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endoplasmic reticulum stress-induced NLRP3 inflammasome activation as a novel mechanism of polystyrene microplastics (PS-MPs)-induced pulmonary inflammation in chickens

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Journal of Zhejiang University-Science B(Biomedicine & Biotechnology) 2024年第3期25卷 233-243页

作者： Hongmin LU Tiantian GUO Yue ZHANG Dewang LIU Lulu HOU Chengxue MA Mingwei XING College of Wildlife and Protected Area Northeast Forestry UniversityHarbin 150040China

Microplastics(MPs)have attracted growing attention worldwide as an increasingly prevalent environmental *** addition,chicken meat is currently the most widely consumed kind of poultry in the global *** demand for chicken is on the rise both at home and *** a result,the safety of chicken raising has also received significant *** lungs play an essential role in the physiological activities of chickens,and they are also the most vulnerable *** injury is difficult to repair after the accumulation of contaminants,and the mortality rate is high,which brings huge economic losses to *** 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 ***,this study explored the effects of exposure to polystyrene microplastics(PS-MPs)at various concentrations for 42 d on chicken ***-MPs could cause lung pathologies and ultrastructural abnormalities,such as endoplasmic reticulum(ER)swelling,inflammatory cell infiltration,chromatin agglutination,and plasma membrane ***,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 *** findings provide new scientific clues for further research o

关键词： Polystyrene microplastics endoplasmic reticulum stress Lung NLRP3 inflammasome Inflammation

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endoplasmic reticulum stress improved chicken tenderness,promoted apoptosis and autophagy during postmortem ageing

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Food Science and Human Wellness 2024年第4期13卷 2141-2151页

作者： Yuwei Chai Lin Chen Shuya Xiang Linxuan Wu Xuebo Liu Jun Luo Xianchao Feng College of Food Science and Engineering Northwest A&F UniversityYangling 712100China College of Animal Science and Technology Northwest A&F UniversityYangling 712100China

In this study,endoplasmic reticulum(ER)stress inducer tunicamycin(TM)and inhibitor 4-phenylbutyric acid(4-PBA)were used to treat postmortem chicken breast muscle to investigate changes in tenderness and effects on apoptosis and autophagy during 5 days ***-induced ER stress reduced shear force,enhanced myofibril fragmentation index(MFI),disrupted myofibril structure,increased desmin degradation,and activatedμ-calpain and *** addition,TM-induced ER stress increased the expression of Bax,Bim,and cytochrome c,and decreased the expression of Bcl-x ***,TM-induced ER stress improved the conversion of LC3I to LC3II,raised the expression of Beclin-1,and decreased the expression of p62,PI3K,and m *** opposite results were observed after 4-PBA *** results suggested that ER stress could improve chicken tenderness,promote apoptosis and autophagy during chicken postmortem ageing.

关键词： endoplasmic reticulum stress Tenderness Apoptosis Autophagy Chicken

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endoplasmic reticulum stress and autophagy in cerebral ischemia/reperfusion injury:PERK as a potential target for intervention

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Neural Regeneration Research 2025年第5期20卷 1455-1466页

作者： Ju Zheng Yixin Li Ting Zhang Yanlin Fu Peiyan Long Xiao Gao Zhengwei Wang Zhizhong Guan Xiaolan Qi Wei Hong Yan Xiao Key Laboratory of Endemic and Ethnic Diseases Ministry of Education&Key Laboratory of Medical Molecular Biology of Guizhou ProvinceGuizhou Medical UniversityGuiyangGuizhou ProvinceChina Guizhou Center for Disease Control and Prevention GuiyangGuizhou ProvinceChina Department of Histology and Embryology Guizhou Medical UniversityGuiyangGuizhou ProvinceChina Collaborative Innovation Center for Prevention and Control of Endemic and Ethnic Regional Diseases Co-constructed by the Province and Ministry GuiyangGuizhou ProvinceChina

