1.Research progress in effects of amino acids on endoplasmic reticulum stress
Wenlong XU ; Mengzhu CUI ; Hongyan LIANG ; Xiaofeng JIANG
International Journal of Laboratory Medicine 2019;40(3):273-276
The occurrence of endoplasmic reticulum stress (ERS) is involved in the development of various diseases in human body.Accurate and effective intervention and regulation of ERS has become a hot spot in recent years.Amino acids are the nutrients that make up the proteins that people need, and they are also important signal transduction molecules in the human body.Intervention and regulation of ERS stress by amino acids is likely to be an important and unexplored area, and it is expected to become a potential target for new prevention strategies such as malignant tumors and cardiovascular diseases.Therefore, in this article, we will briefly review the research progress of the effects of amino acids on cellular ERS stress in recent years.
2.Research progress on the role of matrix protein p17 in human immunodeficiency virus infection and related diseases
Mengzhu LI ; Rui SHEN ; Danhui WU ; Yanqiu LU ; Hong LIU ; Yemiao CHEN ; Hongjuan CUI ; Yaokai CHEN
Chinese Journal of Clinical Infectious Diseases 2023;16(6):475-480
Matrix protein p17 is a structural protein of human immunodeficiency virus(HIV). It not only plays a key role in multiple stages of HIV life cycle,but also is closely associated with HIV-related lymphoma,neurocognitive impairment and breast cancer. This article reviews the role of matrix protein p17 in HIV infection and HIV-related diseases.
3.Effects of long-term noise exposure during sleep on liver circadian clock and lipid metabolism
Xinyao ZHANG ; Xiaojun SHE ; Yiming FU ; Bo FU ; Shuo WANG ; Mengzhu CHENG ; Rui WANG ; Bo CUI
Journal of Environmental and Occupational Medicine 2024;41(1):41-46
Background Long-term exposure to noise during sleep may has adverse effects on metabolic system, and liver lipid metabolism is closely related to circadian clock genes. Objective To investigate the effects of long-term noise exposure during sleep on liver circadian clock and lipid metabolism in mice and its related mechanism. Methods Twenty C57BL/6J male mice were randomly divided into two groups: a noise exposure group and a control group with 10 mice in each group. The mice in the noise exposure group were exposed to white noise at 90 dB sound pressure level (SPL) for 30 consecutive days, 8 h a day, from 9:00 to 17:00. The mice in the control group were exposed to background noise ≤40 dB SPL. After noise exposure, the animals were neutralized at 14:00 (ZT6) and 2:00 (ZT18), 5 animals at each time spot, and the liver tissues were collected. Total cholesterol and triglyceride in liver were determined by cholesterol oxidase method and glycerol phosphate oxidase method respectively. The expressions of circadian clock genes (Clock, Bmal1, Rev-erbα, and Rev-erbβ) and lipid metabolism genes (Srebp1c, Hmgcr, Fasn, Lxrα, Acc1, and Chrebp) in liver were detected by quantitative real-time PCR. Results Compared with the control group, the content of total cholesterol in liver in the noise exposure group increased by 48% (P<0.05) and the content of liver triglyceride increased by 61% (P<0.05) at ZT18. The mRNA expression levels of circadian clock genes Clock and Bmal1 in the noise exposure group was significantly increased at ZT18 and decreased at ZT6 (P<0.05). The mRNA expression level of Rev-erbα decreased at both ZT6 and ZT18 (P<0.05). The mRNA expression level of Rev-erbβ had no significant change at ZT6 and ZT18. The mRNA expression levels of liver lipid metabolism related genes Srebp1c, Hmgcr, Chrebp, and Lxrα in the noise exposure group were higher than those in the control group at ZT18 (P<0.05). The mRNA expression levels of Acc1 and Fasn showed no significant change at ZT6, then an upward trend at ZT18, but no significant difference between the two time spots (P>0.05). Conclusion Long-term noise exposure during sleep can cause circadian clock and lipid metabolism disorders in mice. Among them, suppression of key circadian clock genes may be associated with Rev-erbα-mediated upregulation of the nuclear receptors Srebp1c and Chrebp for lipid synthesis and deposition in the liver, resulting in lipid metabolism disorder.