綠茶表沒食子兒茶素沒食子酸酯調節 HIB1B 棕色前脂肪細胞的自噬途徑

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尤思雅(Deagisti Prima Yoriska) 查詢紙本館藏

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綠茶表沒食子兒茶素沒食子酸酯調節 HIB1B 棕色前脂肪細胞的自噬途徑
(Green Tea Epigallocatechin-3-Gallate Regulates the Autophagy Pathway in HIB1B Brown Preadipocytes)

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至系統瀏覽論文 (2028-1-30以後開放)

摘要(中)

中文摘要

自噬作用是細胞中蛋白質聚集體、多餘脂肪和受損線粒體的回收過程。它可以保護細胞免受壓力條件（如飢餓和氧化應激）的影響，並且通過營養物質進行調節。EGCG是綠茶兒茶素的主要成分之一，已知其可作為肥胖和癌細胞自噬的調節劑，但關於EGCG 對脂肪細胞自噬的影響知之甚少。從我們的研究中，發現 EGCG 在所有血清條件（0%、2% 和 10% FBS）中處理 12、24、36 和 48 小時後會抑制 HIB1B 棕色前脂肪細胞的細胞生長，並且發現與正常血清條件（10% FBS）下相比，較長的治療時間和較低的血清條件（0% 和 2% FBS）中抑制細胞數量甚至更多。處理 12 小時後，我們觀察到 EGCG 在無血清和低血清條件（0% 和 2% FBS）下抑制自噬的啟動以及自噬體的降解，但在正常血清條件下（10% FBS）則不同。特別是，EGCG 在0% FBS 中調節了 Atg3、Atg5、Atg7、Atg13、Atg16L1、LC3B-II/LC3B-I、pp62/p62、pAMPK、AMPK、pAKT 和AKT蛋白的水平。而在 2% FBS 中調節了 Atg7、Atg16L1、LC3B-II/LC3B-I、pp62/p62、pAMPK、pAKT 和AKT 的水平。在 10% FBS 中，發現 EGCG 會調節 Atg3、Atg7、LC3B-II/LC3B-I 和 pp62/p62。基於斑點形成測定，觀察到 EGCG 在 0% FBS 中降低自噬形成能力，導致細胞在早期自噬抑制，但在 2% 和 10% FBS 中則不同。綜上所述，發現EGCG在無血清的條件下通過AMPK和自噬體降解（自噬的後期）抑制自噬的起始（自噬的早期）。此外血清的增加似乎降低了EGCG對自噬的影響。最後，這些發現表明EGCG對HIB1B棕色前脂肪細胞自噬過程的影響取決於血清的比例。

摘要(英)

Abstract

Autophagy is a recycling process for protein aggregates, excess fat, and damaged mitochondria in cells. It protects the cells from stressful conditions (such as starvation and oxidative stress) and can be regulated by nutrients. EGCG, the major component of green tea catechins, has been known to act as a regulator of autophagy of cancer cells. But little information is known about the effect of EGCG on autophagy of fat cells. From our study, EGCG was found to suppress the cell growth in HIB1B brown preadipocytes after 12, 24, 36, and 48 hours of treatment in 0%, 2%, and 10% FBS, and was found to be dependent on the duration of treatment, the dose of EGCG, and the proportion of serum. Upon 12 hours of treatment, EGCG was observed to inhibit the initiation of autophagy as well as the degradation of autophagosomes in no to less serum conditions (0% and 2% FBS), but not in normal serum condition (10% FBS). In particular, EGCG altered the level of Atg3, Atg5, Atg7, Atg13, Atg16L1, LC3B-II/LC3B-I, pp62/p62, pAMPK, AMPK, pAKT, and AKT proteins in 0% FBS. And it altered the level of Atg7, Atg16L1, LC3B-II/LC3B-I, pp62/p62, pAMPK, pAKT, and AKT in 2% FBS. In 10% FBS, EGCG was found to alter Atg3, Atg7, LC3B-II/LC3B-I, and pp62/p62. Based on the puncta formation assay, EGCG was observed to decrease autophagy flux in 0% FBS, causing the cell to undergo an early phase autophagy suppression, but not in 2% and 10% FBS. Taken together, EGCG was found to inhibit the autophagy initiation (early phase of autophagy) through AMPK and autophagosome degradation (late phase of autophagy) in no serum condition (0% FBS). The increase presence of the serum seemed to decrease the effect of EGCG on autophagy. These findings suggest that the effect of EGCG on the autophagy process of HIB1B brown preadipocytes is dependent on the proportion of serum.

