Yuanyuan Li
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Yuanyuan Li has a total of 19 co-authors. Here are the top co-authors by number of shared publications:
Jingjin Hu
School of Public Health, Hangzhou Medical College, Hangzhou, CHINA
2 shared publicationsJunsong Jing
School of Public Health, Hangzhou Medical College, Hangzhou, CHINA
2 shared publicationsRongrong Huang
School of Public Health, Hangzhou Medical College, Hangzhou, CHINA
2 shared publicationsTing Zhou
School of Pharmaceutical Sciences, Hangzhou Medical College, Hangzhou, China
2 shared publicationsXueping Wei
School of Public Health, Hangzhou Medical College, Hangzhou, CHINA
2 shared publicationsYouping Wu
The Children's Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, Hangzhou, China
2 shared publications
Latest Publications
- Open Access
- 7 October 2023
- Published by Elsevier in Journal of Ethnopharmacology
- Vol. 319, 117295
QFAE-nB alleviates pulmonary fibrosis by inhibiting the STING pathway in mice
- 7 October 2023
- Published by Elsevier in Journal of Ethnopharmacology
- Vol. 319, 117295
Open AccessQFAE-nB alleviates pulmonary fibrosis by inhibiting the STING pathway in mice
- Open Access
- 14 April 2023
- Published by Elsevier in Biomedicine & Pharmacotherapy
- Vol. 162, 114691
Doxorubicin downregulates autophagy to promote apoptosis-induced dilated cardiomyopathy via regulating the AMPK/mTOR pathway
- 14 April 2023
- Published by Elsevier in Biomedicine & Pharmacotherapy
- Vol. 162, 114691
Open AccessDoxorubicin downregulates autophagy to promote apoptosis-induced dilated cardiomyopathy via regulating the AMPK/mTOR pathway
- 27 February 2022
- Published by Springer Nature in Current Medical Science
- Vol. 42 (3) , 483-490
Extracts of Bauhinia Championii Alleviate Acute Neuronal Injury After Ischemic Reperfusion by Improving Endoplasmic Reticulum Stress-Mediated Neuronal Apoptosis
Objective Cerebral ischemia/reperfusion (I/R) is a potential factor for lethal injury, and currently lacks effective remedies. Bauhinia championii extracts (BCEs) have been reported to exhibit anti-oxidative and anti-hypoxia properties. The current work aimed to study whether BCE could alleviate neuronal injury caused by I/R. Methods To investigate the protective effects of BCE, oxygen-glucose deprivation/reperfusion (OGD/R) was applied to the HT22 cell line in vitro and to a cerebral I/R mouse model in vivo. Results Under OGD/R, the survival of HT22 cells was significantly prolonged after treatment with BCE. In vivo, BCE significantly reduced the infarct area and decreased neuronal apoptosis caused by I/R. It was further found that OGD/R could trigger endoplasmic reticulum (ER) stress and induce ER stress-mediated neuronal apoptosis in vivo and in vitro, while BCE could effectively alleviate ER stress and neuronal apoptosis. Conclusion These results suggested that BCE exhibits neuroprotective effects by reducing ER stress-mediated apoptosis after cerebral I/R injury. BCE may therefore be an effective therapeutic regimen against cerebral I/R damage.
- 27 February 2022
- Published by Springer Nature in Current Medical Science
- Vol. 42 (3) , 483-490
Extracts of Bauhinia Championii Alleviate Acute Neuronal Injury After Ischemic Reperfusion by Improving Endoplasmic Reticulum Stress-Mediated Neuronal Apoptosis
Objective Cerebral ischemia/reperfusion (I/R) is a potential factor for lethal injury, and currently lacks effective remedies. Bauhinia championii extracts (BCEs) have been reported to exhibit anti-oxidative and anti-hypoxia properties. The current work aimed to study whether BCE could alleviate neuronal injury caused by I/R. Methods To investigate the protective effects of BCE, oxygen-glucose deprivation/reperfusion (OGD/R) was applied to the HT22 cell line in vitro and to a cerebral I/R mouse model in vivo. Results Under OGD/R, the survival of HT22 cells was significantly prolonged after treatment with BCE. In vivo, BCE significantly reduced the infarct area and decreased neuronal apoptosis caused by I/R. It was further found that OGD/R could trigger endoplasmic reticulum (ER) stress and induce ER stress-mediated neuronal apoptosis in vivo and in vitro, while BCE could effectively alleviate ER stress and neuronal apoptosis. Conclusion These results suggested that BCE exhibits neuroprotective effects by reducing ER stress-mediated apoptosis after cerebral I/R injury. BCE may therefore be an effective therapeutic regimen against cerebral I/R damage.