Several studies have shown that activation of unfolded protein response and endoplasmic reticulum(ER)stress plays a crucial role in severe cerebral ischemia/reperfusion *** occurs within hours after cerebral ischemia,but the relationship between ER stress and autophagy remains *** this study,we established experimental models using oxygen-glucose deprivation/reoxygenation in PC12 cells and primary neurons to simulate cerebral ischemia/reperfusion *** found that prolongation of oxygen-glucose deprivation activated the ER stress pathway protein kinase-like endoplasmic reticulum kinase(PERK)/eukaryotic translation initiation factor 2 subunit alpha(e IF2α)-activating transcription factor 4(ATF4)-C/EBP homologous protein(CHOP),increased neuronal apoptosis,and induced ***,inhibition of ER stress using inhibitors or by si RNA knockdown of the PERK gene significantly attenuated excessive autophagy and neuronal apoptosis,indicating an interaction between autophagy and ER stress and suggesting PERK as an essential target for regulating *** autophagy with chloroquine exacerbated ER stress-induced apoptosis,indicating that normal levels of autophagy play a protective role in neuronal injury following cerebral ischemia/reperfusion *** from this study indicate that cerebral ischemia/reperfusion injury can trigger neuronal ER stress and promote autophagy,and suggest that PERK is a possible target for inhibiting excessive autophagy in cerebral ischemia/reperfusion injury.

关键词： apoptosis ATF4 autophagy C/EBP homologous protein cerebral ischemia/reperfusion injury eIF2α endoplasmic reticulum stress PERK

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Molybdenum and cadmium co-induce necroptosis through Th1/Th2 imbalance-mediated endoplasmic reticulum stress in duck ovaries

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Journal of Environmental Sciences 2024年第8期142卷 92-102页

作者： Ting Cui Xueyan Dai Huiling Guo Dianyun Wang Bingyan Huang Wenjing Pu Xuesheng Chu Caiying Zhang Jiangxi Provincial Key Laboratory for Animal Health Institute of Animal Population HealthCollege of Animal Science and TechnologyJiangxi Agricultural UniversityNanchang 330045China

Cadmium(Cd)and excess molybdenum(Mo)pose serious threats to animal *** previous study has determined that Cd and/or Mo exposure can cause ovarian damage of ducks,while the specific mechanism is still *** further investigate the toxic mechanism of Cd and Mo co-exposure in the ovary,forty 8-day-old female ducks were randomly allocated into four groups for 16 weeks,and the doses of Cd and Mo in basic diet per kg were as follows:control group,Mo group(100 mg Mo),Cd group(4 mg Cd),and Mo+Cd group(100 mg Mo+4 mg Cd).Cadmium sulfate 8/3-hydrate(CdSO_(4)·8/3H_(2)O)and hexaammonium molybdate((NH_(4))_(6)Mo_(7)O_(24)·4H_(2)O)were the origins of Cd and Mo,*** the 16th week of the experiment,all ovary tissues were collected for the detection of related *** data indicated that Mo and/or Cd induced trace element disorders and Th1/Th2 balance to divert toward Th1 in the ovary,which activated endoplasmic reticulum(ER)stress and then provoked necroptosis through triggering RIPK1/RIPK3/MLKL signaling pathway,and eventually caused ovarian pathological injuries and necroptosis *** alterations of above indicators were most apparent in the joint *** all,this research illustrates that Mo and/or Cd exposure can initiate necroptosis through Th1/Th2 imbalance-modulated ER stress in duck ovaries,and Mo and Cd combined exposure aggravates ovarian *** research explores the molecular mechanism of necroptosis caused by Mo and/or Cd,which reveals that ER stress attenuation may be a therapeutic target to alleviate necroptosis.

关键词： Molybdenum Cadmium Th1/Th2 imbalance endoplasmic reticulum stress Necroptosis Ovary

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Dietary sodium acetate and sodium butyrate attenuate intestinal damage and improve lipid metabolism in juvenile largemouth bass(Micropterus salmoides) fed a high carbohydrate diet by reducing endoplasmic reticulum stress

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Animal Nutrition 2024年第1期16卷 443-456页

作者： Liulan Zhao Liangshun Cheng Yifang Hu Xiaohui Li Yihui Yang Jin Mu Lianfeng Shen Guojun Hu Kuo He Haoxiao Yan Qiao Liu Song Yang College of Animal Science and Technology Sichuan Agricultural University

