in order to explore the basic principle of regulating autophagy by Chinese herbs and to play a better role in the clinical treatment of cerebral ischemic diseases.
ABSTRACT
Autophagy is a process of degrading the damaged organelles and macromolecules by lysosomes in cells, which belongs to the programmed cell death. Cerebral ischemia is one of the important reasons for activation of autophagy. Studies have showed that autophagy plays a protective role in neuronal death induced by ischemia. However, it has also been found that excessive activation of autophagy could aggravate cerebral ischemia injury. In recent years, more and more Chinese medicine has been proved to regulate the autophagy level of brain neurons and reduce cerebral ischemia injury. In this paper, the main molecular mechanism of autophagy in the process of cerebral ischemic injury and the intervention effects of Chinese herbs on autophagy arereviewed in order to explore the basic principle of regulating autophagy by Chinese herbs and to play a better role in the clinical treatment of cerebral ischemic diseases.
ABSTRACT
Autophagy is a process of degrading the damaged organelles and macromolecules by lysosomes in cells, which belongs to the programmed cell death. Cerebral ischemia is one of the important reasons for activation of autophagy. Studies have showed that autophagy plays a protective role in neuronal death induced by ischemia. However, it has also been found that excessive activation of autophagy could aggravate cerebral ischemia injury. In recent years, more and more Chinese medicine has been proved to regulate the autophagy level of brain neurons and reduce cerebral ischemia injury. In this paper, the main molecular mechanism of autophagy in the process of cerebral ischemic injury and the intervention effects of Chinese herbs on autophagy arereviewed in order to explore the basic principle of regulating autophagy by Chinese herbs and to play a better role in the clinical treatment of cerebral ischemic diseases.
ABSTRACT
Objective To study the regulating effect of freeze-dried substances of Salvia miltiorrhiza and Ligusticum chuanxiong Decoction on lipid metabolism abnormality in focal cerebral ischemia rats. Methods The focal cerebral ischemia rat model was established by monofilament method. The rats were randomly divided into normal group, sham operation group, model group, and drug treatment group. Plasma was collected after the last dosage and UPLC-Q/TOF-MS was used to study the plasma lipidomics. The lipidomics data were analyzed by orthogonal partial least square discriminant analysis (OPLS-DA), and the lipid metabolites changes were examined before and after the intervention of S. miltiorrhiza and L. chuanxiong. Results The focal cerebral ischemia rat model was successfully repeated. The S. miltiorrhiza and L. chuanxiong Decoction freeze-dried substances obviously reversed the abnormal lipid metabolism profile in the focal cerebral ischemia rat model. The plasma lipid biomarkers of ischemia injury rat were PS (21:0/0:0), PG (12:0/17:0), C16 sphinganine, phytosphingosine, PE [18:1 (9Z)/0:0], PC (16:1/2:0), PC (0:0/18:0), PC (16:1/0:0), PC (16:0/0:0), PC (18:2/0:0), PC (18:1/0:0), PC (18:0/0:0), and PC (20:5/0:0), respectively. Conclusion S. miltiorrhiza and L. chuanxiong Decoction freeze-dried substances have protective effects on cerebral ischemia injury, which may be related to the regulation of abnormal lipid metabolism, especially for phosphatidylcholines (PCs).
