BACKGROUND: The present study was undertaken to examine the regulatory effect of hydrogen sulfide(H2S) on endoplasmic reticulum stress in alveolar epithelial cells of rats with acute lung injury(ALI) induced by oleic ...BACKGROUND: The present study was undertaken to examine the regulatory effect of hydrogen sulfide(H2S) on endoplasmic reticulum stress in alveolar epithelial cells of rats with acute lung injury(ALI) induced by oleic acid(OA).METHODS: Seventy-two male Sprague Dawley(SD) rats were divided into control group, oleic acid-induced ALI group(OA group), oleic acid-induced ALI with sodium hydrosulfide(Na HS) pretreatment group(OA+Na HS group), and sodium hydrosulfide treatment group(Na HS group). Rats of each group were further subdivided into 3 subgroups. Index of quantitative assessment of histological lung injury(IQA), wet/dry weight ratio(W/D) and H2 S level of lung tissues were measured. The expressions of endoplasmic reticulum stress markers including glucose-regulated protein 78(GRP78) and α-subunit of eukaryotic translation initiation factor-2(el F2α) in lung tissues were measured by immunohistochemical staining and Western blotting.RESULTS: The IQA score and W/D ratio of lung tissues at the three time points significantly increased in rats injected with OA, but significantly decreased in other rats injected with OA and Na HS. The level of H2 S in lung tissue at the three time points significantly decreased in rats injected with OA, but significantly increased in other rats injected with both OA and Na HS. GRP78 and el F2α decreased in rats injected with OA, but increased in other rats injected with both OA and Na HS, especially at 4-hour and 6-hour time points.CONCLUSION: The results suggested that H2 S could promote alveolar epithelial cell endoplasmic reticulum stress in rats with ALI.展开更多
In this review,the databases searched were PubMed and Web of Science.It is believed that the main causes of acute lung injury(ALI)and acute respiratory distress syndrome(ARDS)are inflammatory response disorders,excess...In this review,the databases searched were PubMed and Web of Science.It is believed that the main causes of acute lung injury(ALI)and acute respiratory distress syndrome(ARDS)are inflammatory response disorders,excessive oxidative stress,cell death,endoplasmic reticulum stress,coagulation dysfunction,and weakened aquaporin function.展开更多
Microplastics(MPs)have attracted growing attention worldwide as an increasingly prevalent environmental pollutant.In addition,chicken meat is currently the most widely consumed kind of poultry in the global market.Con...Microplastics(MPs)have attracted growing attention worldwide as an increasingly prevalent environmental pollutant.In addition,chicken meat is currently the most widely consumed kind of poultry in the global market.Consumer demand for chicken is on the rise both at home and abroad.As a result,the safety of chicken raising has also received significant attention.The lungs play an essential role in the physiological activities of chickens,and they are also the most vulnerable organs.Lung injury is difficult to repair after the accumulation of contaminants,and the mortality rate is high,which brings huge economic losses to farmers.The research on the toxicity of MPs has mainly focused on the marine ecosystem,while the mechanisms of toxicity and lung damage in chickens have been poorly studied.Thus,this study explored the effects of exposure to polystyrene microplastics(PS-MPs)at various concentrations for 42 d on chicken lungs.PS-MPs could cause lung pathologies and ultrastructural abnormalities,such as endoplasmic reticulum(ER)swelling,inflammatory cell infiltration,chromatin agglutination,and plasma membrane rupture.Simultaneously,PS-MPs increased the expression of genes related to the heat shock protein family(Hsp60,Hsp70,and Hsp90),ER stress signaling(activating) transcription factor 6(ATF0),ATF4,protein kinase RNA-like ER kinase(PERK),and eukaryotic translation initiation factor 2 subunitα(eIF2a),pyroptosis-related genes(NOD)-,LRR-and pyrin domain-containing protein 3(NLRP3),apoptosis-associated speck-like protein containing a caspase recruitment domain(ASC),interleukin-1β(IL-1β),cysteinyl aspartate-specific proteinase 1(Caspasel),and gasdermin-D(GSDMD),and the inflammatory signaling pathway(nuclear factor-kB(NF-kB),inducible nitric oxide synthase(iNOS),and cyclooxygenase-2(COX-2).The above results showed that PS-MP exposure could result in lung stress,ER stress,pyroptosis,and inflammation in broilers.Our findings provide new scientific clues for further research on the mechanisms of physical health and toxicology regardingMPs.展开更多