Keywords: Autophagy, EGCG, brown preadipocytes

關鍵字(中)

★ 自噬
★ EGCG
★ 棕色前脂肪細胞

關鍵字(英)

★ Autophagy
★ EGCG
★ brown preadipocytes

論文目次

Table of Contents

Abstract i
中文提要 ii
Acknowledgement iii
Table of Contents iv
List of Tables vi
List of Figures vii
Abbreviation viii
CHAPTER 1 INTRODUCTION 1
1.1 Obesity 1
1.2 Green tea catechins 1
1.3 Types of adipocytes 3
1.4 Autophagy 4
1.4.1 History and function 4
1.4.2 Mechanism 4
1.5 EGCG, adipocytes, and autophagy 5
1.6 Research motives and purposes 6
CHAPTER 2 MATERIALS AND METHODS 8
2.1 Experimental materials 8
2.2 Cell culture 8
2.3 Trypan blue exclusion method 8
2.4 Western blot (Immunoblot)analysis 8
2.4.1 Gel production 9
2.4.2 Sample preparation 9
2.4.3 Gel electrophoresis 9
2.4.4 Transfer proteins 9
2.4.5 Blocking and antibody identification 9
2.4.6 Stripping 10
2.4.7 quantifying protein band 10
2.5 Puncta formation assay 10
2.6 Statistical analysis 11

CHAPTER 3 RESULTS 12
3.1 EGCG and autophagy inhibitors suppressed cell growth in HIB1B brown
preadipocytes 12
3.2 EGCG regulates autophagy markers and autophagy-related protein expressions
in HIB1B brown preadipocytes 13
3.3 Treatment of CQalone and combined treatment of EGCG and CQ altered
autophagy markers and autophagy-related protein expressions in HIB1B
brown preadipocytes 14
3.4 Treatment of 3-MAalone and combined treatment of EGCG and 3-MA
altered autophagy markers and autophagy-relatedprotein expressions in
HIB1B brown preadipocytes 15
3.5 The presence of serum affected EGCG effects on autophagy flux in HIB1B
brown preadipocytes 16
CHAPTER 4 DISCUSSION 18
CHAPTER 5 CONCLUSIONS 24
REFERENCES 26

