To study the biological and morphological characters of bovine mammary epithelial cells in response to heat stress, the cells were exposed to temperatures from 37 ℃to 41℃ for 1 hour, and the cell activities and morp...To study the biological and morphological characters of bovine mammary epithelial cells in response to heat stress, the cells were exposed to temperatures from 37 ℃to 41℃ for 1 hour, and the cell activities and morphological characters were measured by MTT, trypan blue dying, transmission microscopy, and flow cytometry. Results were shown as follows: (1) Cell proliferation was inhibited. The cell number in the treatment groups was significantly lower than that in the control(P<0.05). During the recovery period, 6-18 hours at 37 ℃ after treatment,the cell numbers were lower and mitotic phases were shorter in heat-treated groups (treated for more than 5 days)than those in the control group(P<0.05). (2)In response to heat stress, the mammary cell nuclei shrank and splintered,the organelles deformed and vacuolated, and the damaged cells developed into apoptosis bodies.(3)By flow cytometric analysis,the numbers of mammary cells arrested at G2 phase after heat shock was significantly higher than in controls(P<0.01). It is concluded that heat stress inhibites mammary epithelial cell proliferation and induces cell apoptosis.展开更多
There have been recent extensive studies and rapid advancement on the pathogenesis underlying idiopathic pulmonary fibrosis(IPF),and intricate pathogenesis of IPF has been suggested.The purpose of this study was to cl...There have been recent extensive studies and rapid advancement on the pathogenesis underlying idiopathic pulmonary fibrosis(IPF),and intricate pathogenesis of IPF has been suggested.The purpose of this study was to clarify the logical relationship between these mechanisms.An extensive search was undertaken of the PubMed using the following keywords:"etiology,""pathogenesis,""alveolar epithelial cell(AEC),""fibroblast,""lymphocyte,""macrophage,""epigenomics,""histone,"acetylation,""methylation,""endoplasmic reticulum stress,""mitochondrial dysfunction,""telomerase,""proteases,""plasminogen,""epithelial-mesenchymal transition,""oxidative stress,""inflammation,""apoptosis,"and"idiopathic pulmonary fibrosis."This search covered relevant research articles published up to April 30,2020.Original articles,reviews,and other articles were searched and reviewed for content;240 highly relevant studies were obtained after screening.IPF is likely the result of complex interactions between environmental,genetic,and epigenetic factors:environmental exposures affect epigenetic marks;epigenetic processes translate environmental exposures into the regulation of chromatin;epigenetic processes shape gene expression profiles;in turn,an individual’s genetic background determines epigenetic marks;finally,these genetic and epigenetic factors act in concert to dysregulate gene expression in IPF lung tissue.The pathogenesis of IPF involves various imbalances including endoplasmic reticulum,telomere length homeostasis,mitochondrial dysfunction,oxidant/antioxidant imbalance,Th1/Th2 imbalance,M1-M2 polarization of macrophages,protease/antiprotease imbalance,and plasminogen activation/inhibition imbalance.These affect each other,promote each other,and ultimately promote AEC/fibroblast apoptosis imbalance directly or indirectly.Excessive AEC apoptosis and impaired apoptosis of fibroblasts contribute to fibrosis.IPF is likely the result of complex interactions between environmental,genetic,and epigenetic factors.The pathogenesis of IPF involve展开更多