Objective:To evaluate the protective effect of dexmedetomidine and its mechanism on the lung after myocardial ischemia reperfusion in diabetic mice.Methods:Adult diabetic db/db mice aged 15 weeks were selected.The sha...Objective:To evaluate the protective effect of dexmedetomidine and its mechanism on the lung after myocardial ischemia reperfusion in diabetic mice.Methods:Adult diabetic db/db mice aged 15 weeks were selected.The sham operation group(S group),ischemic reperfusion group(IR group),dexmedetomidine post-treatment group(POST-D)and dexmedetomidine pre-treatment group(PRE-D)were set respectively.The IR group of mice underwent ligation of anterior descending branch of left coronary artery for 30min and readministration for 120min.The post-D group and the pre-D group were intraperitoneally injected with 50 ug/kg DEX before surgery and during reperfusion,respectively.Orbital blood was extracted at 120min of reperfusion,serum levels of creatine kinase isoenzyme MB and inflammatory cytokines IL-6,IFN-γand IL-10 were detected,then mice were sacrificed and lung tissue was taken,the ratio of wet and dry weight(W/D)was determined,lung histopathological morphology was observed under light microscope,superoxide dismutase(SOD)and malondialdehyde(MDA)contents were determined,Western Blot was used to detect the expressions of Sirt1,GRP78 and CHOP in lung tissue.Results:Compared with the S group,the IR group rats had severe lung injury,including increased lung W/D value,increased serum CK-MB、IL-6 and IFN-γlevels,decreased serum IL-10,increased serum MDA content,decreased SOD activity,down-regulated Sirt1 expression,up-regulated GRP78 and CHOP expression.Compared with IR group,lung histopathological injury was reduced in post-D group and pre-D group,lung W/D value was decreased,serum CK-MB、IL-6 and IFN-γlevels were decreased,serum IL-10 was increased,serum MDA content was reduced,SOD activity was rised,the expression of Sirt1 was up-regulated,and GRP78 and CHOP were down-regulated.Compared with the post-D group,the degree of lung tissue injury in the pre-D group was reduced,but the differences in various indicators were not statistically significant.Conclusion:Dexmedetomidine can alleviate acute lung injury after myocardial ischemia reperfusion in diabetic mice,and the mechanism may be related to the up-regulation of Sirt1 and the inhibition of endoplasmic reticulum stress.展开更多
A two-photon ratiometric fluorescent sensor for Cu^+ in endoplasmic reticulum(ER), CNSB, was developed via coumarin/ASBD integration based on FRET mechanism. In solution, CNSB shows reversible, highly-specific ratiome...A two-photon ratiometric fluorescent sensor for Cu^+ in endoplasmic reticulum(ER), CNSB, was developed via coumarin/ASBD integration based on FRET mechanism. In solution, CNSB shows reversible, highly-specific ratiometric response to Cu^+ .Moreover, CNSB exhibits suitable K_d value, suggesting the possibility of detecting Cu^+ in the living cells. The probe can enter the MCF-7 cells easily and specifically locates in the ER. The highly specific ratiometric response of CNSB toward Cu^+ in MCF-7 cells provides the sensor the capacity to visualize both exogenous and endogenous Cu^+ in the ER via fluorescence imaging.Next, CNSB was utilized to detect the fluctuation and distribution of Cu^+ under ER stress in MCF-7 cells, which confirmed directly the relationship between Cu^+ enhancement and ER stress. Meanwhile, the two-photon ability of coumarin facilitated the sensor to visualize Cu^+ fluctuation via two-photon fluorescence imaging. In addition, the spatial distribution of Cu^+ in the heart slice of the 14-day-old rat was demonstrated using CNSB. This study demonstrates the promising potential of CNSB in clarifying the Cu^+ -dependent signaling in the ER stress-related diseases.展开更多
