OBJECTIVE:To investigate the protective effect and possible mechanism of sodium Danshensu(SDSS)against pressure injury caused by ischemia/reperfusion(I/R)injury.METHODS:Sprague-Dawley rats were randomly divided into f...OBJECTIVE:To investigate the protective effect and possible mechanism of sodium Danshensu(SDSS)against pressure injury caused by ischemia/reperfusion(I/R)injury.METHODS:Sprague-Dawley rats were randomly divided into five groups of eight rats each:control group,model group,10 mg/kg SDSS-treated group,20 mg/kg SDSS-treated group,and 40 mg/kg SDSS-treated group.We used two round ferrite magnetic plates of 15 mm diameter and 3 mm thickness to establish stage 2 pressure injury model rats.Each rat was subjected to five cycles of ischemia and reperfusion to induce pressure injury.One cycle consisted of 2 h of ischemia and 0.5 h of reperfusion,which meant that each cycle included2 h of pressure and 0.5 h of pressure relief.The outline of the wound was delineated by butter paper and marker pen,and histopathological changes were observed by hematoxylin and eosin staining.In addition,the number of apoptotic cells and the activity of caspase-3 were assessed by terminal deoxynucleotidyl transferase-mediated nick end labeling and caspase-3 assay kits,respectively.The expression of apoptosis-regulatory proteins and inflammatory mediators was investigated by enzyme-linked immunosorbent assay.RESULTS:Results showed that treatment with SDSS for 7 d after establishing the pressure injury model remarkably improved the healing rate of the wound.SDSS also inhibited the levels of tumor necrosis factor-α,myeloperoxidase,and intercellular cell adhesion molecule-1;decreased the number of apoptotic cells;increased the ratio of B-cell lymphoma-2(Bcl-2)/Bcl-2-associated X(Bax);and regulated the expression and activity of caspase-3.CONCLUSION:Our results suggest that SDSS exhibits a treatment efficacy for pressure injury caused by I/R injury possibly by inhibiting apoptosis and inflammatory response.展开更多
BACKGROUND： The high concentration of glutamate release is the main cause for neuronal cell death. The relationship between glutamate level and apoptosis during ischemia/reperfusion injury is still unclear. OBJECTIVE...BACKGROUND： The high concentration of glutamate release is the main cause for neuronal cell death. The relationship between glutamate level and apoptosis during ischemia/reperfusion injury is still unclear. OBJECTIVE： To observe the neuronal apoptosis at 24 and 72 hours following cerebral ischemia/reperfusion in rats, and analyze the possible influencing factors. DESIGN： A randomized controlled animal experiment. SETTING： School of Medicine, Southern Yangtze University. MATERIALS： Totally 30 male adult Sprague Dawley （SD） rats of clean grade, weighing 240 - 290 g, were obtained from Shanghai Experimental Animal Center, Chinese Academy of Sciences. The rats were randomly divided into sham-operated group （n=10） and model group （n=20）. Each group was observed at 24 and 72 hours after ischemia/reperfusion, 5 rats at each time point in the sham-operated group, whereas 12 at 24 hours and 8 at 72 hours in the model group. Kits for determining apoptosis and Bcl-2 were bought from Wuhan Boster Biological Technology, Co., Ltd.; Kit for calcineurin from Nanjing Jiancheng Bioengineering Institute. METHODS： The experiment was carried out in the Functional Scientific Research Room of Southern Yangtze University from June to October in 2006.①Right middle cerebral artery was occluded by inserting a thread through internal carotid artery （ICA）. The surgical process for the sham-operated rats was the same as that in the model group except a nylon suture inserted the ICA. According to Longa five-degree standard, the neurological deficit evaluation of rats was evaluated after surgery, and grades 1 - 3 were taken as successful model establishment. The blood was recirculated by withdrawing the nylon filament under anesthesia at 2 hours after ischemia in successful rat models. ②After reperfusion, the brain tissue was quickly removed at 24 or 72 hours and the slices were obtained from optic chiasma to funnel manubrium. The changes of the number of apoptotic cells were observed using the terminal deoxynucl展开更多
