Background:Chronic heat stress has a negative impact on poultry meat quality.Although this has been extensively investigated,previous studies have primarily focused on metabolic alterations and oxidative stress in the...Background:Chronic heat stress has a negative impact on poultry meat quality.Although this has been extensively investigated,previous studies have primarily focused on metabolic alterations and oxidative stress in the pectoralis major(PM)muscle under chronic heat stress,and not all of the underlying molecular mechanisms are completely understood.Methods:A total of 144 male Arbor Acres broilers(28 d old)were randomly allocated into 3 treatment groups:(1)the normal control(NC)group,with broilers raised at 22℃and fed a basal diet;(2)the heat stress(HS)group,with birds raised at 32℃and fed a basal diet;and(3)the pair-fed(PF)group,with birds raised at 22℃and fed the amount of feed equal to the feed consumed on the previous day by the HS group.The experiment lasted for 14 d.Results:Chronic heat stress decreased the average daily feed intake and average daily gain,increased feed:gain ratio(P<0.05);and increased drip loss,cooking loss,shear force,hardness,and decreased p H,redness(a*);and springiness of PM muscle(P<0.05).Furthermore,chronic heat stress decreased muscle fiber density,increased connective tissue,and led to intracellular vacuolation.The transcriptome analyses indicated that the effect of chronic heat stress on meat quality was not only related to metabolism and oxidative stress,but also to signal transduction,immune system,transport and catabolism,cell growth and death,and muscle structure.Conclusions:Chronic heat stress has a negative impact on the growth performance,meat quality,and the PM muscle structure of broilers.Transcriptome analysis revealed a comprehensive understanding of the mechanism of the chronic heat stress-induced deterioration of broiler meat quality at the transcriptional level.展开更多
Background:Previous studies had shown that short-term acute heat stress(HS)affected the host’s metabolism and intestinal microbiota independent of feed intake(FI)reduction,and long-term calorie restriction caused int...Background:Previous studies had shown that short-term acute heat stress(HS)affected the host’s metabolism and intestinal microbiota independent of feed intake(FI)reduction,and long-term calorie restriction caused intestinal morphological injuries and gut microbial alterations.However,research on the effects of constant chronic HS on intestinal microbial composition and the roles of FI reduction played in is limited.This study aimed to investigate the effects of 7-day constant chronic HS on the composition of intestinal microbes in growing-finishing pigs,and its relationship with pigs’performance,intestinal morphology,and ileal immune response.Twenty-four growingfinishing pigs(Duroc×Large White×Landrace,30±1 kg body weight)were randomly assigned to three treatments(n=8),1)thermal neutral(TN)conditions(25±1℃)with ad libitum FI,2)HS conditions(35±1℃)with ad libitum FI,3)pair-fed(PF)with HS under TN conditions to discriminate the confounding effects of dissimilar FI,and the FI was the previous day’s average FI of HS.The small intestinal segments(duodenum,jejunum,and ileum)and feces were collected on d 8.Results:Results indicated that HS drastically declined(P<0.05)average daily gain(ADG)and average daily feed intake(ADFI)(about 61%)in comparison with TN,and caused hyperpyrexia,meanwhile PF caused hypothermia.Morphological observation by light and electron microscopes showed that both HS and PF treatment decreased(P<0.05)the villus and microvillus height compared with TN.Additionally,HS increased(P<0.05)protein expression of heat shock protein 70 in the duodenum,jejunum,and ileum.Furthermore,the expression of tight junction protein zonula occluden-1(ZO-1)in the duodenum and ileum,and Occludin in the ileum were enhanced(P<0.05)compared with TN and PF.Moreover,HS significantly enhanced(P<0.05)the mRNA relative expression of inflammatory cytokines(TLR-2,TLR-4,and tumor necrosis factor-α(TNF-α),IL-6,IL-8,PG1–5,β-defensin 2(pBD-2)),mucins(mucin-1 and mucin-2)and P65 protein level in the ileal mucosa tissue.Intestinal microbiota analysis by 16S rRNA sequencing showed lower(P<0.10)αdiversity in both HS and PF,and a separated cluster ofβdiversity among groups.Compared with TN,HS but not PF mainly reduced(FDR<0.05)Bacteroidetes(phylum),Bacteroidia(class)and elevated the proportions of Proteobacteria(phylum,FDR<0.05),Bacillales(order,FDR<0.05),Planococcaceae(family,FDR<0.05),Kurthia(genus,FDR<0.05),Streptococcaceae(family,FDR<0.10)and Streptococcus(genus,FDR<0.10).Notably,Lactobacillales(order)was decreased(FDR<0.05)by PF alone.Furthermore,the Spearman correlation analysis indicated that the microbes prevalent in HS were positively(P<0.05)associated with intestinal morphological injuries indicators and ileal immune response parameters,and the microbes reduced in HS were negatively(P<0.05)with the performance data.Conclusions:Intestinal morphological injuries and ileal immune response caused by constant chronic HS independent of FI showed close connections with alterations in intestinal microbiota in growing-finishing pigs.展开更多