參考文獻

REFERENCES

1. WHO. Obesity and Overweight. 2018, February 16 [cited 2019 December 10]; Available from: https://www.who.int/news-room/fact-sheets/detail/obesity-and-overweight.
2. Yeomans, M.R., Adverse Effects of Consuming High Fat–Sugar Diets on Cognition: Implications for Understanding Obesity. Proceedings of the Nutrition Society 76, 2017: p. 455–465.
3. Dinh, T.C., et al., The Effects of Green Tea on Lipid Metabolism and Its Potential Applications for Obesity and Related Metabolic Disorders - An Existing Update. Diabetes & Metabolic Syndrome: Clinical Research & Reviews 13, 2019: p. 1667-1673.
4. Saris, W.H.M., S. N. Blair, M. A. Van Baak, S. B. Eaton, P. S. W. Davies, L. Di Pietro, M. Fogelholm, A. Rissanen D., Schoeller, B. Swinburn, A. Tremblay, K. R. Westerterp, H. Wyatt, How much physical activity is enough to prevent unhealthy weight gain? Outcome of the IASO 1st Stock Conference and consensus statement. Obesity Reviews, 2003. 4(2): p. 101-114.
5. Trigueros, L., S. Peña , A. V. Ugidos , E. Sayas-Barberá , J. A. Pérez-Álvarez, and E. Sendra, Food Ingredients as Anti-Obesity Agents: A Review. Critical Reviews in Food Science and Nutrition, 2013. 53(9): p. 929-942.
6. Son, J.W.a.S.K., Comprehensive Review of Current and Upcoming Anti-Obesity Drugs. Diabetes & Metabolism Journal, 2020. 44: p. 802-818.
7. Müller, T.D., Matthias Blüher, Matthias H. Tschöp, and Richard D. DiMarchi, Anti-obesity drug discovery: advances and challenges. Nature Reviews, 2022. 21: p. 201-223.
8. Chacko, S.M., et al., Beneficial Effects of Green Tea: A Literature Review. Chinese Medicine Vol. 5, No. 13, 2010: p. 1-9.
9. Rusak, G., Drazenka Komes, Saša Likic, Dunja Horzic, Maja Kovac, Phenolic content and antioxidative capacity of green and white tea extracts depending on extraction conditions and the solvent used. Food Chem, 2008. 110: p. 852– 858.
10. Legeay, S., Marion Rodier, Laetitia Fillon, Sébastien Faure, and Nicolas Clere, Epigallocatechin Gallate: A Review of Its Beneficial Properties to Prevent Metabolic Syndrome. Nutrients, 2015. 7: p. 5443-5468.
11. Yang Chung S., H.W., Cancer Preventive Activities of Tea Catechins. Molecules, 2016. 21(12): p. 1-19.
12. Murray, M., Chelsey Walchuk, Miyoung Suh and Peter J. Jones, Green tea catechins and cardiovascular disease risk factors: Should a health claim be made by the United States Food and Drug Administration? Trends in Food Science & Technology, 2015. 41: p. 188-197.
13. Pastoriza, S., M. Mesías, C. Cabrera, and J. A. Rufián-Henares, Healthy properties of green and white teas: an update. Food & Function, 2017. 8: p. 2650-2662
14. Bimonte, S., Vittorio Albino, Mauro Piccirillo, Aurelio Nasto, Carlo Molino, Raffaele Palaia, and Marco Cascella, Epigallocatechin-3-gallate in the prevention and treatment of hepatocellular carcinoma: experimental findings and translational perspectives. Drug Design, Development and Therapy, 2019. 13: p. 611-621.
15. Nedergaard, J., Tore Bengtsson, and Cannon Barbara, Unexpected evidence for active brown adipose tissue in adult humans. Am. J. Physiol. Endocrinol Metab., 2007. 293(2): p. E444–E452.
16. Zingaretti, M.C., Francesca Crosta,Alessandra Vitali, Mario Guerrieri, Andrea Frontini, Barbara Cannon, Jan Nedergaard, and Saverio Cinti, The presence of UCP1 demonstrates that metabolically active adipose tissue in the neck of adult humans truly represents brown adipose tissue. FASEB J., 2009. 23(9): p. 3113-3120.
17. Cypess, A.M., Sanaz Lehman, Gethin Williams, Ilan Tal, Dean Rodman, Allison B Goldfine, Frank C. Kuo, Edwin L. Palmer, Yu-Hua Tseng, Alessandro Doria, Gerald M. Kolodny, and C. Ronald Kahn, Identification and importance of brown adipose tissue in adult humans. N. Engl. J. Med., 2009. 360(15): p. 1509-1517.
