Nicotinic acid shields liver from reperfusion injury, reveals research

The team's findings demonstrate that nicotinic acid matches or even exceeds NAC's protective effects by targeting the root cause: damaged mitochondria. In experiments using both mice and primary hepatocytes, pretreatment with nicotinic acid markedly lowered markers of liver injury (ALT, AST, LDH), suppressed inflammation, and reduced cell death driven by ferroptosis, an iron-dependent form of programmed cell death.

Notably, nicotinic acid markedly restored mitochondrial quality. “It did not just act as an antioxidant-it actively promoted mitophagy (the cleanup of broken mitochondria) and mitochondrial biogenesis (the creation of new ones),” says Yao. “This dual action stabilized the mitochondrial permeability transition pore, boosted ATP production, and rebalanced cellular redox status.”

The authors noted that given its safety, low cost, and widespread availability, nicotinic acid could be rapidly translated into clinical use-potentially improving outcomes for patients undergoing liver surgery. Human trials are now being planned to confirm these benefits in real-world settings.

Reference:

Qian Zeng, Yina Sun, Mengzhen Lei, Zihan Liu, Xijing Yan, Rong Li, Jun Zheng, Jiandong Zha, Lijun Zhang, Xiaoling Guan, Jia Yao, Nicotinic acid protects against hepatic ischemia-reperfusion injury via suppressing mitochondrial damage-induced ferroptosis, Liver Research, https://doi.org/10.1016/j.livres.2025.11.001.