Background:Chronic heat stress(CHS)disrupts hepatic metabolic homeostasis and jeopardizes product quality of pigs.Selenium(Se)may regulate the metabolic state through affect selenoprotein.Thus,we investigate the prote...Background:Chronic heat stress(CHS)disrupts hepatic metabolic homeostasis and jeopardizes product quality of pigs.Selenium(Se)may regulate the metabolic state through affect selenoprotein.Thus,we investigate the protective effect of dietary hydroxy-4-methylselenobutanoic acid(HMSeBA)on CHS induced hepatic metabolic disorder in growing pigs,and the corresponding response of selenoprotein.Methods:Forty crossbreed growing pigs were randomly assigned to five groups:control group raised in the thermoneutral environment(22±2℃)with basal diet;four CHS groups raised in hyperthermal condition(33±2℃)with basal diet and supplied with 0.0,0.2,0.4,and 0.6 mg Se/kg HMSeBA,respectively.The trial lasted 28 d.The serum biochemical,hepatic metabolism related enzyme,protein and gene expression and 25 selenoproteins in liver tissue were determined by real-time PCR,ELISA and western blot.Results:CHS significantly increased the rectal temperature,respiration rate,serum aspartate aminotransferase(AST)and low-density lipoprotein cholesterol(LDL-C)of pigs,up-regulated hepatic heat shock protein 70(HSP70)and induced lower liver weight,glycogen content,hepatic glucokinase and glutathione peroxidase(GSH-Px).The CHSinduced liver metabolic disorder was associated with the aberrant expression of 6 metabolism-related gene and 11 selenoprotein encoding genes,and decreased the protein abundance of GCK,GPX4 and SELENOS.HMSeBA improved anti-oxidative capacity of liver.0.4 or 0.6 mg Se/kg HMSeBA supplementation recovered the liver weight,glycogen content and rescue of mRNA abundance of genes related to metabolism and protein levels of GCK.HMSeBA supplementation changed expressions of 15 selenoprotein encoding genes,and enhanced protein expression of GPX1,GPX4 and SELENOS in the liver affected by CHS.CHS alone showed no impact while HMSeBA supplementation increased protein levels of p-AMPKαin the liver.Conclusions:In summary,HMSeBA supplementation beyond nutrient requirement mitigates CHS-induced hepatic metabolic disorder,recovered the liver glycogen content and the processes that are associated with the activation of AMPK signal and regulation of selenoproteins in the liver of growing pigs.展开更多
In the present study,the chronic heat stress(CHS)broiler model was developed to investigate the potential protection mechanism of organic selenium(selenomethionine,SeMet)on CHS-induced skeletal muscle growth retardati...In the present study,the chronic heat stress(CHS)broiler model was developed to investigate the potential protection mechanism of organic selenium(selenomethionine,SeMet)on CHS-induced skeletal muscle growth retardation and poor meat quality.Four hundred Arbor Acres male broilers(680±70 g,21 d old)were grouped into 5 treatments with 8 replicates of 10 broilers per replicate.Broilers in the control group were raised in a thermoneutral environment(22±2°C)and fed with a basal diet.The other four treatments were exposed to hyperthermic conditions(33±2°C,24 h in each day)and fed on the basal diet supplied with SeMet at 0.0,0.2,0.4,and 0.6 mg Se/kg,respectively,for 21 d.Results showed that CHS reduced(P<0.05)the growth performance,decreased(P<0.05)the breast muscle weight and impaired the meat quality of breast muscle in broilers.CHS induced protein metabolic disorder in breast muscle,which increased(P<0.05)the expression of caspase 3,caspase 8,caspase 9 and ubiquitin proteasome system related genes,while decreased the protein expression of P-4EBP1.CHS also decreased the antioxidant capacity and induced mitochondrial stress and endoplasmic reticulum(ER)stress in breast muscle,which increased(P<0.05)the ROS levels,decreased the concentration of ATP,increased the protein expression of HSP60 and CLPX,and increased(P<0.05)the expression of ER stress biomarkers.Dietary SeMet supplementation linearly increased(P<0.05)breast muscle Se concentration and exhibited protective effects via up-regulating the expression of the selenotranscriptome and several key selenoproteins,which increased(P<0.05)body weight,improved meat quality,enhanced antioxidant capacity and mitigated mitochondrial stress and ER stress.What's more,SeMet suppressed protein degradation and improved protein biosynthesis though inhibiting the caspase and ubiquitin proteasome system and promoting the mTOR-4EBP1 pathway.In conclusion,dietary SeMet supplementation increases the expression of several key selenoproteins,alleviates mitochondrial dysfunction and ER stress,improves protein biosynthesis,suppresses protein degradation,thus increases the body weight and improves meat quality of broilers exposed to CHS.展开更多