18. Loncar, D., B. A. Afzelius, and B. Cannon, Epididymal white adipose tissue after cold stress in rats. I. Nonmitochondrial changes. J. Ultrastruct Mol. Struct. Res., 1988. 101(2-3): p. 109-122.
19. Mika, A., Filippo Macaluso, Rosario Barone, Valentina Di Felice, and Tomasz Sledzinski Effect of Exercise on Fatty Acid Metabolism and Adipokine Secretion in Adipose Tissue. Front Physiol., 2019. 10(26): p. 1-7.
20. Wang, S., Min-Hsiung Pan, Wei-Lun Hung, Yen-Chen Tung, and Chi-Tang Ho, From white to beige adipocytes: therapeutic potential of dietary molecules against obesity and their molecular mechanisms. Food Funct., 2019. 10(3): p. 1263-1279.
21. Kaisanlahti, A., and T. Glumoff, Browning of white fat: agents and implications for beige adipose tissue to type 2 diabetes. J. Physiol. Biochem., 2019. 75(1): p. 1-10.
22. Ikeda, K., Pema Maretich, and Shingo Kajimura, The common and distinct features of brown and beige adipocytes. Trends Endocrinol Metab., 2018. 29(3): p. 191-200.
23. Giordano, A., Arianna Smorlesi, Andrea Frontini, Giorgio Barbatelli, and Saverio Cinti, White, brown and pink adipocytes: the extraordinary plasticity of the adipose organ. Eur. J. Endocrinol., 2014. 170(5): p. R159-171.
24. Cinti, S., Pink Adipocytes. Trends Endocrinol Metab., 2018. 29(9): p. 651-666.
25. Yang, Z., and Daniel J. Klionsky, Mammalian autophagy: core molecular machinery and signaling regulation. Curr Opin Cell Biol. 2010, 2010. 22(2): p. 124–131.
26. Choi, A.M.K., Stefan W. Ryter, and Beth Levine, Autophagy in Human Health and Disease. The New England Journal of Medicine, 2013. 368(7): p. 651-662.
27. Mizushima, N., Tamotsu Yoshimori, and Beth Levine, Methods in Mammalian Autophagy Research. Cell, 2010. 140: p. 313-326.
28. Klionsky, D.J.a.P.C., The Mechanism and Physiological Function of Macroautophagy. Journal of Innate Immunity, 2013. 5: p. 427-433.
29. Abounit, K., Tiziano M Scarabelli, and Roy B McCauley, Autophagy in mammalian cells. World Journal of Biological Chemistry, 2012. 3(1): p. 1-6.
30. Hansen, M., David C. Rubinsztein, and David W. Walker, Autophagy as a promoter of longevity: insights from model organisms. Nature Reviews Molecular Cell Biology, 2018. 19(9): p. 579-593.
31. Mähler, A., Jochen Steiniger, Markus Bock, Lars Klug, Nadine Parreidt, Mario Lorenz, Benno F Zimmermann, Alexander Krannich, Friedemann Paul, and Michael Boschmann, Metabolic response to epigallocatechin-3-gallate in relapsing-remitting multiple sclerosis: a randomized clinical trial. Am J Clin Nutr, 2015. 101(3): p. 487-495.
32. Huang J., Y.W., Z. Xie, Y. Zhou, Y. Zhang, and X. Wan The anti-obesity effects of green tea in human intervention and basic molecular studies. European Journal of Clinical Nutrition, 2014. 68: p. 1075-1087.
33. Lee, M.-S., Yoonjin Shin, Sunyoon Jung, and Yangha Kim, Effects of epigallocatechin-3-gallate on thermogenesis and mitochondrialbiogenesis in brown adipose tissues of diet-induced obese mice. Food & Nutrition Research, 2017. 61: p. 1-9.
34. Batubara, N.C., Green Tea Epigallocatechin-3-Gallate Regulates the Autophagy Pathway in 3T3-L1 Preadipocytes, in Life Sciences2019, National Central University: Taiwan.
35. Meng, J., Cuicui Chang, Yuhua Chen, Fangfang Bi, Chen Ji, and Wei Liu, EGCG overcomes gefitinib resistance by inhibiting autophagy and augmenting cell death through targeting ERK phosphorylation in NSCLC. OncoTargets and Therapy, 2019. 12: p. 6033-6043.
36. Kim, H.S., Vedrana Montana, Hyun Ju Jang, Vladimir Parpura, Jeong A Kim, Epigallocatechin Gallate (EGCG) Stimulates Autophagy in Vascular Endothelial Cells. The Journal of Biological Chemistry, 2013. 288(31): p. 22693-22705.
37. Kim, S.N., Hyun Jung Kwon, Seun Akindehin, Hyun Woo Jeong, Yun Hee Lee, Effects of Epigallocatechin-3-Gallate on Autophagic Lipolysis in Adipocytes. Nutrients, 2017. 9(680): p. 1-14.
