Guoqing Ouyang
Liver surgery researcher at Guangxi Medical University and senior author of a 2026 study in which the plant compound notoginsenoside R1 eased paracetamol liver injury by boosting autophagy
Division of Hepatobiliary Surgery, The First Affiliated Hospital of Guangxi Medical University (2026) · Department of General Surgery, Liuzhou People's Hospital affiliated to Guangxi Medical University (2024)
An overdose of acetaminophen (paracetamol) is one of the commonest causes of sudden liver failure. Guoqing Ouyang is last author of a 2026 study testing notoginsenoside R1, a compound from the medicinal plant Panax notoginseng, in this kind of injury (LIS2026). The compound reduced liver cell death and oxidative damage, and it worked by boosting autophagy, the cell's recycling system, through changes in MAPK and mTOR signalling. mTOR normally holds autophagy back, so easing it lets damaged cells clean up. The work was done in laboratory models; there is no evidence yet that the compound helps people with overdose.
Ouyang's PubMed record is in liver disease at Guangxi Medical University in Nanning. Recent papers include a 2024 study, as first author from Liuzhou People's Hospital affiliated to the university, that grouped liver cancers by genes of a cell-death programme called PANoptosis and built a survival score, and work with Songqing He's hepatobiliary surgery group on alcohol-related liver disease. A Frontiers profile lists Ouyang at the Division of Hepatobiliary Surgery of the First Affiliated Hospital as a doctoral-level researcher, but no institutional page was found, so the position shown is the one on the 2026 paper.
Milestones in the Atlas
A selection, not a full bibliography: only papers that meet the Atlas inclusion criteria.
| Year | Evidence | Study |
|---|---|---|
| 2026 | A | Notoginsenoside R1 Alleviates Acetaminophen-Induced Liver Injury via MAPK/mTOR-Mediated Autophagy. LIS2026 Last author: led the study showing that notoginsenoside R1 eases acetaminophen liver injury by promoting protective autophagy via MAPK/mTOR. |
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