ABSTRACT
OBJECTIVE： To observe the effects of dihydroquercetin （DHQ） on hemorheology and other relevant related indexes in local cerebral ischemic injury model rats. METHODS： SD rats were randomly divided into sham operation group， model group， nimodipine group （positive control， 20 mg/kg） and DHQ low-dose， medium-dose and high-dose groups （15， 30， 60 mg/kg）， with 10 rats in each group. Administration groups were given relevant medicine intragastrically， sham operation group and model group were given constant volume of 0.4％ Sodium carboxymethyl cellulose solution， once a day， for consecutive 14 d. After last administration， local cerebral ischemic injury model was induced by bilateral common carotid artery ligation in other groups except for sham operation group. After 24 h of cerebral ischemia， histopathological changes of brain tissue in rats of each group were observed； the levels of hemorheology indexes [whole blood viscosity （low， medium and high shear）， whole blood reduced viscosity （low， medium and high shear）， plasma viscosity]， erythrocyte parameters （hematocrit， EAI， DI， IR）， coagulation function indexes （APTT， PT， TT， FIB） were detected. RESULTS： Compared with sham operation group， the cells in the brain tissue of model group were loose， the gap was obvious， and the neurons around the ischemic area were damaged obviously； the levels of whole blood viscosity， whole blood reduced viscosity， plasma viscosity， hematocrit， EAI， IR and FIB were increased significantly， while the levels of DI， APTT， PT and TT were decreased or shortened significantly （P＜0.05 or P＜0.01）. Compared with model group， above symptoms of administration groups were improved to different extents， whole blood viscosity， plasma viscosity， EAI and IR of nimodipine group， whole blood viscosity and hematocrit of DHQ high-dose group， plasma viscosity and EAI of DHQ groups， and IR of DHQ medium-dose and high-dose groups were decreased significantly； DI， APTT， PT and TT of nimodipine group， DI， APTT and TT of DHQ groups and PT of DHQ high-dose group were increased or prolonged significantly （P＜0.05 or P＜0.01）. There was no statistical significance in other indexes among those groups （P＞0.05）. CONCLUSIONS： DHQ can protect against local cerebral ischemic injury model rats， the mechanism of which may be associated with improving hemorheology indexes and coagulation function disorder.
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Objective To explore the effect of the total saponins of Panax notoginseng (TSPN) on the expression of GFAP in hippocampus and brain water content in rats subjected global cerebral ischemia injury. Methods Using four-vessel occlusion method built the global cerebral ischemia model. Rats were divided into Sham group, vehicle group, and TSPN group. The rats in the TSPN group were administered TSPN intraperitoneally 30 min post-brain ischemia. The dose of TSPN (75 mg/kg) was suspended in 0.9% saline, once per day for days 1, 3, 7, and 14 after reperfusion. While rats in the vehicle group was treated with equal volume of 0.9% saline, one injection per day until the rats were sacrificed at either days 1, 3, 7, and 14 after brain ischemia. The brain water contentwas detected by dry-wet technique and GFAP expression in the dentate subgranular zone (SGZ) was assessed by immunohistochemistry. Moreover, immunofluorescence was applied to detect the GFAP/DCX in the SGZ, and western-blot was adopted to test the protein level of GFAP. Results The brain water content in the TSPN group was significantly lower than the vehicle group (P < 0.05); There was statistical difference in the GFAP+ cells density in SGZ at the 3th, 7th, 14th day in two groups (P < 0.05). Furthermore, compared with the vehicle group, the ratio of the GFAP/DCX to DCX in the SGZ at 7th, 14th d of TSPN group was significantly different (P < 0.05), and the protein level of GFAP on days 3, 7, 14 in the TSPN group was higher (P < 0.05). Conclusion TSPN could play a neuroprotective effect through promoting gliosis, neuroregeneration in the SGZ, and alleviating brain water content of rats following global cerebral ischemia.
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Objective To investigate neurological function, volume of cerebral infarction, changes of lipid peroxidation, and the intervention effect of compound angelica injection (CAI) on rats with focal cerebral ischemia injury. Methods Models of rat with cerebral ischemia were reproduced by middle cerebral artery occlusion (MCAO). All animals were randomly divided into sham-operation group, model group, CAI group, and edaravone group. 1 hour after the models were established, rats in the sham-operation group and model group received intraperitoneal injection with normal saline, while rats in CAI group and edaravone group received intraperitoneal injection with relevant medicine for continuing 7 days. Volume of cerebral infarction was detected by Tetrazole staining method, neurologic function were detected by neuroethology, and concentration of MDA in brain tissue was also detected. Results After 7-day cerebral ischemia, compared with the model group, volume of cerebral infarction in CAI group was significantly reduced (P<0.05), and the concentration of MDA was a little lower. Conclusion CAI has significant protective effects which can significantly improve neurological function, reduce volume of cerebral infarction, and alleviate the effects of lipid peroxidation of rats with focal cerebral ischemia injury.