38. Holczer, M., Boglárka Besze, Veronika Zámbó, Miklós Csala, Gábor Bánhegyi , Orsolya Kapuy, Epigallocatechin-3-Gallate (EGCG) Promotes Autophagy-Dependent Survival via Influencing the Balance of mTOR-AMPK Pathways upon Endoplasmic Reticulum Stress. Oxidative Medicine and Cellular Longevity, 2018. 2018: p. 1-15.
39. Zhou, J., Benjamin Livingston Farah, Rohit Anthony Sinha, Yajun Wu, Brijesh Kumar Singh, Boon-Huat Bay, Chung S. Yang, Paul Michael Yen, Epigallocatechin-3-Gallate (EGCG), a Green Tea Polyphenol, Stimulates Hepatic Autophagy and Lipid Clearance. PLOS ONE, 2014. 9(1): p. 1-10.
40. Zhao, L., Shengtang Liu, Jiaying Xu, Wei Li, Guangxin Duan, Haichao Wang, Huilin Yang, Zaixing Yang, and Ruhong Zhou, A new molecular mechanism underlying the EGCG-mediated autophagic modulation of AFP in HepG2 cells. Cell Death and Disease, 2017. 8: p. 1-10.
41. Lee, Y.M., Mi Kyoung Kim, Hyunah Choo, Youhoon Chong, Conjugation with Phenylalanine Enhances Autophagy-Inducing Activity of (−)-Epigallocatechin Gallate in Hepatic Cells. Journal of Agricultural and Food Chemistry, 2018. 66: p. 12741-12747.
42. Meng, J., Yuhua Chen, Junzhe Wang, Junling Qiu, Cuicui Chang, Fangfang Bi, Xiaopeng Wu, and Wei Liu, EGCG protects vascular endothelial cells from oxidative stress-induced damage by targeting the autophagy-dependent PI3K-AKT-mTOR pathway. Annals of Translational Medicine, 2020. 8(5): p. 1-12.
43. Choi, C., Hyun-Doo Song, Yeonho Son, Yoon Keun Cho, Sang-Yeop Ahn, Young-Suk Jung, Young Cheol Yoon, Sung Won Kwon, and Yun-Hee Lee, Epigallocatechin-3-Gallate Reduces Visceral Adiposity Partly through the Regulation of Beclin1-Dependent Autophagy in White Adipose Tissues. Nutrients, 2020. 12: p. 1-10.
44. Kao, Y.-H., Richard A. Hiipakka, and Shutsung Liao, Modulation of Endocrine Systems and Food Intake by Green Tea Epigallocatechin Gallate. Endocrinology, 2000. 141(3): p. 980-987.
45. Wang, C.-T., Hsin-Huei Chang, Chiao-Hsin Hsiao, Meng-Jung Lee, Hui-Chen Ku, Yu-Jung Hu, and Yung-Hsi Kao, The effects of green tea (-)-epigallocatechin-3-gallate on reactive oxygen species in 3T3-L1 preadipocytes and adipocytes depend on the glutathione and 67 kDa laminin receptor pathways. Mol. Nutr. Food Res., 2009. 53(3): p. 349-360.
46. Ku, H.-C., Hsin-Huei Chang,* Hsien-Chun Liu, Chiao-Hsin Hsiao, Meng-Jung Lee, Yu-Jung Hu, Pei-Fang Hung, Chi-Wei Liu, and Yung-Hsi Kao, Green tea (-)-epigallocatechin gallate inhibits insulin stimulation of 3T3-L1 preadipocyte mitogenesis via the 67-kDa laminin receptor pathway. Am J Physiol Cell Physiol, 2009. 297: p. C121-C132.
47. Rai, S.a.R.M., Fluorescence microscopy: A tool to study autophagy. AIP Advances 2015. 5: p. 1-8.
48. Mauthe, M., Idil Orhon, Cecilia Rocchi, Xingdong Zhou, Morten Luhr, Kerst-Jan Hijlkema, Robert P. Coppes, Nikolai Engedal, Muriel Mari & Fulvio Reggiori, Chloroquine inhibits autophagic flux by decreasing autophagosome-lysosome fusion. Autophagy, 2018. 18(8): p. 1435-1455.
49. Wu, Y.-T., Hui-Ling Tan, Guanghou Shui, Chantal Bauvy, Qing Huang, Markus R. Wenk, Choon-Nam Ong, Patrice Codogno, and Han-Ming Shen, Dual Role of 3-Methyladenine in Modulation of Autophagy via Different Temporal Patterns of Inhibition on Class I and III Phosphoinositide 3-Kinase. THE JOURNAL OF BIOLOGICAL CHEMISTRY, 2010. 285(14): p. 10850–10861.
50. Zhang, C., Yingke He, Mitsuhara Okutsu, Lai Chun Ong, Yi Jin, Lin Zheng, Pierce Chow, Sidney Yu, Mei Zhang, and Zhen Yan, Autophagy is involved in adipogenic differentiation by repressesing proteasome-dependent PPARγ2 degradation. American Journal of Physiology Endocrinology and Metabolism, 2013. 305(4): p. 530-539.