文摘BACKGROUND: The present study was undertaken to examine the regulatory effect of hydrogen sulfide(H2S) on endoplasmic reticulum stress in alveolar epithelial cells of rats with acute lung injury(ALI) induced by oleic acid(OA).METHODS: Seventy-two male Sprague Dawley(SD) rats were divided into control group, oleic acid-induced ALI group(OA group), oleic acid-induced ALI with sodium hydrosulfide(Na HS) pretreatment group(OA+Na HS group), and sodium hydrosulfide treatment group(Na HS group). Rats of each group were further subdivided into 3 subgroups. Index of quantitative assessment of histological lung injury(IQA), wet/dry weight ratio(W/D) and H2 S level of lung tissues were measured. The expressions of endoplasmic reticulum stress markers including glucose-regulated protein 78(GRP78) and α-subunit of eukaryotic translation initiation factor-2(el F2α) in lung tissues were measured by immunohistochemical staining and Western blotting.RESULTS: The IQA score and W/D ratio of lung tissues at the three time points significantly increased in rats injected with OA, but significantly decreased in other rats injected with OA and Na HS. The level of H2 S in lung tissue at the three time points significantly decreased in rats injected with OA, but significantly increased in other rats injected with both OA and Na HS. GRP78 and el F2α decreased in rats injected with OA, but increased in other rats injected with both OA and Na HS, especially at 4-hour and 6-hour time points.CONCLUSION: The results suggested that H2 S could promote alveolar epithelial cell endoplasmic reticulum stress in rats with ALI.
基金Yunnan Fundamental Research Projects(202201AU070167,202301AT070258)Yunnan Key Laboratory of Formulated Granules(202105AG070014).
文摘In this review,the databases searched were PubMed and Web of Science.It is believed that the main causes of acute lung injury(ALI)and acute respiratory distress syndrome(ARDS)are inflammatory response disorders,excessive oxidative stress,cell death,endoplasmic reticulum stress,coagulation dysfunction,and weakened aquaporin function.
基金This work was supported by the Key Projects of Natural Science Foundation of Heilongjiang Province of China(No.ZD2020C005).
文摘Microplastics(MPs)have attracted growing attention worldwide as an increasingly prevalent environmental pollutant.In addition,chicken meat is currently the most widely consumed kind of poultry in the global market.Consumer demand for chicken is on the rise both at home and abroad.As a result,the safety of chicken raising has also received significant attention.The lungs play an essential role in the physiological activities of chickens,and they are also the most vulnerable organs.Lung injury is difficult to repair after the accumulation of contaminants,and the mortality rate is high,which brings huge economic losses to farmers.The research on the toxicity of MPs has mainly focused on the marine ecosystem,while the mechanisms of toxicity and lung damage in chickens have been poorly studied.Thus,this study explored the effects of exposure to polystyrene microplastics(PS-MPs)at various concentrations for 42 d on chicken lungs.PS-MPs could cause lung pathologies and ultrastructural abnormalities,such as endoplasmic reticulum(ER)swelling,inflammatory cell infiltration,chromatin agglutination,and plasma membrane rupture.Simultaneously,PS-MPs increased the expression of genes related to the heat shock protein family(Hsp60,Hsp70,and Hsp90),ER stress signaling(activating) transcription factor 6(ATF0),ATF4,protein kinase RNA-like ER kinase(PERK),and eukaryotic translation initiation factor 2 subunitα(eIF2a),pyroptosis-related genes(NOD)-,LRR-and pyrin domain-containing protein 3(NLRP3),apoptosis-associated speck-like protein containing a caspase recruitment domain(ASC),interleukin-1β(IL-1β),cysteinyl aspartate-specific proteinase 1(Caspasel),and gasdermin-D(GSDMD),and the inflammatory signaling pathway(nuclear factor-kB(NF-kB),inducible nitric oxide synthase(iNOS),and cyclooxygenase-2(COX-2).The above results showed that PS-MP exposure could result in lung stress,ER stress,pyroptosis,and inflammation in broilers.Our findings provide new scientific clues for further research on the mechanisms of physical health and toxicology regardingMPs.