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Objective To explore the effects of Buyang Huanwu decoction(BYHWD)on expressions of nuclear factor-κB p65(NF-κBp65)and its inhibitor( I-κB)in signal transduction of NF-κB in brain tissue of rats with focal cerebral ischemia injury. Methods 180 Sprague-Dawley(SD)rats were randomly divided into normal group,sham-operated group,model group,pynolidine dithiocarbamate(PDTC)group,minocycline(MC)group and BYHWD treatment group,each group 30 rats. The rats of PDTC group were given PDTC 100 mg?kg-1?d-1 by intra-peritoneal injection. In MC group,MC was given by filling the stomach,the dose was 2.35 g?kg-1?d-1,the drug solution was prepared by adding the distilled water,and the total volume of drug solution to fill the stomach was kept at the same volume in various groups,thus the concentration of the drug was different. In BYHWD group,BYHWD was given,the dose was reduced to 5 g?kg-1?d-1 according to the body surface area dose conversion formula about people and animals. In sham-operated group and model group,the distilled water was given in the same volume as other drug solution. The protein expression levels of NF-κBp65 and I-κB in ischemic tissues were examined by using immunohistochemical method on the time points 7,14 and 21 days after treatment in each group. Results Compared with model group, the cell numbers with expression of NF-κBp65 in PDTC group,MC group and BYHWD group were significantly decreased along with the prolongation of therapy time,the decrease in number was more and more,until 21 days,it reached the valley level(cell/400 times HP:44.00±6.91,45.33±6.55,18.67±2.14 vs. 126.00±5.78,all P0.05). After treatment for 7 days,the number of cells with positive expression of I-κB protein in BYHWD group was less than that in MC group(cell/400 times HP:55.00±3.40 vs. 72.50±4.29,P0.05),and after treatment for 21 days,the number in BYHWD group was significantly higher than that in MC group(88.83±4.95 vs. 71.17±7.16, P<0.05). Conclusion BYHWD can regulate the expressions of inflammatory cytokine I-κB and NF-κB in signal transduction of NF-κB in ischemic brain tissue to inhibit the inflammatory reaction,thus it has the protective effect on cerebral ischemia.
ABSTRACT
This thesis discourse upon blood stagnant in cerebral venation is the pivotal pathogenesis of cerebral ischemia stroke,and discuss once the cerebral ischemia occur,it can derive more phlegms,toxic heat and other pathological outcomes,resulting in inflammatory injury of cerebral ischemia,forming a vicious circle of "inflammation-thrombus",so that aggravating the injury with ischemia and anoxia of never cells,even causing inreversible putrescence of cerebral ischemia.And this condition should be the springs of the development and aggravation of the illness.Therefore,applying promoting blood circulation for removing blood stasis measures can removing blood stasis,eliminating pathogenic wind-fire and cleanning out phlegm,so the pyogenic infections can be dispelled,and the pathological state of inflammation,injury and microcirculation obstacle in the brain can be meliorated.Then,the brain vascula become smooth and the blood supply resume,the symptoms with never functional impairment alleviate or meliorate,thereby,the rate of death and cripple decrease obviously.
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OBJECTIVE:To study the intervention mechanism of puerarin on expressions of HSP70 and Fas proteinum in rats with acute cerebral ischemia injury.METHODS:12 rats with acute cerebral ischemia injury were randomly divided into ischemia control group(saline) and puerarin treated control group,with 6 in each group,each rat under took own control by ischemia side(exp.group) and non-ischemia side(control group);And rats with acute cerebral ischemia injury were randomly divided into control group (saline,ischemia side),puerarin treated control group and normal group (non-ischemia side),with 6 in each group.And then the expressions of HSP70 and Fas proteinum is determined by HE staining and immunochistochemistry SP.RESULTS: The expression of HSP70 was negative or weakly positive in ischemia control group and puerarin treated control group, while that in ischemia experiment group and puerarin treated experiment group was significantly increased(P0.05);The numbers of dead cells in control group and puerarin group were found to be significantly larger than that in normal group(P