51. Pellegrini, C., Marta Columbaro, Elisa Schena, Sabino Prencipe, Davide Andrenacci, Patricia Iozzo, Maria Angela Guzzardi, Cristina Capanni, Elisabetta Mattioli, Manuela Loi, David Araujo-Vilar, Stefano Squarzoni, Saverio Cinti, Paolo Morselli, Assuero Giorgetti, Laura Zanotti, Alessandra Gambineri, and Giovanna Lattanzi, Altered adipocyte differentiation and unbalanced autophagy in type 2 Familial Partial Lipodystrophy: an in vitro and in vivo study of adipose tissue browning. Experimental & Molecular Medicine, 2019. 51(89): p. 1-17.
52. Satoh, M., Yukitoshi Takemura, Hironobu Hamada, Yoshitaka Sekido, and Shunichiro Kubota, EGCG induces human mesothelioma cell death by inducing reactive oxygen species and autophagy. Cancer Cell International, 2013. 13(19): p. 1-8.
53. Wu, B.-T., Pei-Fang Hung, Hui-Chian Chen, Rong-Nan Huang, Hsin-Huei Chang, and Yung-Hsi Kao, The Apoptotic Effect of Green Tea (-)-Epigallocatechin Gallate on 3T3-L1 Preadipocytes Depends on the Cdk2 Pathway. Journal of Agricultural and Food Chemistry, 2005. 53: p. 5695-5701.
54. Hung, P.-F., Bo-Tsung Wu, Hui-Chian Chen, Yen-Hang Chen, Chia-Lin Chen, Ming-Hua Wu, Hsien-Chun Liu, Meng-Jung Lee, and Yung-Hsi Kao, Antimitogenic effect of green tea (-)-epigallocatechin gallate on 3T3-L1 preadipocytes depends on the ERK and Cdk2 pathways. Am J Physiol Cell Physiol, 2005(288): p. 1094-1108.
55. Zhang, Y., Nai-Di Yang, Fan Zhou, Ting Shen, Ting Duan, Jing Zhou, Yin Shi, Xin-Qiang Zhu, and Han-Ming Shen, (-)-Epigallocatechin-3-Gallate Induces Non-Apoptotic Cell Death in Human Cancer Cells via ROS-Mediated Lysosomal Membrane Permeabilization. PLoS ONE, 2012. 7(10): p. 1-13.
56. Zhang, Y., Yu-Ying Xu, Wen-Jie Sun, Mo-Han Zhang, Yi-Fan Zheng, Han-Ming Shen, Jun Yang, and Xin-Qiang Zhu, FBS or BSA Inhibits EGCG Induced Cell Death through Covalent Binding and the Reduction of Intracellular ROS Production. BioMed Research International, 2016. 2016: p. 1-8.
57. Klionsky, D.J., et al., Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition). Autophagy, 2016. 12(1): p. 1-222.
58. Hale, A.N., Dan J. Ledbetter, Thomas R. Gawriluk, and Edmund B. Rucker, III, Autophagy Regulation and role in development. Autophagy, 2013. 9(7): p. 951-972.
59. Li, T.Y., Shu-Yong Lin, and Sheng-Cai Lin, Mechanism and Physiological Significance of Growth Factor-Related Autophagy. Physiology, 2013. 28: p. 423-431.
60. Nitulescu, G.M., Maryna Van De Venter, Georgiana Nitulescu, Anca Ungurianu, Petras Juzenas, Qian Peng, Octavian Tudorel Olaru, Daniela Grădinaru, Aristides Tsatsakis, Dimitris Tsoukalas, Demetrios A. Spandidos, and Denisa Margina, The Akt pathway in oncology therapy and beyond (Review). International Journal of Oncology, 2018. 53: p. 2319-2331.
61. Hemmings, B.A.a.D.F.R., PI3K-PKB/Akt Pathway. Cold Spring Harbor Perspectives in Biology, 2012. 4(9): p. 1-3.
62. Zhang, X.-j., Sheng Chen, Kai-xing Huang, and Wei-dong Le, Why should autophagic flux be assessed? Acta Pharmacologica Sinica, 2013. 34: p. 595-599.
63. Kuma, A.a.N.M., Physiological role of autophagy as an intracellular recycling system: With an emphasis on nutrient metabolism. Seminars in Cell & Developmental Biology, 2010. 21: p. 683-690.
64. Yoshii, S.R., and Noboru Mizushima, Monitoring and Measuring Autophagy. International Journal of Molecular Sciences, 2017. 18(1865): p. 1-13.
65. Information, N.C.f.B. Chloroquine phosphate. 2022 [cited 2022 December 19]; Available from: https://pubchem.ncbi.nlm.nih.gov/compound/Chloroquine-phosphate.
66. Information, N.C.f.B. 3-Methyladenine. 2022 [cited 2022 December 19]; Available from: https://pubchem.ncbi.nlm.nih.gov/compound/3-Methyladenine.
67. Gaspar, R.C., Vitor Rosetto Muñoz, Ana Paula Azevêdo Macêdo, Renan Fudoli Lins Vieira, and José Rodrigo Pauli, A Palette of Adipose Tissue: Multiple Functionality and Extraordinary Plasticity. Herald Scholarly Open Access Trens in Anatomy and Physiology, 2021. 4: p. 013.

指導教授

高永旭(Yung-Hsi Kao)

審核日期

2023-1-18

推文