Long-Term Consumption of Hydrogen-Rich Water Mitigates Oxidative Stress, Hepatic Inflammation, and Apoptosis in Rats with LPS-Induced Chronic Liver Injury.

Abstract

Chronic hepatic inflammation underlies the progression of various metabolic liver diseases, yet the long-term effects of hydrogen-rich water (HRW) on this condition had not been well characterized. Sprague-Dawley rats received HRW for 8 months before and during exposure to lipopolysaccharide (LPS) to establish a chronic liver injury model. Sustained HRW administration suppressed inflammatory cell infiltration in hepatic tissue, blunted abnormal rises in pro-inflammatory mediators, and stabilized anti-inflammatory factor expression. Apoptotic signaling through the death receptor, mitochondrial, and endoplasmic reticulum stress pathways—reflected by Bax, cytochrome c, Caspase-3, -8, -9, -12, CHOP, and GRP78—was attenuated, while the anti-apoptotic protein Bcl-2 was preserved. These findings indicate that long-term HRW consumption may delay chronic inflammation-driven liver injury by concurrently reducing oxidative stress, mitochondrial dysfunction, and apoptotic activity.

Mechanism

HRW suppresses pro-apoptotic signaling via the death receptor, mitochondrial, and ER stress pathways—downregulating Bax, Caspase-3/-8/-9/-12, CHOP, and GRP78—while maintaining Bcl-2 expression, thereby reducing hepatocyte apoptosis and oxidative stress-driven liver injury.