OBJECTIVE:To investigate the effect of moxibustion-acupoint treatment with acupoints of Zusanli(ST 36) and Zhongwan(RN 12) on cell apoptosis and the expressions of heat shock protein(HSP) 60,HSP70 and second mitochond...OBJECTIVE:To investigate the effect of moxibustion-acupoint treatment with acupoints of Zusanli(ST 36) and Zhongwan(RN 12) on cell apoptosis and the expressions of heat shock protein(HSP) 60,HSP70 and second mitochondrial activator of caspase(Smac) in rat models of acute gastric mucosal lesion(AGML),and explore the mechanisms underlying protection of gastric mucosal lesion.METHODS:Twenty-four Sprague Dawley rats were divided into 3 groups,blank controlled group(group A),controlled-point group(group B) and acupoint group(group C),8 for each.After 8-day moxibustion treatment in group B and C,gastric lavage of anhydrous ethanol was used to created AGML in all three groups.The Guth method was employed to measure the ulcer index(UI) of gastric mucosal lesion and immunohistochemistry used to measure apoptosis with apoptosis index(AI) and examinetheexpressionsofHSP60,HSP70and Smac.RESULTS:Compared with group A,the expressions of UI,AI,Smac and HSP60 were markedly elevated in group B(P<0.05 or P<0.01).However the expression of HSP70 showed no obvious change(P>0.05);the expressions of UI,HSP60 and HSP70 were markedly elevated in group C(P<0.01) while those of AI and Smac became obviously suppressed(P<0.01).Compared with group B,the expressions of UI,AI and Smac decreased significantly in group C(P< 0.01) while those of HSP60 and HSP70 increased markedly(P<0.01),and the expressions of HSP60 and HSP70 were considerably up-regulated(P< 0.01).CONCLUSION:The moxibustion treatment could alleviate the gastric mucosal lesion caused by anhydrous ethanol,induce the over-expressions of HSP60 and HSP70,and down-regulate the expression of Smac,which could suppress cell apoptosis.展开更多
Objective： To determine whether spinal cord decompression plays a role in neural cell apoptosis after spinal cord injury. Study design： We used an animal model of compressive spinal cord injury with incomplete parap...Objective： To determine whether spinal cord decompression plays a role in neural cell apoptosis after spinal cord injury. Study design： We used an animal model of compressive spinal cord injury with incomplete paraparesis to evaluate neural cell apoptosis after decompression. Apoptosis and cellular damage were assessed by staining with terminal deoxynucleotidyl transferase （TdT）-mediated deoxyuridine triphosphate nick-end labelling （TUNEL） and immunostaining for caspase-3, Bcl-2 and Bax. Methods： Experiments were conducted in male Sprague-Dawley rats （n-78） weighing 300-400 g. The spinal cord was compressed posteriorly at T10 level using a custom-made screw for 6 h, 24 h or continuously, followed by decompression by removal of the screw. The rats were sacrificed on Day I or 3 or in Week 1 or 4 post-decompression. The spinal cord was removed en bloc and examined at lesion site, rostral site and caudal site （7.5 mm away from the lesion）. Results： The numbers of TUNEL-positive cells were significantly lower at the site of decompression on Day 1, and also at the rostral and caudal sites between Day 3 and Week 4 post-decompression, compared with the persistently compressed group. The numbers of cells between Day 1 and Week 4 were immunoreactive to caspase-3 and B-cell lymphoma-2 （Bcl-2）-associated X-protein （Bax）, but not to Bcl-2, correlated with those of TUNEL-positive cells. Conclusion： Our results suggest that decompression reduces neural cell apoptosis following spinal cord injury.展开更多
Sirtuin 2(SIRT2)inhibition or Sirt2 knocko ut in animal models protects against the development of neurodegenerative diseases and cerebral ischemia.However,the role of SIRT2 in traumatic brain injury(TBI)remains uncle...Sirtuin 2(SIRT2)inhibition or Sirt2 knocko ut in animal models protects against the development of neurodegenerative diseases and cerebral ischemia.However,the role of SIRT2 in traumatic brain injury(TBI)remains unclear.In this study,we found that knockout of Sirt2 in a mouse model of TBI reduced brain edema,attenuated dis ruption of the blood-brain barrie r,decreased expression of the nucleotide-binding oligomerization domain-like receptor protein 3(NLRP3)inflammasome,reduced the activity of the effector caspase-1,reduced neuroinflammation and neuronal pyroptosis,and improved neurological function.Knoc kout of Sirt2 in a mechanical stretch injury cell model in vitro also decreased expression of the NLRP3 inflammasome and pyroptosis.Our findings suggest that knockout of Sirt2 is neuro protective against TBI;therefore.Sirt2 could be a novel to rget for TBI treatment.展开更多