High-carbohydrate(HC) diets decrease the intestinal levels of sodium acetate(SA) and sodium butyrate(SB) and impair the gut health of largemouth bass; however, SA and SB have been shown to enhance immunity and improve intestinal health in farmed animals. Thus, the present study was to investigate the effects of dietary SA and SB on HC diet-induced intestinal injury and the potential mechanisms in juvenile largemouth bass. The experiment set five isonitrogenous and isolipidic diets, including a lowcarbohydrate diet(9% starch)(LC), a high carbohydrate diet(18% starch)(HC), and the HC diet supplemented with 2 g/kg SA(HCSA), 2 g/kg SB(HCSB) or a combination of 1 g/kg SA and 1 g/kg SB(HCSASB).The feeding experiment was conducted for 8 weeks. A total of 525 juvenile largemouth bass with an initial body weight of 7.00 ± 0.20 g were used. The results showed that dietary SA and SB improved the weight gain rate and specific growth rate (Pendoplasmic reticulum stress(P<0.05). Further results revealed that dietary SA and SB reduced HC-induced intestinal fat deposition by inhibiting adipogenesis and promoting lipolysis(P<0.05). In summary, this study demonstrated that dietary SA and SB attenuated HC-induced intestinal damage and reduced excessive intestinal fat deposition in largemouth bass.

关键词： Sodium acetate Sodium butyrate High carbohydrate diet endoplasmic reticulum stress Intestine health Lipid metabolism

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Treatment with β-sitosterol ameliorates the effects of cerebral ischemia/reperfusion injury by suppressing cholesterol overload, endoplasmic reticulum stress, and apoptosis

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Neural Regeneration Research 2024年第3期19卷 642-649页

作者： Xiuling Tang Tao Yan Saiying Wang Qingqing Liu Qi Yang Yongqiang Zhang Yujiao Li Yumei Wu Shuibing Liu Yulong Ma Le Yang Precision Pharmacy&Drug Development Center Department of PharmacyTangdu HospitalAir Force Medical UniversityXi’anShaanxi ProvinceChina Department of Clinical Pharmacy Jinling HospitalMedical School of Nanjing UniversityNanjingJiangsu ProvinceChina Department of Pharmacology School of PharmacyAir Force Medical UniversityXi’anShaanxi ProvinceChina Department of Anesthesiology The First Medical Center of Chinese PLA General HospitalBeijingChina Department of Anatomy Histology and Embryology and K.K.Leung Brain Research CentreAir Force Medical UniversityXi’anShaanxi ProvinceChina

β-Sitosterol is a type of phytosterol that occurs naturally in *** studies have shown that it has anti-oxidant,anti-hyperlipidemic,anti-inflammatory,immunomodulatory,and anti-tumor effects,but it is unknown whetherβ-sitosterol treatment reduces the effects of ischemic *** we found that,in a mouse model of ischemic stroke induced by middle cerebral artery occlusion,β-sitosterol reduced the volume of cerebral infarction and brain edema,reduced neuronal apoptosis in brain tissue,and alleviated neurological dysfunction;moreover,β-sitosterol increased the activity of oxygen-and glucose-deprived cerebral cortex neurons and reduced *** investigation showed that the neuroprotective effects ofβ-sitosterol may be related to inhibition of endoplasmic reticulum stress caused by intracellular cholesterol accumulation after ischemic *** addition,β-sitosterol showed high affinity for NPC1L1,a key transporter of cholesterol,and antagonized its *** conclusion,β-sitosterol may help treat ischemic stroke by inhibiting neuronal intracellular cholesterol overload/endoplasmic reticulum stress/apoptosis signaling pathways.

关键词： apoptosis blood-brain barrier β-sitosterol cerebral ischemia/reperfusion injury cholesterol overload cholesterol transport endoplasmic reticulum stress ischemic stroke molecular docking NPC1L1

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Asperuloside Promotes Apoptosis of Cervical Cancer Cells through endoplasmic reticulum stress-Mitochondrial Pathway

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Chinese Journal of Integrative Medicine 2024年第1期30卷 34-41页

作者： QI Zhi-min WANG Xia LIU Xia ZHAO Juan Medical Examination Center Hebei Province Hospital of Chinese MedicineShijiazhuang(050011)China Department of Gynaecology and Obstetrics Hebei Province Hospital of Chinese MedicineShijiazhuang(050011)China Experimental Center for Teaching Hebei Medical UniversityShijiazhuang(050017)China