Although high temperatures influence gut health,data on underlying mechanisms remains scant.Using a pig model,this study performed a global analysis on how chronic heat stress affects the transport and immune function...Although high temperatures influence gut health,data on underlying mechanisms remains scant.Using a pig model,this study performed a global analysis on how chronic heat stress affects the transport and immune function of the gut through transcriptome,proteome,microbial diversity and flow cytometry.A total of 27 pigs with similar body weights were assigned into 3 groups,control(Con)group(23℃),chronic heat stressed(HS)group(33°C),and pair-fed(PF)group,in a controlled environment for 21 days.Our results showed that pigs in the HS group had reduced growth performance and diminished height of ileal villi(P<0.01).Transcriptome and proteome analyses demonstrated notable modification of expression of nutrients and ion transport-related transporters and gut mechanical barrier-related genes by chronic heart stress(P<0.05),suggesting damage of transport functions and the gut barrier.Chronic heat stress-induced endoplasmic reticulum stress also increased the synthesis of misfolded proteins,leading to upregulation of misfolded protein degradation and synthesis,as well as vesicle transport disorder(P<0.05).Energy supply processes were enhanced in the mitochondrion(P<0.05)to maintain biological processes with high energy demands.Furthermore,chronic heat stress activated complement cascade response-related genes and proteins in the gut mucosa(P<0.05).Our flow cytometry assays showed that the proportion of gut lymphocytes(CD4^(+)T cells,T cells,B cells in Peyer’s patch lymphocytes and CD4^(+)CD25^(+)T cells in intraepithelial lymphocytes)were significantly altered in the HS group pigs(P<0.05).In addition,the occurrence of gut microbial dysbiosis in the HS group pigs was characterized by increased potential pathogens(e.g.,Asteroleplasma,Shuttleworthia,Mycoplasma)and suppression of beneficial bacteria(e.g.,Coprococcus and Aeriscardovia),which are associated with gut immune function.Altogether,our data demonstrated that chronic heat stress induced gut transport and immune function disorder associated with endoplasmic reticulum stress in growing pigs.展开更多
The effects of cigarette smoke extract (CSE) on the expression of heat stress protein 70 (Hsp70) in human bronchi smooth muscle cells were investigated in vitro, and the changes in Hsp70 mRNA in the patients with chro...The effects of cigarette smoke extract (CSE) on the expression of heat stress protein 70 (Hsp70) in human bronchi smooth muscle cells were investigated in vitro, and the changes in Hsp70 mRNA in the patients with chronic obstructive pulmonary disease and their significance were explored. Human bronchi smooth muscle cells were cultured with CSE at the different concentrations. The expression of Hsp70 mRNA and Hsp70 was detected by reverse translation-polymerase chain reaction (RT-PCR) and Western blotting respectively. Levels of Hsp70 mRNA and Hsp70 in lymphocytes from 20 patients with COPD and 20 healthy smoking control subjects were measured by RT-PCR and Western blotting. The results showed the expression of both Hsp70 mRNA and Hsp70 was decreased conformably in human bronchi smooth muscle cells treated with CSE at certain concentration in vitro. The A values of the Hsp70 mRNA expression were 0.24±0.11 and 0.42±0.13 respectively in COPD patients and healthy smoking controls with the difference being significant (P<0.01). There was also significant difference in the A values of the Hsp70 expression between COPD patients and healthy smoking controls (20.9±9.9 vs 44.8±15.3, P<0.01). The levels of Hsp70 mRNA had strongly positive correlation with Hsp70 protein (r = 0.85, P<0 01). It was suggested that the expression of Hsp70 mRNA was in concordance with the expression of Hsp70, which could provide a basis on the study of Hsp70 gene regulation and Hsp70 gene in the development of COPD.展开更多