INTRODUCTIONGastric epithelial dysplasia (GED) hypothetically is a straight-forward concept: dysplastic epithelium replacing the normal gastric epithelium of the stomach [1].In the stomach ,like any other segment of t...INTRODUCTIONGastric epithelial dysplasia (GED) hypothetically is a straight-forward concept: dysplastic epithelium replacing the normal gastric epithelium of the stomach [1].In the stomach ,like any other segment of the gut ,it is defined as an unequivocal non-invasive epithelial change[2,3].The observation of gastric dysplasia as a cancerous lesion was recognized over a century ago ,but it is only after the advent of gastroscopy that its clinical significance has been stressed[4-7].展开更多
Objective:By observing the effects of electroacupuncture(EA)on the apoptosis of conjunctival cells of rabbits with dry eye syndrome(DES)and the expressions of apoptosis-related proteins Caspase-3,Fas and Bcl-2,to disc...Objective:By observing the effects of electroacupuncture(EA)on the apoptosis of conjunctival cells of rabbits with dry eye syndrome(DES)and the expressions of apoptosis-related proteins Caspase-3,Fas and Bcl-2,to discuss the mechanism of EA in the treatment of DES from the perspective of cell apoptosis.Methods:Male New Zealand rabbits were randomly divided into a normal group(NG),a model group(MG),an EA group(EAG)and a sham EA group(SEAG).DES rabbit model was developed by eye drop of 0.1%benzalkonium chloride.The rabbit tear secretion and tear film break-up time(BUT)were measured;terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling(TUNEL)assay was used to detect the apoptosis of conjunctival cells;the expressions of Caspase-3,Fas and Bcl-2 proteins in conjunctival cells were detected by immunohistochemistry.Results:Compared with the NG,the rabbit tear secretion decreased and the BUT was shortened in the MG(both P<0.01);compared with the MG and the SEAG,the rabbit tear secretion increased and the BUT was prolonged in the EAG(all P<0.05).Compared with the NG,the apoptosis of rabbit conjunctival cells increased(P<0.01),the expressions of Caspase-3 and Fas proteins increased(both P<0.05),and the expression of Bcl-2 protein decreased(P<0.01)in the MG;compared with the MG and the SEAG,the apoptosis of rabbit conjunctival cells decreased(both P<0.01),the expressions of Caspase-3 and Fas proteins decreased(all P<0.05),and the expression of Bcl-2 protein increased(both P<0.01)in the EAG.Conclusion:EA can inhibit the apoptosis of rabbit conjunctival cells,down-regulate the expressions of apoptosis-related proteins Caspase-3 and Fas,and up-regulate the expression of Bcl-2 protein,which may be one of the mechanisms of EA in treatment of DES.展开更多
基金Supported by Grant of National Natural Science Foundation of China (No. 81072867,307727707)
文摘OBJECTIVE:To investigate the effect of moxibustion-acupoint treatment with acupoints of Zusanli(ST 36) and Zhongwan(RN 12) on cell apoptosis and the expressions of heat shock protein(HSP) 60,HSP70 and second mitochondrial activator of caspase(Smac) in rat models of acute gastric mucosal lesion(AGML),and explore the mechanisms underlying protection of gastric mucosal lesion.METHODS:Twenty-four Sprague Dawley rats were divided into 3 groups,blank controlled group(group A),controlled-point group(group B) and acupoint group(group C),8 for each.After 8-day moxibustion treatment in group B and C,gastric lavage of anhydrous ethanol was used to created AGML in all three groups.The Guth method was employed to measure the ulcer index(UI) of gastric mucosal lesion and immunohistochemistry used to measure apoptosis with apoptosis index(AI) and examinetheexpressionsofHSP60,HSP70and Smac.RESULTS:Compared with group A,the expressions of UI,AI,Smac and HSP60 were markedly elevated in group B(P<0.05 or P<0.01).However the expression of HSP70 showed no obvious change(P>0.05);the expressions of UI,HSP60 and HSP70 were markedly elevated in group C(P<0.01) while those of AI and Smac became obviously suppressed(P<0.01).Compared with group B,the expressions of UI,AI and Smac decreased significantly in group C(P< 0.01) while those of HSP60 and HSP70 increased markedly(P<0.01),and the expressions of HSP60 and HSP70 were considerably up-regulated(P< 0.01).CONCLUSION:The moxibustion treatment could alleviate the gastric mucosal lesion caused by anhydrous ethanol,induce the over-expressions of HSP60 and HSP70,and down-regulate the expression of Smac,which could suppress cell apoptosis.
