脂多糖和玉米赤霉烯酮介導的內(nèi)質網(wǎng)應激對山羊子宮內(nèi)膜基質細胞的作用
發(fā)布時間:2024-12-26 04:23
繁殖障礙,特別是懷孕早期胚胎丟失會造成嚴重的經(jīng)濟損失。導致早期胚胎丟失的原因很多,如環(huán)境中的細菌感染和玉米赤霉烯酮污染。脂多糖(LPS)是革蘭式陰性菌的主要毒力因子,是由脂質和由O-抗原組成的多糖組成的大分子,外核和內(nèi)核通過共價鍵連接。有證據(jù)表明LPS導致家畜流產(chǎn)。玉米赤霉烯酮(ZEA)是由一些鐮刀菌屬和赤霉屬物種產(chǎn)生的一種的雌激素類似物,具有熱穩(wěn)定性,并且在世界范圍內(nèi)的許多谷類作物中發(fā)現(xiàn)了赤霉烯酮,例如玉米,大麥,燕麥,小麥,水稻和高粱。玉米赤霉烯酮已經(jīng)被證明是主要的毒素,會導致不育、流產(chǎn)或其他繁殖問題。進一步揭示和分析LPS和ZEA對子宮內(nèi)膜細胞作用的機制具有重要意義。據(jù)報道,有幾個因素在胚胎著床階段起著關鍵作用,包括激素、血管活性基因、細胞因子、生長因子和環(huán)境因素。然而,在胚胎植入過程中,胚胎植入前的發(fā)育和胚胎-子宮相互作用的分子途徑仍不清楚。在本研究中,我們關注植入階段并研究脂質多糖和玉米赤霉烯酮感染的山羊子宮內(nèi)膜基質細胞(GESCs)的病理生理變化。LPS和/或ZEA用作影響細胞氧化應激的模型。1.內(nèi)質網(wǎng)應激參與脂多糖誘導的山羊子宮內(nèi)膜基質細胞的炎癥反應和細胞凋亡內(nèi)質網(wǎng)應激(E...
【文章頁數(shù)】:64 頁
【學位級別】:博士
【文章目錄】:
ABSTRACT
摘要
Review and Literature
Chapter Ⅰ:The ER stress and Effects of Lipopolysaccharide and Zearalenone
1.Endoplasmic reticulum stress
2.Pre-implantation embryos development
3.Lipopolysaccharide and/or Zearalenone induced cell apoptosis
4.Lipopolysaccharide and/or Zearalenone induced cell proliferation
5.Lipopolysaccharide and/or Zearalenone induced autophagy
6.Lipopolysaccharide and/or Zearalenone induced activation of ER stress
7.Lipopolysaccharide and/or Zearalenone induced inflammatory cytokines
8.Some ways to blocked endoplasmic reticulum stress
Experimental research
Chapter Ⅱ:Endoplasmic Reticulum Stress is Involved in Lipopolysaccharide Induced Inflammatory Response and Apoptosis in Goat Endometrial Stromal Cells
1.MATERIALS AND METHODS
1.1 Cell culture and drug treatment
1.2 Cell viability
1.3 Apoptosis analysis
1.4 Total RNA extraction and real-time quantitative PCR
1.5 ELISA
1.6 Western blot analysis
1.7 Knock down ATF6 and IRE1 genes with small interfering RNA
1.8 Statistical analysis
2.RESULTS
2.1 Functional role of LPS on ESC cell proliferation
2.2 Effect of LPS on ESC apoptosis and PCNA,MKI67 expression
2.3 LPS activated Endoplasmic reticulum stress
2.4 LPS affected on expression of autophagy and mitochondria-related genes
2.5 LPS increased inflammatory cytokines secretion
2.6 4-phenylbutyrate inhibited the expression of ER stress protein,autophagy and pro-inflammatory cytokines under LPS treatment
2.7 Effect of ATF6 and IRE1 on promoting autophagy
DISCUSSION
Chapter Ⅲ:Endoplasmic Reticulum Stress is Involved in Mycotoxin Zearalenone Induced Inflammatory Response,Proliferation,and Apoptosis in Goat Endometrial Stromal Cells
1.Materials and methods
1.1 Chemicals
1.2 Cell culture and treatments
1.3 Cell proliferation
1.4 Cell apoptosis assay
1.5 ELISA
1.6 Western blot
1.7 Knockdown ERN1 gene by small interfering RNA
1.8 Statistical analysis
2.Results
2.1 Dynamic role of ZEA on ESC proliferation and apoptosis assay
