Hydrogen Therapy Protects Heart Cells from Diabetes-Related Damage
- Authors
- Hong Jiang, Pan Yu, De-Hui Qian, Zhe-Xue Qin, Xue-Jun Sun, Jie Yu, Lan Huang
- Journal
- International Journal of Molecular Medicine
- Year
- 2013
- DOI
- 10.3892/ijmm.2013.1334
- Study Type
- Cell Culture
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Diabetes Mellitus
- Body System
- Cardiovascular
TL;DR
Adding hydrogen to the environment of blood vessel cells protects them from damage caused by harmful compounds that accumulate with age.
Key Finding
Hydrogen-rich medium reduced advanced glycation end product-induced cell death in cultured blood vessel cells from 21.61% to 11.32%, while simultaneously decreasing harmful reactive oxygen species and enhancing antioxidant enzyme expression.
Summary
Researchers grew blood vessel cells in a lab and exposed them to advanced glycation end products (AGEs)—harmful compounds that build up in diabetes and aging. They tested whether hydrogen-rich medium (water with extra dissolved hydrogen) could protect these cells from damage. Hydrogen-rich medium reduced cell death by about half and decreased harmful reactive oxygen species (unstable molecules that damage cells) while boosting the cells' natural antioxidant defenses.
Practical Takeaway
This laboratory study suggests hydrogen may help protect blood vessel cells from AGE-related damage through antioxidant mechanisms. However, this is early-stage cell culture research with no human testing, so it's unclear whether these effects would occur in the human body or translate to health benefits. Much more research, including animal and human studies, would be needed before any therapeutic claims could be made.
Abstract
The purpose of the present study was to determine whether using hydrogen-rich medium (HRM) to increase hydrogen levels in endothelial cells (ECs) protects ECs from apoptosis induced by advanced glycation end products (AGEs). The thoracic aorta was removed from 2-3-year-old Sprague-Dawley rats, and ECs were isolated and cultured. After culturing ECs in the presence of AGEs and/or with HRM for 24 h, Annexin V/7-AAD and TUNEL staining were carried out to detect apoptosis. Intracellular ROS were detected by fluorescent probe and quantified by flow cytometry. The expression of antioxidative enzymes (superoxide dismutase, glutathione peroxidase) was determined by real-time PCR analysis and enzymatic assay. The relative expression levels of Bcl-2 and Bax were analyzed by western blotting. The addition of AGEs increased the apoptosis of ECs in a concentration-dependent manner and HRM reduced the AGE (400 µg/ml)-induced apoptosis from 21.61±2.52 to 11.32±1.75%. HRM also significantly attenuated the AGE-induced intracellular ROS induction and decrease in the expression of antioxidative enzymes. In conclusion, hydrogen exhibits significant protective effects against AGE-induced EC injury possibly through reducing ROS generation, intracellular antioxidant enzyme system protection and elevation of the Bcl-2/Bax ratio.