Acute pancreatitis is an inflammatory disorder of the pancreas that may cause life-threatening complications.Etiologies of pancreatitis vary,with gallstones accounting for the majority of all cases,followed by alcohol...Acute pancreatitis is an inflammatory disorder of the pancreas that may cause life-threatening complications.Etiologies of pancreatitis vary,with gallstones accounting for the majority of all cases,followed by alcohol.Other causes of pancreatitis include trauma,ischemia,mechanical obstruction,infections,autoimmune,hereditary,and drugs.The main events occurring in the pancreatic acinar cell that initiate and propagate acute pancreatitis include inhibition of secretion,intracellular activation of proteases,and generation of inflammatory mediators.Small cytokines known as chemokines are released from damaged pancreatic cells and attract inflammatory cells,whose systemic action ultimately determined the severity of the disease.Indeed,severe forms of pancreatitis may result in systemic inflammatory response syndrome and multiorgan dysfunction syndrome,characterized by a progressive physiologic failure of several interdependent organ systems.Stress occurs when homeostasis is threatened,and stressors can include physical or mental forces,or combinations of both.Depending on the timing and duration,stress can result in beneficial or harmful consequences.While it is well established that a previous acute-short-term stress decreases the severity of experimentally-induced pancreatitis,the worsening effects of chronic stress on the exocrine pancreas have received relatively little attention.This review will focus on the influence of both prior acute-short-term and chronic stress in acute pancreatitis.展开更多
Increasing evidence suggests that heat shock factor 1 exerts endogenous protective effects on working memory under conditions of chronic psychological stress. However, the precise underlying mechanisms remain poorly u...Increasing evidence suggests that heat shock factor 1 exerts endogenous protective effects on working memory under conditions of chronic psychological stress. However, the precise underlying mechanisms remain poorly understood. This study examined the protective factors affecting working memory in heat shock transcription factor 1 gene knockout mice. The results indicated that the number of correct T maze alternations decreased following mild chronic psychological stress in knockout mice. This change was accompanied by a decrease in neurogenesis and an increase in neuronal apoptosis in the hippocampal dentate gyrus. The number of correct T maze alternations was positively correlated with neurogenesis in hippocampal dentate gyrus, and negatively correlated with neuronal apoptosis. In wild type mice, no significant difference was detected in the number of correct T maze alternations or neuronal apoptosis in hippocampal dentate gyrus. These results indicate that the heat shock factor 1 gene has an endogenous protective role in working memory during mild chronic psychological stress associated with dentate gyrus neuronal apoptosis Moreover, dentate gyrus neurogenesis appears to participate in the protective mechanism.展开更多
基金the National Natural Science Foundation of China(32072780,31872374)the National Key Research and Development Program of China(2016YFD0500501,2018YFD0500405)the Earmarked Fund for Jiangsu Agricultural Industry Technology System(JATS[2021]459)。
文摘Background:Chronic heat stress has a negative impact on poultry meat quality.Although this has been extensively investigated,previous studies have primarily focused on metabolic alterations and oxidative stress in the pectoralis major(PM)muscle under chronic heat stress,and not all of the underlying molecular mechanisms are completely understood.Methods:A total of 144 male Arbor Acres broilers(28 d old)were randomly allocated into 3 treatment groups:(1)the normal control(NC)group,with broilers raised at 22℃and fed a basal diet;(2)the heat stress(HS)group,with birds raised at 32℃and fed a basal diet;and(3)the pair-fed(PF)group,with birds raised at 22℃and fed the amount of feed equal to the feed consumed on the previous day by the HS group.The experiment lasted for 14 d.Results:Chronic heat stress decreased the average daily feed intake and average daily gain,increased feed:gain ratio(P<0.05);and increased drip loss,cooking loss,shear force,hardness,and decreased p H,redness(a*);and springiness of PM muscle(P<0.05).Furthermore,chronic heat stress decreased muscle fiber density,increased connective tissue,and led to intracellular vacuolation.The transcriptome analyses indicated that the effect of chronic heat stress on meat quality was not only related to metabolism and oxidative stress,but also to signal transduction,immune system,transport and catabolism,cell growth and death,and muscle structure.Conclusions:Chronic heat stress has a negative impact on the growth performance,meat quality,and the PM muscle structure of broilers.Transcriptome analysis revealed a comprehensive understanding of the mechanism of the chronic heat stress-induced deterioration of broiler meat quality at the transcriptional level.