Objective: To investigate the effects of asperuloside on cervical cancer based on endoplasmic reticulum(ER) stress and mitochondrial pathway. Methods: Different doses(12.5–800 μg/mL) of asperuloside were used to treat cervical cancer cell lines Hela and CaSki to calculate the half maximal inhibitory concentration(IC_(50)) of asperuloside. The cell proliferation was analyzed by clone formation assay. Cell apoptosis, intracellular reactive oxygen species(ROS) and mitochondrial membrane potential were determined by flow cytometry. The protein expressions of cleaved-caspase-3, Bcl-2, Bax, Cyt-c, cleaved-caspase-4 and glucose-regulated protein 78(GRP78) were analyzed by Western blot. And the inhibitor of ER stress, 4-phenyl butyric acid(4-PBA) was used to treat cervical cancer cells to further verify the role of ER stress in the apoptosis of cervical cancer cells induced by asperuloside. Results: Asperuloside of 325, 650, and 1300 μg/mL significantly inhibited the proliferation and promoted apoptosis of Hela and CaSki cells(Pstress-mitochondrial pathway.

关键词： asperuloside Chinese medicine cervical cancer endoplasmic reticulum stress mitochondrial damage apoptosis

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XBP1 splicing contributes to endoplasmic reticulum stress-induced human islet amyloid polypeptide up-regulation

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Genes & Diseases 2024年第5期11卷 350-359页

作者： Yun Zhang Susan Lin Jing Yao Wantong Cai Huaqiu Chen Ailikemu Aierken Zhe Wang Weihong Song National Clinical Research Center for Geriatric Disorders Xuanwu HospitalCapital Medical UniversityBeijing 100053China Townsend Family Laboratories Department of PsychiatryThe University of British Columbia2255 Wesbrook MallVancouverBC V6T 1Z3Canada Institute of Aging Key Laboratory of Alzheimer’s Disease of Zhejiang ProvinceSchool of Mental Health and the Affiliated Kangning HospitalWenzhou Medical UniversityWenzhouZhejiang 325000China Oujiang Laboratory(Zhejiang Lab for Regenerative Medicine Vision and Brain Health)WenzhouZhejiang 325001China

As a pathological hallmark of type 2 diabetes mellitus(T2DM),islet amyloid is formed by the aggregation of islet amyloid polypeptide(IAPP).endoplasmic reticulum(ER)stress interacts with IAPP aggregates and has been implicated in the pathogenesis of *** examine the role of ER stress in T2DM,we cloned the hIAPP promoter and analyzed its promoter activity in human *** found that ER stress significantly enhanced hIAPP promoter activity and expression in human b-cells via triggering X-box binding protein 1(XBP1)*** identified a binding site of XBP1 in the hIAPP *** of this binding site by substitution or deletion mutagenesis significantly diminished the effects of ER stress on hIAPP promoter *** of XBP splicing by MKC3946 treatment inhibited ER stress-induced hIAPP up-regulation and improved human b-cell survival and *** study uncovers a link between ER stress and IAPP at the transcriptional level and may provide novel insights into the role of ER stress in IAPP cytotoxicity and the pathogenesis of T2DM.

关键词： b-cell function endoplasmic reticulum stress Islet amyloid polypeptide Type 2 diabetes mellitus XBP1

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Selenomethionine alleviates chronic heat stress-induced breast muscle injury and poor meat quality in broilers via relieving mitochondrial dysfunction and endoplasmic reticulum stress

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Animal Nutrition 2024年第1期16卷 363-375页

作者： Jinzhong Jing Jiayi Wang Xiaoyu Xiang Shenggang Yin Jiayong Tang Longqiong Wang Gang Jia Guangmang Liu Xiaoling Chen Gang Tian Jingyi Cai Bo Kang Lianqiang Che Hua Zhao Key Laboratory for Animal Disease-Resistance Nutrition of Ministry of Education of China Ministry of Agriculture and Rural Affairsof Sichuan ProvinceAnimal Nutrition InstituteSichuan Agricultural University College of Animal Science and Technology Sichuan Agricultural University