基金Project (No. Y207216) supported by the Natural Science Foundation of Zhejiang Province, China
文摘Objective： To determine whether spinal cord decompression plays a role in neural cell apoptosis after spinal cord injury. Study design： We used an animal model of compressive spinal cord injury with incomplete paraparesis to evaluate neural cell apoptosis after decompression. Apoptosis and cellular damage were assessed by staining with terminal deoxynucleotidyl transferase （TdT）-mediated deoxyuridine triphosphate nick-end labelling （TUNEL） and immunostaining for caspase-3, Bcl-2 and Bax. Methods： Experiments were conducted in male Sprague-Dawley rats （n-78） weighing 300-400 g. The spinal cord was compressed posteriorly at T10 level using a custom-made screw for 6 h, 24 h or continuously, followed by decompression by removal of the screw. The rats were sacrificed on Day I or 3 or in Week 1 or 4 post-decompression. The spinal cord was removed en bloc and examined at lesion site, rostral site and caudal site （7.5 mm away from the lesion）. Results： The numbers of TUNEL-positive cells were significantly lower at the site of decompression on Day 1, and also at the rostral and caudal sites between Day 3 and Week 4 post-decompression, compared with the persistently compressed group. The numbers of cells between Day 1 and Week 4 were immunoreactive to caspase-3 and B-cell lymphoma-2 （Bcl-2）-associated X-protein （Bax）, but not to Bcl-2, correlated with those of TUNEL-positive cells. Conclusion： Our results suggest that decompression reduces neural cell apoptosis following spinal cord injury.
基金supported by the National Nature Science Foundation of China,Nos.81671207 and 81974189(both to HLT)。
文摘Sirtuin 2(SIRT2)inhibition or Sirt2 knocko ut in animal models protects against the development of neurodegenerative diseases and cerebral ischemia.However,the role of SIRT2 in traumatic brain injury(TBI)remains unclear.In this study,we found that knockout of Sirt2 in a mouse model of TBI reduced brain edema,attenuated dis ruption of the blood-brain barrie r,decreased expression of the nucleotide-binding oligomerization domain-like receptor protein 3(NLRP3)inflammasome,reduced the activity of the effector caspase-1,reduced neuroinflammation and neuronal pyroptosis,and improved neurological function.Knoc kout of Sirt2 in a mechanical stretch injury cell model in vitro also decreased expression of the NLRP3 inflammasome and pyroptosis.Our findings suggest that knockout of Sirt2 is neuro protective against TBI;therefore.Sirt2 could be a novel to rget for TBI treatment.
基金Supported by the Science Fund of Health Department,No.95A2141.and the Science Fund of Health Bureau of Shanghai.No.982019
文摘INTRODUCTIONGastric epithelial dysplasia (GED) hypothetically is a straight-forward concept: dysplastic epithelium replacing the normal gastric epithelium of the stomach [1].In the stomach ,like any other segment of the gut ,it is defined as an unequivocal non-invasive epithelial change[2,3].The observation of gastric dysplasia as a cancerous lesion was recognized over a century ago ,but it is only after the advent of gastroscopy that its clinical significance has been stressed[4-7].
文摘Objective:By observing the effects of electroacupuncture(EA)on the apoptosis of conjunctival cells of rabbits with dry eye syndrome(DES)and the expressions of apoptosis-related proteins Caspase-3,Fas and Bcl-2,to discuss the mechanism of EA in the treatment of DES from the perspective of cell apoptosis.Methods:Male New Zealand rabbits were randomly divided into a normal group(NG),a model group(MG),an EA group(EAG)and a sham EA group(SEAG).DES rabbit model was developed by eye drop of 0.1%benzalkonium chloride.The rabbit tear secretion and tear film break-up time(BUT)were measured;terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling(TUNEL)assay was used to detect the apoptosis of conjunctival cells;the expressions of Caspase-3,Fas and Bcl-2 proteins in conjunctival cells were detected by immunohistochemistry.Results:Compared with the NG,the rabbit tear secretion decreased and the BUT was shortened in the MG(both P<0.01);compared with the MG and the SEAG,the rabbit tear secretion increased and the BUT was prolonged in the EAG(all P<0.05).Compared with the NG,the apoptosis of rabbit conjunctival cells increased(P<0.01),the expressions of Caspase-3 and Fas proteins increased(both P<0.05),and the expression of Bcl-2 protein decreased(P<0.01)in the MG;compared with the MG and the SEAG,the apoptosis of rabbit conjunctival cells decreased(both P<0.01),the expressions of Caspase-3 and Fas proteins decreased(all P<0.05),and the expression of Bcl-2 protein increased(both P<0.01)in the EAG.Conclusion:EA can inhibit the apoptosis of rabbit conjunctival cells,down-regulate the expressions of apoptosis-related proteins Caspase-3 and Fas,and up-regulate the expression of Bcl-2 protein,which may be one of the mechanisms of EA in treatment of DES.