基金Natural Science Foundation of Xinjiang Uygur Autonomous Region(No.2019D01C298)。
文摘Objective:To evaluate the protective effect of dexmedetomidine and its mechanism on the lung after myocardial ischemia reperfusion in diabetic mice.Methods:Adult diabetic db/db mice aged 15 weeks were selected.The sham operation group(S group),ischemic reperfusion group(IR group),dexmedetomidine post-treatment group(POST-D)and dexmedetomidine pre-treatment group(PRE-D)were set respectively.The IR group of mice underwent ligation of anterior descending branch of left coronary artery for 30min and readministration for 120min.The post-D group and the pre-D group were intraperitoneally injected with 50 ug/kg DEX before surgery and during reperfusion,respectively.Orbital blood was extracted at 120min of reperfusion,serum levels of creatine kinase isoenzyme MB and inflammatory cytokines IL-6,IFN-γand IL-10 were detected,then mice were sacrificed and lung tissue was taken,the ratio of wet and dry weight(W/D)was determined,lung histopathological morphology was observed under light microscope,superoxide dismutase(SOD)and malondialdehyde(MDA)contents were determined,Western Blot was used to detect the expressions of Sirt1,GRP78 and CHOP in lung tissue.Results:Compared with the S group,the IR group rats had severe lung injury,including increased lung W/D value,increased serum CK-MB、IL-6 and IFN-γlevels,decreased serum IL-10,increased serum MDA content,decreased SOD activity,down-regulated Sirt1 expression,up-regulated GRP78 and CHOP expression.Compared with IR group,lung histopathological injury was reduced in post-D group and pre-D group,lung W/D value was decreased,serum CK-MB、IL-6 and IFN-γlevels were decreased,serum IL-10 was increased,serum MDA content was reduced,SOD activity was rised,the expression of Sirt1 was up-regulated,and GRP78 and CHOP were down-regulated.Compared with the post-D group,the degree of lung tissue injury in the pre-D group was reduced,but the differences in various indicators were not statistically significant.Conclusion:Dexmedetomidine can alleviate acute lung injury after myocardial ischemia reperfusion in diabetic mice,and the mechanism may be related to the up-regulation of Sirt1 and the inhibition of endoplasmic reticulum stress.
基金supported by the National Basic Research Program of China (2015CB856300)the National Natural Science Foundation of China (21571099, 21731004)the Natural Science Foundation of Jiangsu (BK20150054)
文摘A two-photon ratiometric fluorescent sensor for Cu^+ in endoplasmic reticulum(ER), CNSB, was developed via coumarin/ASBD integration based on FRET mechanism. In solution, CNSB shows reversible, highly-specific ratiometric response to Cu^+ .Moreover, CNSB exhibits suitable K_d value, suggesting the possibility of detecting Cu^+ in the living cells. The probe can enter the MCF-7 cells easily and specifically locates in the ER. The highly specific ratiometric response of CNSB toward Cu^+ in MCF-7 cells provides the sensor the capacity to visualize both exogenous and endogenous Cu^+ in the ER via fluorescence imaging.Next, CNSB was utilized to detect the fluctuation and distribution of Cu^+ under ER stress in MCF-7 cells, which confirmed directly the relationship between Cu^+ enhancement and ER stress. Meanwhile, the two-photon ability of coumarin facilitated the sensor to visualize Cu^+ fluctuation via two-photon fluorescence imaging. In addition, the spatial distribution of Cu^+ in the heart slice of the 14-day-old rat was demonstrated using CNSB. This study demonstrates the promising potential of CNSB in clarifying the Cu^+ -dependent signaling in the ER stress-related diseases.