基金supported by National Key Research and Development Program of China(2016YFD0500501)the China Agriculture Research System of MOF and MARA+1 种基金the Science and Technology Program of Guangdong Academy of Agricultural Sciences(R2020PY-JG009,202106TD)the Project of Swine Innovation Team in Guangdong Modern Agricultural Research System(2021KJ126)。
文摘Background:Previous studies had shown that short-term acute heat stress(HS)affected the host’s metabolism and intestinal microbiota independent of feed intake(FI)reduction,and long-term calorie restriction caused intestinal morphological injuries and gut microbial alterations.However,research on the effects of constant chronic HS on intestinal microbial composition and the roles of FI reduction played in is limited.This study aimed to investigate the effects of 7-day constant chronic HS on the composition of intestinal microbes in growing-finishing pigs,and its relationship with pigs’performance,intestinal morphology,and ileal immune response.Twenty-four growingfinishing pigs(Duroc×Large White×Landrace,30±1 kg body weight)were randomly assigned to three treatments(n=8),1)thermal neutral(TN)conditions(25±1℃)with ad libitum FI,2)HS conditions(35±1℃)with ad libitum FI,3)pair-fed(PF)with HS under TN conditions to discriminate the confounding effects of dissimilar FI,and the FI was the previous day’s average FI of HS.The small intestinal segments(duodenum,jejunum,and ileum)and feces were collected on d 8.Results:Results indicated that HS drastically declined(P<0.05)average daily gain(ADG)and average daily feed intake(ADFI)(about 61%)in comparison with TN,and caused hyperpyrexia,meanwhile PF caused hypothermia.Morphological observation by light and electron microscopes showed that both HS and PF treatment decreased(P<0.05)the villus and microvillus height compared with TN.Additionally,HS increased(P<0.05)protein expression of heat shock protein 70 in the duodenum,jejunum,and ileum.Furthermore,the expression of tight junction protein zonula occluden-1(ZO-1)in the duodenum and ileum,and Occludin in the ileum were enhanced(P<0.05)compared with TN and PF.Moreover,HS significantly enhanced(P<0.05)the mRNA relative expression of inflammatory cytokines(TLR-2,TLR-4,and tumor necrosis factor-α(TNF-α),IL-6,IL-8,PG1–5,β-defensin 2(pBD-2)),mucins(mucin-1 and mucin-2)and P65 protein level in the ileal mucosa tissue.Intestinal microbiota analysis by 16S rRNA sequencing showed lower(P<0.10)αdiversity in both HS and PF,and a separated cluster ofβdiversity among groups.Compared with TN,HS but not PF mainly reduced(FDR<0.05)Bacteroidetes(phylum),Bacteroidia(class)and elevated the proportions of Proteobacteria(phylum,FDR<0.05),Bacillales(order,FDR<0.05),Planococcaceae(family,FDR<0.05),Kurthia(genus,FDR<0.05),Streptococcaceae(family,FDR<0.10)and Streptococcus(genus,FDR<0.10).Notably,Lactobacillales(order)was decreased(FDR<0.05)by PF alone.Furthermore,the Spearman correlation analysis indicated that the microbes prevalent in HS were positively(P<0.05)associated with intestinal morphological injuries indicators and ileal immune response parameters,and the microbes reduced in HS were negatively(P<0.05)with the performance data.Conclusions:Intestinal morphological injuries and ileal immune response caused by constant chronic HS independent of FI showed close connections with alterations in intestinal microbiota in growing-finishing pigs.
基金supported partly by the National Natural Science Foundation of China(No.31772643)the Special Research Funding for Discipline Construction in Sichuan Agricultural University(No.03570126).