Background Cisplatin （DDP） is one of most effective and most commonly used therapeutic agent in treating tumors,it can accumulate in the kidney and lead to acute renal failure.MicroRNA-181a can induce cell apoptosis...Background Cisplatin （DDP） is one of most effective and most commonly used therapeutic agent in treating tumors,it can accumulate in the kidney and lead to acute renal failure.MicroRNA-181a can induce cell apoptosis by suppressing the expression of Bcl-2 family.In the present study,we investigated the role of microRNA-181a in the apoptosis of tubular epithelial cell induced by DDP.Methods HK-2 cells were cultured,transfected with microRNA-181a inhibitor for 48 hours,and stimulated with 50 μmol/L cisplatin for 24 hours.MicroRNA-181a expression was analyzed by real time PCR,and cell apoptosis was detected by flow cytometry.Moreover,Bcl-2 and Bcl-2-associated X protein （Bax） expression were measured by Western blotting.Results MicroRNA-181a expression significantly down-regulated in cells transfected with microRNA-181a inhibitor,compared with that in untransfectd cells （21.19±2.01 vs.38.87±1.97,P 〈0.05）.Cell apoptosis induced by DDP significantly decreased in cells transfected with MicroRNA-181a inhibitor.Compared with DDP treated cells alone,Bcl-2 expression strikingly was up-regulated and Bax expression was down-regulated in cells transfected with microRNA-181a inhibitor.Conclusion One pathway of DDP induces apoptosis of tubular epithelial cell by suppressing Bcl-2 expression is achieved by regulating the target gene of MicroRNA-181a.展开更多
Objective:To study the protective effect of resveratrol on lens epithelial cell apoptosis in diabetic cataract rat.Methods:A total of 84 Wistar rats were divided into 4 groups:12 in Group A(control group).24 in Group ...Objective:To study the protective effect of resveratrol on lens epithelial cell apoptosis in diabetic cataract rat.Methods:A total of 84 Wistar rats were divided into 4 groups:12 in Group A(control group).24 in Group B(diabetic cataract group),24 in Group C(therapeutic-dose of resveratrol group) and 24 in Group D(low-dose of resveratrol group).Rats in Group B-D were given with60 mg/kg streptozotocin through intraperitoneal injection.Rats in Group C were given with 100mg/kg resveratrol and rats in Group D were given with 20 mg/kg resveratrol.The caspase-3expression levels and apoptosis ratios of LEC among each group were observed:the degrees of lens opacity in Group B-D after 12 weeks were compared.Results:There were significant differences in caspase-3 expression levels,apoptosis ratios of T.F.C among groups at 4 w,8 w and12 w(P<0.05).After 12 weeks,in Group B the degree of lens opacity was as follow:0(0.00%) in grade Ⅰ,3(37.50%) in grade Ⅱ,2(25.00%)in grade Ⅲ,2(25.00%)grade Ⅳ,and 1(12.50%) in gradeⅤ:in Group C:2(25.00%)in grade Ⅰ,4(50.00%) in grade Ⅱ.2(25.00%)in grade Ⅲ,0(0.00%)gradeⅣ,and 0(0.00%) in grade Ⅴ;in Group D:1(12.50%)in grade Ⅰ,4(50.00%) in grade Ⅱ,2(25.00%)in grade Ⅲ,1(12.50%) grade Ⅳ,and 0(0.00%) in grade Ⅴ.The.difference among Group B-D was statistically significant(P<0.05).Conclusions:Resveratrol has protective effect on lens epithelial cell apoptosis in diabetic cataract rat,and the effect is relative to its dose.展开更多
文摘To study the biological and morphological characters of bovine mammary epithelial cells in response to heat stress, the cells were exposed to temperatures from 37 ℃to 41℃ for 1 hour, and the cell activities and morphological characters were measured by MTT, trypan blue dying, transmission microscopy, and flow cytometry. Results were shown as follows: (1) Cell proliferation was inhibited. The cell number in the treatment groups was significantly lower than that in the control(P<0.05). During the recovery period, 6-18 hours at 37 ℃ after treatment,the cell numbers were lower and mitotic phases were shorter in heat-treated groups (treated for more than 5 days)than those in the control group(P<0.05). (2)In response to heat stress, the mammary cell nuclei shrank and splintered,the organelles deformed and vacuolated, and the damaged cells developed into apoptosis bodies.(3)By flow cytometric analysis,the numbers of mammary cells arrested at G2 phase after heat shock was significantly higher than in controls(P<0.01). It is concluded that heat stress inhibites mammary epithelial cell proliferation and induces cell apoptosis.