基金Supported by the Health Commission of Zhejiang Province(Exploring the Mechanism of Danshensu Anti-apoptosis Effect in Rat Models of Stage 2 Pressure Injury Based on PI3K/AKT Pathway,No.2019KY470)。
文摘OBJECTIVE:To investigate the protective effect and possible mechanism of sodium Danshensu(SDSS)against pressure injury caused by ischemia/reperfusion(I/R)injury.METHODS:Sprague-Dawley rats were randomly divided into five groups of eight rats each:control group,model group,10 mg/kg SDSS-treated group,20 mg/kg SDSS-treated group,and 40 mg/kg SDSS-treated group.We used two round ferrite magnetic plates of 15 mm diameter and 3 mm thickness to establish stage 2 pressure injury model rats.Each rat was subjected to five cycles of ischemia and reperfusion to induce pressure injury.One cycle consisted of 2 h of ischemia and 0.5 h of reperfusion,which meant that each cycle included2 h of pressure and 0.5 h of pressure relief.The outline of the wound was delineated by butter paper and marker pen,and histopathological changes were observed by hematoxylin and eosin staining.In addition,the number of apoptotic cells and the activity of caspase-3 were assessed by terminal deoxynucleotidyl transferase-mediated nick end labeling and caspase-3 assay kits,respectively.The expression of apoptosis-regulatory proteins and inflammatory mediators was investigated by enzyme-linked immunosorbent assay.RESULTS:Results showed that treatment with SDSS for 7 d after establishing the pressure injury model remarkably improved the healing rate of the wound.SDSS also inhibited the levels of tumor necrosis factor-α,myeloperoxidase,and intercellular cell adhesion molecule-1;decreased the number of apoptotic cells;increased the ratio of B-cell lymphoma-2(Bcl-2)/Bcl-2-associated X(Bax);and regulated the expression and activity of caspase-3.CONCLUSION:Our results suggest that SDSS exhibits a treatment efficacy for pressure injury caused by I/R injury possibly by inhibiting apoptosis and inflammatory response.
文摘BACKGROUND： The high concentration of glutamate release is the main cause for neuronal cell death. The relationship between glutamate level and apoptosis during ischemia/reperfusion injury is still unclear. OBJECTIVE： To observe the neuronal apoptosis at 24 and 72 hours following cerebral ischemia/reperfusion in rats, and analyze the possible influencing factors. DESIGN： A randomized controlled animal experiment. SETTING： School of Medicine, Southern Yangtze University. MATERIALS： Totally 30 male adult Sprague Dawley （SD） rats of clean grade, weighing 240 - 290 g, were obtained from Shanghai Experimental Animal Center, Chinese Academy of Sciences. The rats were randomly divided into sham-operated group （n=10） and model group （n=20）. Each group was observed at 24 and 72 hours after ischemia/reperfusion, 5 rats at each time point in the sham-operated group, whereas 12 at 24 hours and 8 at 72 hours in the model group. Kits for determining apoptosis and Bcl-2 were bought from Wuhan Boster Biological Technology, Co., Ltd.; Kit for calcineurin from Nanjing Jiancheng Bioengineering Institute. METHODS： The experiment was carried out in the Functional Scientific Research Room of Southern Yangtze University from June to October in 2006.①Right middle cerebral artery was occluded by inserting a thread through internal carotid artery （ICA）. The surgical process for the sham-operated rats was the same as that in the model group except a nylon suture inserted the ICA. According to Longa five-degree standard, the neurological deficit evaluation of rats was evaluated after surgery, and grades 1 - 3 were taken as successful model establishment. The blood was recirculated by withdrawing the nylon filament under anesthesia at 2 hours after ischemia in successful rat models. ②After reperfusion, the brain tissue was quickly removed at 24 or 72 hours and the slices were obtained from optic chiasma to funnel manubrium. The changes of the number of apoptotic cells were observed using the terminal deoxynucl
