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Wando Mount Pleasant Library
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Calycosin Enhances Heat Shock Related-Proteins in H9c2 Cells to Modulate Survival and Apoptosis against Heat Shock.
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- Author(s): Lai, Pei-Fang (AUTHOR); Mahendran, Ramasamy (AUTHOR); Tsai, Bruce Chi-Kang (AUTHOR); Lu, Cheng-You (AUTHOR); Kuo, Chia-Hua (AUTHOR); Lin, Kuan-Ho (AUTHOR); Lu, Shang-Yeh (AUTHOR); Wu, Yu-Ling (AUTHOR); Chang, Yung-Ming (AUTHOR); Kuo, Wei-Wen (AUTHOR); Huang, Chih-Yang (AUTHOR)
- Source:
American Journal of Chinese Medicine. 2024, Vol. 52 Issue 4, p1173-1193. 21p. - Source:
- Additional Information
- Subject Terms: FLOW cytometry; ASTRAGALUS (Plants); DATA analysis; RESEARCH funding; ISOFLAVONES; PHYSIOLOGICAL effects of heat; CELL physiology; APOPTOSIS; FEVER; FLUORESCENT antibody technique; CELLULAR signal transduction; DESCRIPTIVE statistics; HEAT shock proteins; RATS; CELL culture; ANIMAL experimentation; WESTERN immunoblotting; MYOCARDIUM; ONE-way analysis of variance; STATISTICS; CELL survival; MOLECULAR chaperones; STAINS & staining (Microscopy); DATA analysis software; HEART cells; IMMUNOBLOTTING
- Abstract: Heat shock proteins (HSPs), which function as chaperones, are activated in response to various environmental stressors. In addition to their role in diverse aspects of protein production, HSPs protect against harmful protein-related stressors. Calycosin exhibits numerous beneficial properties. This study aims to explore the protective effects of calycosin in the heart under heat shock and determine its underlying mechanism. H9c2 cells, western blot, TUNEL staining, flow cytometry, and immunofluorescence staining were used. The time-dependent effects of heat shock analyzed using western blot revealed increased HSP expression for up to 2 h, followed by protein degradation after 4 h. Hence, a heat shock damage duration of 4 h was chosen for subsequent investigations. Calycosin administered post-heat shock demonstrated dose-dependent recovery of cell viability. Under heat shock conditions, calycosin prevented the apoptosis of H9c2 cells by upregulating HSPs, suppressing p-JNK, enhancing Bcl-2 activation, and inhibiting cleaved caspase 3. Calycosin also inhibited Fas/FasL expression and activated cell survival markers (p-PI3K, p-ERK, p-Akt), indicating their cytoprotective properties through PI3K/Akt activation and JNK inhibition. TUNEL staining and flow cytometry confirmed that calycosin reduced apoptosis. Moreover, calycosin reversed the inhibitory effects of quercetin on HSF1 and Hsp70 expression, illustrating its role in enhancing Hsp70 expression through HSF1 activation during heat shock. Immunofluorescence staining demonstrated HSF1 translocation to the nucleus following calycosin treatment, emphasizing its cytoprotective effects. In conclusion, calycosin exhibits pronounced protective effects against heat shock-induced damages by modulating HSP expression and regulating key signaling pathways to promote cell survival in H9c2 cells. [ABSTRACT FROM AUTHOR]
- Abstract: Copyright of American Journal of Chinese Medicine is the property of World Scientific Publishing Company and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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