基金National Natural Science Foundation of China(No.81970083)。
文摘There have been recent extensive studies and rapid advancement on the pathogenesis underlying idiopathic pulmonary fibrosis(IPF),and intricate pathogenesis of IPF has been suggested.The purpose of this study was to clarify the logical relationship between these mechanisms.An extensive search was undertaken of the PubMed using the following keywords:"etiology,""pathogenesis,""alveolar epithelial cell(AEC),""fibroblast,""lymphocyte,""macrophage,""epigenomics,""histone,"acetylation,""methylation,""endoplasmic reticulum stress,""mitochondrial dysfunction,""telomerase,""proteases,""plasminogen,""epithelial-mesenchymal transition,""oxidative stress,""inflammation,""apoptosis,"and"idiopathic pulmonary fibrosis."This search covered relevant research articles published up to April 30,2020.Original articles,reviews,and other articles were searched and reviewed for content;240 highly relevant studies were obtained after screening.IPF is likely the result of complex interactions between environmental,genetic,and epigenetic factors:environmental exposures affect epigenetic marks;epigenetic processes translate environmental exposures into the regulation of chromatin;epigenetic processes shape gene expression profiles;in turn,an individual’s genetic background determines epigenetic marks;finally,these genetic and epigenetic factors act in concert to dysregulate gene expression in IPF lung tissue.The pathogenesis of IPF involves various imbalances including endoplasmic reticulum,telomere length homeostasis,mitochondrial dysfunction,oxidant/antioxidant imbalance,Th1/Th2 imbalance,M1-M2 polarization of macrophages,protease/antiprotease imbalance,and plasminogen activation/inhibition imbalance.These affect each other,promote each other,and ultimately promote AEC/fibroblast apoptosis imbalance directly or indirectly.Excessive AEC apoptosis and impaired apoptosis of fibroblasts contribute to fibrosis.IPF is likely the result of complex interactions between environmental,genetic,and epigenetic factors.The pathogenesis of IPF involve
基金This work was supported by the National Natural Science Foundation of China （No.61101218 and No.81102673）,the New Star Program of Beijing Science and Technology Commission （No.2011111） and the National Basic Research Program of China （No.2011 CB944004）.
文摘Background Cisplatin （DDP） is one of most effective and most commonly used therapeutic agent in treating tumors,it can accumulate in the kidney and lead to acute renal failure.MicroRNA-181a can induce cell apoptosis by suppressing the expression of Bcl-2 family.In the present study,we investigated the role of microRNA-181a in the apoptosis of tubular epithelial cell induced by DDP.Methods HK-2 cells were cultured,transfected with microRNA-181a inhibitor for 48 hours,and stimulated with 50 μmol/L cisplatin for 24 hours.MicroRNA-181a expression was analyzed by real time PCR,and cell apoptosis was detected by flow cytometry.Moreover,Bcl-2 and Bcl-2-associated X protein （Bax） expression were measured by Western blotting.Results MicroRNA-181a expression significantly down-regulated in cells transfected with microRNA-181a inhibitor,compared with that in untransfectd cells （21.19±2.01 vs.38.87±1.97,P 〈0.05）.Cell apoptosis induced by DDP significantly decreased in cells transfected with MicroRNA-181a inhibitor.Compared with DDP treated cells alone,Bcl-2 expression strikingly was up-regulated and Bax expression was down-regulated in cells transfected with microRNA-181a inhibitor.Conclusion One pathway of DDP induces apoptosis of tubular epithelial cell by suppressing Bcl-2 expression is achieved by regulating the target gene of MicroRNA-181a.
基金supported by Wenzhou Science and Technology Project(Y20080087)
文摘Objective:To study the protective effect of resveratrol on lens epithelial cell apoptosis in diabetic cataract rat.Methods:A total of 84 Wistar rats were divided into 4 groups:12 in Group A(control group).24 in Group B(diabetic cataract group),24 in Group C(therapeutic-dose of resveratrol group) and 24 in Group D(low-dose of resveratrol group).Rats in Group B-D were given with60 mg/kg streptozotocin through intraperitoneal injection.Rats in Group C were given with 100mg/kg resveratrol and rats in Group D were given with 20 mg/kg resveratrol.The caspase-3expression levels and apoptosis ratios of LEC among each group were observed:the degrees of lens opacity in Group B-D after 12 weeks were compared.Results:There were significant differences in caspase-3 expression levels,apoptosis ratios of T.F.C among groups at 4 w,8 w and12 w(P<0.05).After 12 weeks,in Group B the degree of lens opacity was as follow:0(0.00%) in grade Ⅰ,3(37.50%) in grade Ⅱ,2(25.00%)in grade Ⅲ,2(25.00%)grade Ⅳ,and 1(12.50%) in gradeⅤ:in Group C:2(25.00%)in grade Ⅰ,4(50.00%) in grade Ⅱ.2(25.00%)in grade Ⅲ,0(0.00%)gradeⅣ,and 0(0.00%) in grade Ⅴ;in Group D:1(12.50%)in grade Ⅰ,4(50.00%) in grade Ⅱ,2(25.00%)in grade Ⅲ,1(12.50%) grade Ⅳ,and 0(0.00%) in grade Ⅴ.The.difference among Group B-D was statistically significant(P<0.05).Conclusions:Resveratrol has protective effect on lens epithelial cell apoptosis in diabetic cataract rat,and the effect is relative to its dose.
