Tianyou Li
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Tianyou Li has a total of 6 co-authors. Here are the top co-authors by number of shared publications:
- Dawei Wang
Research Center for Nutrition and Food Safety, Chongqing Key Laboratory of Nutrition and Health, Chongqing Medical Nutrition Research Center, Institute of Military Preventive Medicine, Third Military Medical University, Chongqing 400038, China
1 shared publication - Jining Yang
Research Center for Nutrition and Food safety, Chongqing Key Laboratory of Nutrition and Food Safety, Institute of Military Preventive Medicine, Third Military Medical University, Chongqing 400038, China
1 shared publication - Long Yi
Research Center for Nutrition and Food safety, Chongqing Key Laboratory of Nutrition and Food Safety, Institute of Military Preventive Medicine, Third Military Medical University, Chongqing 400038, China
1 shared publication - Mantian Mi
Chongqing Key Laboratory of Nutrition and Health, Research Center for Nutrition and Food Safety, Chongqing Medical Nutrition Research Center, Institute of Military Preventive Medicine Army Medical University (Third Military Medical University) Chongqing China
1 shared publication - Xinxin Guo
Research Center for Nutrition and Food safety, Chongqing Key Laboratory of Nutrition and Food Safety, Institute of Military Preventive Medicine, Third Military Medical University, Chongqing 400038, China
1 shared publication - Yingquan Xie
Research Center for Nutrition and Food safety, Chongqing Key Laboratory of Nutrition and Food Safety, Institute of Military Preventive Medicine, Third Military Medical University, Chongqing 400038, China
1 shared publication
Latest Publications
- Open Access
Sulforaphane Inhibits Exhaustive Exercise-Induced Liver Injury and Transcriptome-Based Mechanism Analysis
Exhaustive exercise (EE) induces liver injury and has recently gained much attention. Sulforaphane (SFN) can protect the liver from inflammation and oxidative stress. However, the effects of SFN on EE-induced liver injury and its underlying mechanisms are still unclear. C57BL/6J mice swimming to exhaustion for seven days were used to simulate the liver injury caused by EE. Different doses of SFN (10, 30, 90 mg/kg body weight) were gavage-fed one week before and during the exercise. SFN intervention significantly reduced the EE-induced lactate dehydrogenase (LDH), creatine kinase (CK), alanine aminotransferase (ALT), and aspartate aminotransferase (AST) in the serum, as well as attenuating liver tissue morphological abnormality, oxidative stress injury, and inflammation. Liver transcriptomic analysis showed that the differentially expressed genes altered by SFN intervention in the exercise model were mainly enriched in glucose and lipid metabolism pathways. The most altered gene by SFN intervention screened by RNA-seq and validated by qRT-PCR is Ppp1r3g, a gene involved in regulating hepatic glycogenesis, which may play a vital role in the protective effects of SFN in EE-induced liver damage. SFN can protect the liver from EE-induced damage, and glucose and lipid metabolism may be involved in the mechanism of the protective effects.
Open AccessSulforaphane Inhibits Exhaustive Exercise-Induced Liver Injury and Transcriptome-Based Mechanism Analysis
Exhaustive exercise (EE) induces liver injury and has recently gained much attention. Sulforaphane (SFN) can protect the liver from inflammation and oxidative stress. However, the effects of SFN on EE-induced liver injury and its underlying mechanisms are still unclear. C57BL/6J mice swimming to exhaustion for seven days were used to simulate the liver injury caused by EE. Different doses of SFN (10, 30, 90 mg/kg body weight) were gavage-fed one week before and during the exercise. SFN intervention significantly reduced the EE-induced lactate dehydrogenase (LDH), creatine kinase (CK), alanine aminotransferase (ALT), and aspartate aminotransferase (AST) in the serum, as well as attenuating liver tissue morphological abnormality, oxidative stress injury, and inflammation. Liver transcriptomic analysis showed that the differentially expressed genes altered by SFN intervention in the exercise model were mainly enriched in glucose and lipid metabolism pathways. The most altered gene by SFN intervention screened by RNA-seq and validated by qRT-PCR is Ppp1r3g, a gene involved in regulating hepatic glycogenesis, which may play a vital role in the protective effects of SFN in EE-induced liver damage. SFN can protect the liver from EE-induced damage, and glucose and lipid metabolism may be involved in the mechanism of the protective effects.