文摘Background:Chronic heat stress(CHS)disrupts hepatic metabolic homeostasis and jeopardizes product quality of pigs.Selenium(Se)may regulate the metabolic state through affect selenoprotein.Thus,we investigate the protective effect of dietary hydroxy-4-methylselenobutanoic acid(HMSeBA)on CHS induced hepatic metabolic disorder in growing pigs,and the corresponding response of selenoprotein.Methods:Forty crossbreed growing pigs were randomly assigned to five groups:control group raised in the thermoneutral environment(22±2℃)with basal diet;four CHS groups raised in hyperthermal condition(33±2℃)with basal diet and supplied with 0.0,0.2,0.4,and 0.6 mg Se/kg HMSeBA,respectively.The trial lasted 28 d.The serum biochemical,hepatic metabolism related enzyme,protein and gene expression and 25 selenoproteins in liver tissue were determined by real-time PCR,ELISA and western blot.Results:CHS significantly increased the rectal temperature,respiration rate,serum aspartate aminotransferase(AST)and low-density lipoprotein cholesterol(LDL-C)of pigs,up-regulated hepatic heat shock protein 70(HSP70)and induced lower liver weight,glycogen content,hepatic glucokinase and glutathione peroxidase(GSH-Px).The CHSinduced liver metabolic disorder was associated with the aberrant expression of 6 metabolism-related gene and 11 selenoprotein encoding genes,and decreased the protein abundance of GCK,GPX4 and SELENOS.HMSeBA improved anti-oxidative capacity of liver.0.4 or 0.6 mg Se/kg HMSeBA supplementation recovered the liver weight,glycogen content and rescue of mRNA abundance of genes related to metabolism and protein levels of GCK.HMSeBA supplementation changed expressions of 15 selenoprotein encoding genes,and enhanced protein expression of GPX1,GPX4 and SELENOS in the liver affected by CHS.CHS alone showed no impact while HMSeBA supplementation increased protein levels of p-AMPKαin the liver.Conclusions:In summary,HMSeBA supplementation beyond nutrient requirement mitigates CHS-induced hepatic metabolic disorder,recovered the liver glycogen content and the processes that are associated with the activation of AMPK signal and regulation of selenoproteins in the liver of growing pigs.
基金supported by the National Natural Science Foundation of China(No.31772643)the Special Research Funding for Discipline Construction in Sichuan Agricultural University(No.03570126)
文摘In the present study,the chronic heat stress(CHS)broiler model was developed to investigate the potential protection mechanism of organic selenium(selenomethionine,SeMet)on CHS-induced skeletal muscle growth retardation and poor meat quality.Four hundred Arbor Acres male broilers(680±70 g,21 d old)were grouped into 5 treatments with 8 replicates of 10 broilers per replicate.Broilers in the control group were raised in a thermoneutral environment(22±2°C)and fed with a basal diet.The other four treatments were exposed to hyperthermic conditions(33±2°C,24 h in each day)and fed on the basal diet supplied with SeMet at 0.0,0.2,0.4,and 0.6 mg Se/kg,respectively,for 21 d.Results showed that CHS reduced(P<0.05)the growth performance,decreased(P<0.05)the breast muscle weight and impaired the meat quality of breast muscle in broilers.CHS induced protein metabolic disorder in breast muscle,which increased(P<0.05)the expression of caspase 3,caspase 8,caspase 9 and ubiquitin proteasome system related genes,while decreased the protein expression of P-4EBP1.CHS also decreased the antioxidant capacity and induced mitochondrial stress and endoplasmic reticulum(ER)stress in breast muscle,which increased(P<0.05)the ROS levels,decreased the concentration of ATP,increased the protein expression of HSP60 and CLPX,and increased(P<0.05)the expression of ER stress biomarkers.Dietary SeMet supplementation linearly increased(P<0.05)breast muscle Se concentration and exhibited protective effects via up-regulating the expression of the selenotranscriptome and several key selenoproteins,which increased(P<0.05)body weight,improved meat quality,enhanced antioxidant capacity and mitigated mitochondrial stress and ER stress.What's more,SeMet suppressed protein degradation and improved protein biosynthesis though inhibiting the caspase and ubiquitin proteasome system and promoting the mTOR-4EBP1 pathway.In conclusion,dietary SeMet supplementation increases the expression of several key selenoproteins,alleviates mitochondrial dysfunction and ER stress,improves protein biosynthesis,suppresses protein degradation,thus increases the body weight and improves meat quality of broilers exposed to CHS.