2.2 Endoplasmic reticulum stress-activated by ZEA on Goat endometrial stromal cells
2.3 Autophagy and inflammatory cytokine affected with ZEA on ESCs
2.4 knockdown IRE1 and affected on promoting autophagy and inflammation
DISCUSSION
Conclusion
General Conclusion
REFERENCES
Acknowledgements
作者簡介
本文編號:4020526
【文章頁數(shù)】:64 頁
【學位級別】:博士
【文章目錄】:
ABSTRACT
摘要
Review and Literature
Chapter Ⅰ:The ER stress and Effects of Lipopolysaccharide and Zearalenone
1.Endoplasmic reticulum stress
2.Pre-implantation embryos development
3.Lipopolysaccharide and/or Zearalenone induced cell apoptosis
4.Lipopolysaccharide and/or Zearalenone induced cell proliferation
5.Lipopolysaccharide and/or Zearalenone induced autophagy
6.Lipopolysaccharide and/or Zearalenone induced activation of ER stress
7.Lipopolysaccharide and/or Zearalenone induced inflammatory cytokines
8.Some ways to blocked endoplasmic reticulum stress
Experimental research
Chapter Ⅱ:Endoplasmic Reticulum Stress is Involved in Lipopolysaccharide Induced Inflammatory Response and Apoptosis in Goat Endometrial Stromal Cells
1.MATERIALS AND METHODS
1.1 Cell culture and drug treatment
1.2 Cell viability
1.3 Apoptosis analysis
1.4 Total RNA extraction and real-time quantitative PCR
1.5 ELISA
1.6 Western blot analysis
1.7 Knock down ATF6 and IRE1 genes with small interfering RNA
1.8 Statistical analysis
2.RESULTS
2.1 Functional role of LPS on ESC cell proliferation
2.2 Effect of LPS on ESC apoptosis and PCNA,MKI67 expression
2.3 LPS activated Endoplasmic reticulum stress
2.4 LPS affected on expression of autophagy and mitochondria-related genes
2.5 LPS increased inflammatory cytokines secretion
2.6 4-phenylbutyrate inhibited the expression of ER stress protein,autophagy and pro-inflammatory cytokines under LPS treatment
2.7 Effect of ATF6 and IRE1 on promoting autophagy
DISCUSSION
Chapter Ⅲ:Endoplasmic Reticulum Stress is Involved in Mycotoxin Zearalenone Induced Inflammatory Response,Proliferation,and Apoptosis in Goat Endometrial Stromal Cells
1.Materials and methods
1.1 Chemicals
1.2 Cell culture and treatments
1.3 Cell proliferation
1.4 Cell apoptosis assay
1.5 ELISA
1.6 Western blot
1.7 Knockdown ERN1 gene by small interfering RNA
1.8 Statistical analysis
2.Results
2.1 Dynamic role of ZEA on ESC proliferation and apoptosis assay
2.2 Endoplasmic reticulum stress-activated by ZEA on Goat endometrial stromal cells
2.3 Autophagy and inflammatory cytokine affected with ZEA on ESCs
2.4 knockdown IRE1 and affected on promoting autophagy and inflammation
DISCUSSION
Conclusion
General Conclusion
REFERENCES
Acknowledgements
作者簡介
本文編號:4020526
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