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 *** hundred Arbor Acres male broilers （680±70 g,21 d old） were grouped into 5 treatments with 8 replicates of 10 broilers per *** in the control group were raised in a thermoneutral environment （22±2°C） and fed with a basal *** 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 *** showed that CHS reduced （Pstress and endoplasmic reticulum （ER） stress in breast muscle,which increased （Pstress *** SeMet supplementation linearly increased （Pstress and ER ***'s more,SeMet suppressed protein degradation and improved protein biosynthesis though inhibiting the caspase and ubiquitin proteasome system and promoting the mTOR-4EBP1 *** conclusion,dietary SeMet supplementation increases the expression of

关键词： Broiler Chronic heat stress Skeletal muscle Meat quality Mitochondrial dysfunction endoplasmic reticulum stress

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Mechanisms underlying the role of endoplasmic reticulum stress in the placental injury and fetal growth restriction in an ovine gestation model

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Journal of Animal Science and Biotechnology 2024年第1期15卷 201-217页

作者： Hao Zhang Xia Zha Yi Zheng Xiaoyun Liu Mabrouk Elsabagh Hongrong Wang Honghua Jiang Mengzhi Wang Laboratory of Metabolic Manipulation of Herbivorous Animal Nutrition College of Animal Science and TechnologyYangzhou UniversityYangzhou 225009P.R.China Joint International Research Laboratory of Agriculture and Agri‑Product Safety Ministry of Education of ChinaYangzhou UniversityYangzhou 225009P.R.China Department of Animal Production and Technology Faculty of Agricultural Sciences and TechnologiesNiğde Omer Halisdemir UniversityNigde 51240Turkey Department of Nutrition and Clinical Nutrition Faculty of Veterinary MedicineKafrelsheikh UniversityKafrelSheikhEgypt Department of Pediatrics Northern Jiangsu People’s HospitalClinical Medical CollegeYangzhou UniversityYangzhou 225001China State Key Laboratory of Sheep Genetic Improvement and Healthy Production Xinjiang Academy of Agricultural Reclamation ScienceShihezi 832000China

Background Exposure to bisphenol A(BPA),an environmental pollutant known for its endocrine-disrupting properties,during gestation has been reported to increase the risk of fetal growth restriction(FGR)in an ovine model of *** hypothesized that the FGR results from the BPA-induced insufficiency and barrier dysfunction of the placenta,oxidative stress,inflammatory responses,autophagy and endoplasmic reticulum stress(ERS).However,precise mechanisms underlying the BPA-induced placental dysfunction,and subsequently,FGR,as well as the potential involvement of placental ERS in these complications,remain to be *** In vivo experiment,16 twin-pregnant(from d 40 to 130 of gestation)Hu ewes were randomly distributed into two groups(8 ewes each).One group served as a control and received corn oil once a day,whereas the other group received BPA(5 mg/kg/d as a subcutaneous injection).In vitro study,ovine trophoblast cells(OTCs)were exposed to 4 treatments,6 replicates *** OTCs were treated with 400μmol/L BPA,400μmol/L BPA+0.5μg/m L tunicamycin(Tm;ERS activator),400μmol/L BPA+1μmol/L 4-phenyl butyric acid(4-PBA;ERS antagonist)and DMEM/F12 complete medium(control),for 24 *** In vivo experiments,pregnant Hu ewes receiving the BPA from 40 to 130 days of pregnancy experienced a decrease in placental efficiency,progesterone(P4)level and fetal weight,and an increase in placental estrogen(E2)level,together with barrier dysfunctions,OS,inflammatory responses,autophagy and ERS in type A *** vitro experiment,the OTCs exposed to BPA for 24 h showed an increase in the E2 level and related protein and gene expressions of autophagy,ERS,pro-apoptosis and inflammatory response,and a decrease in the P4 level and the related protein and gene expressions of antioxidant,anti-apoptosis and barrier ***,treating the OTCs with Tm aggravated BPA-induced dysfunction of barrier and endocrine(the increased E2 level and decreased P4 level),OS,inflamm

关键词： Autophagy Bisphenol A endoplasmic reticulum stress Fetal growth restriction Inflammatory responses Sheep

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