基金National Key R&D Program of China(2016YFD0500501)the Agricultural Science and Technology Innovation Programof China(ASTIP-IAS07)the Seed Project of State Key Laboratory of Animal Nutrition of China(2004DA125184G2102)。
文摘Although high temperatures influence gut health,data on underlying mechanisms remains scant.Using a pig model,this study performed a global analysis on how chronic heat stress affects the transport and immune function of the gut through transcriptome,proteome,microbial diversity and flow cytometry.A total of 27 pigs with similar body weights were assigned into 3 groups,control(Con)group(23℃),chronic heat stressed(HS)group(33°C),and pair-fed(PF)group,in a controlled environment for 21 days.Our results showed that pigs in the HS group had reduced growth performance and diminished height of ileal villi(P<0.01).Transcriptome and proteome analyses demonstrated notable modification of expression of nutrients and ion transport-related transporters and gut mechanical barrier-related genes by chronic heart stress(P<0.05),suggesting damage of transport functions and the gut barrier.Chronic heat stress-induced endoplasmic reticulum stress also increased the synthesis of misfolded proteins,leading to upregulation of misfolded protein degradation and synthesis,as well as vesicle transport disorder(P<0.05).Energy supply processes were enhanced in the mitochondrion(P<0.05)to maintain biological processes with high energy demands.Furthermore,chronic heat stress activated complement cascade response-related genes and proteins in the gut mucosa(P<0.05).Our flow cytometry assays showed that the proportion of gut lymphocytes(CD4^(+)T cells,T cells,B cells in Peyer’s patch lymphocytes and CD4^(+)CD25^(+)T cells in intraepithelial lymphocytes)were significantly altered in the HS group pigs(P<0.05).In addition,the occurrence of gut microbial dysbiosis in the HS group pigs was characterized by increased potential pathogens(e.g.,Asteroleplasma,Shuttleworthia,Mycoplasma)and suppression of beneficial bacteria(e.g.,Coprococcus and Aeriscardovia),which are associated with gut immune function.Altogether,our data demonstrated that chronic heat stress induced gut transport and immune function disorder associated with endoplasmic reticulum stress in growing pigs.
基金This project was supported by grants from the NationalKey Technologies R&D Program of the Tenth five year plan[2001BA703B03 ( B)], the Clinical Intensive Discipline of Ministry of Public Health ([ 2001 ] 321 ) and the National Natural Sciences Foundation of China (No. 30400194).
文摘The effects of cigarette smoke extract (CSE) on the expression of heat stress protein 70 (Hsp70) in human bronchi smooth muscle cells were investigated in vitro, and the changes in Hsp70 mRNA in the patients with chronic obstructive pulmonary disease and their significance were explored. Human bronchi smooth muscle cells were cultured with CSE at the different concentrations. The expression of Hsp70 mRNA and Hsp70 was detected by reverse translation-polymerase chain reaction (RT-PCR) and Western blotting respectively. Levels of Hsp70 mRNA and Hsp70 in lymphocytes from 20 patients with COPD and 20 healthy smoking control subjects were measured by RT-PCR and Western blotting. The results showed the expression of both Hsp70 mRNA and Hsp70 was decreased conformably in human bronchi smooth muscle cells treated with CSE at certain concentration in vitro. The A values of the Hsp70 mRNA expression were 0.24±0.11 and 0.42±0.13 respectively in COPD patients and healthy smoking controls with the difference being significant (P<0.01). There was also significant difference in the A values of the Hsp70 expression between COPD patients and healthy smoking controls (20.9±9.9 vs 44.8±15.3, P<0.01). The levels of Hsp70 mRNA had strongly positive correlation with Hsp70 protein (r = 0.85, P<0 01). It was suggested that the expression of Hsp70 mRNA was in concordance with the expression of Hsp70, which could provide a basis on the study of Hsp70 gene regulation and Hsp70 gene in the development of COPD.
基金Supported by KB and Associates Representing Certification International(United Kingdom)Limited
文摘Acute pancreatitis is an inflammatory disorder of the pancreas that may cause life-threatening complications.Etiologies of pancreatitis vary,with gallstones accounting for the majority of all cases,followed by alcohol.Other causes of pancreatitis include trauma,ischemia,mechanical obstruction,infections,autoimmune,hereditary,and drugs.The main events occurring in the pancreatic acinar cell that initiate and propagate acute pancreatitis include inhibition of secretion,intracellular activation of proteases,and generation of inflammatory mediators.Small cytokines known as chemokines are released from damaged pancreatic cells and attract inflammatory cells,whose systemic action ultimately determined the severity of the disease.Indeed,severe forms of pancreatitis may result in systemic inflammatory response syndrome and multiorgan dysfunction syndrome,characterized by a progressive physiologic failure of several interdependent organ systems.Stress occurs when homeostasis is threatened,and stressors can include physical or mental forces,or combinations of both.Depending on the timing and duration,stress can result in beneficial or harmful consequences.While it is well established that a previous acute-short-term stress decreases the severity of experimentally-induced pancreatitis,the worsening effects of chronic stress on the exocrine pancreas have received relatively little attention.This review will focus on the influence of both prior acute-short-term and chronic stress in acute pancreatitis.
基金the National Natural Science Foundation of China, No. 30170326
文摘Increasing evidence suggests that heat shock factor 1 exerts endogenous protective effects on working memory under conditions of chronic psychological stress. However, the precise underlying mechanisms remain poorly understood. This study examined the protective factors affecting working memory in heat shock transcription factor 1 gene knockout mice. The results indicated that the number of correct T maze alternations decreased following mild chronic psychological stress in knockout mice. This change was accompanied by a decrease in neurogenesis and an increase in neuronal apoptosis in the hippocampal dentate gyrus. The number of correct T maze alternations was positively correlated with neurogenesis in hippocampal dentate gyrus, and negatively correlated with neuronal apoptosis. In wild type mice, no significant difference was detected in the number of correct T maze alternations or neuronal apoptosis in hippocampal dentate gyrus. These results indicate that the heat shock factor 1 gene has an endogenous protective role in working memory during mild chronic psychological stress associated with dentate gyrus neuronal apoptosis Moreover, dentate gyrus neurogenesis appears to participate in the protective mechanism.
文摘【目的】研究慢性热应激对黄羽肉鸡肝脏和肌肉的抗氧化能力与内质网应激以及腓肠肌肌纤维类型的影响.【方法】试验选用20只47日龄黄羽肉鸡,随机分为常温组和慢性热应激组,每组10只.鸡只饲养在人工气候室,试验期30 d.试验结束采集血液、肝脏和腓肠肌样品,利用试剂盒法检测血清生化指标、血清激素以及血清和肝脏抗氧化指标.利用实时荧光定量PCR法检测内质网应激(Endoplasmic reticulum stress,ERS)相关基因和腓肠肌不同肌纤维肌球蛋白重链(Myosin heavy chain,My HC)基因mRNA的表达.【结果和结论】慢性热应激显著降低肉鸡平均日增质量、血清甘油三酯(TG)、甲状腺激素(T3和T4)、胰岛素样生长因子1(Insulin-like growth factor 1,IGF-1),显著升高血清皮质酮(CORT)水平(P<0.05).同时,慢性热应激显著升高血清中丙二醛(MDA)含量,降低血清和肝脏谷胱甘肽过氧化物酶(GSH-PX)活性和肝脏总抗氧化能力(T-AOC)(P<0.05).此外,慢性热应激显著提高肉鸡肝脏和腓肠肌中热休克蛋白70(Heat shock protein 70,HSP70)基因以及腓肠肌中转录激活因子4(Activating transcription factor 4,ATF4)基因mRNA的表达(P<0.05),降低腓肠肌中葡萄糖调节蛋白78(Glucose-regulated protein 78,GRP78)基因mRNA的表达,而对肝脏中ATF4和GRP78基因mRNA的表达量无显著影响.最后,慢性热应激显著降低腓肠肌慢肌(Slow myofiber,SM)My HC基因mRNA表达量(P<0.05)而对快红肌(Fast red myofiber,FRM)和快白肌(Fast white myofiber,FWM)My HC基因mRNA表达量无影响.研究结果提示,慢性热应激可能通过降低血清生长和代谢激素、机体抗氧化能力以及引发细胞内质网应激影响肉鸡生长和腓肠肌纤维类型.