2017 · Li — Protective Effects of Molecular Hydrogen on Steroid-Induced Osteonecrosis in Rabbits via Reducing Oxidative Stress and Apoptosis
Super-Abstract
In rabbits given high-dose steroids, treatment with molecular hydrogen (injected intraperitoneally) reduced the incidence of bone death (osteonecrosis) from 68% to 29% by suppressing oxidative damage, vascular injury, and cell death (apoptosis). This is a preclinical animal study; human steroid-induced osteonecrosis has not been studied with H₂.
Commentary
Steroid-induced osteonecrosis of the femoral head is a debilitating complication of high-dose corticosteroid treatment — common in patients receiving immunosuppressive therapy after organ transplant or for autoimmune conditions. Oxidative stress and vascular injury in bone tissue are key mechanisms. This study randomised 60 rabbits to a standard steroid-induction protocol, with half receiving intraperitoneal hydrogen injections for seven consecutive days. The key finding is striking: osteonecrosis incidence dropped from 68% (model group) to 28.6% (hydrogen group). Mechanistic markers — oxidative damage (8-OHdG, MDA), vascular injury (sTM), and apoptosis (TUNEL assay) — were all significantly lower in the hydrogen group. Notably, cholesterol and triglyceride levels did not differ, suggesting that H₂ acts directly on oxidative and vascular mechanisms rather than on lipid metabolism. The study is well-designed for a preclinical experiment, but the intraperitoneal injection route is not directly translatable to human H₂ delivery methods, and the species and steroid protocol differ substantially from clinical scenarios.
Key quotes
- „The incidence of steroid-induced ON was significantly lower in hydrogen group (28.6%) than that in model group (68.0%).“ — the headline result: a roughly 2.5-fold reduction in osteonecrosis incidence
- „Oxidative injury, vascular injury and apoptosis were attenuated in the hydrogen group compared with those in the model group in vivo.“ — the three mechanistic pathways through which H₂ acts
- „These results suggested that molecular hydrogen prevents steroid-induced osteonecrosis in rabbits by suppressing oxidative injury, vascular injury and apoptosis.“ — authors' conclusion on the protective mechanism
Our assessment
This is a preclinical animal study — results cannot be directly transferred to humans. The finding is notable: a substantial reduction in osteonecrosis incidence in a rabbit model, with mechanistic data supporting three plausible pathways (antioxidant, vasoprotective, anti-apoptotic). Limitations: rabbits differ from humans in bone biology and steroid metabolism; intraperitoneal injection of H₂ solution is not a standard human H₂ delivery method; sample sizes per group are not explicitly stated; long-term bone recovery was not assessed. Human clinical trials for this specific application do not yet exist.
Study design
- Type: animal experiment · Model: rabbits, steroid-induced osteonecrosis model · n: 60 rabbits (model group and hydrogen group) · H₂ delivery: intraperitoneal injection of molecular hydrogen solution, 10 ml/kg body weight for 7 consecutive days
- Outcome: osteonecrosis incidence 28.6% (H₂) vs. 68.0% (model, p<0.05); reduced oxidative markers (8-OHdG, MDA), vascular injury marker (sTM), and apoptosis (TUNEL); cholesterol and triglycerides unchanged
Abstract
BACKGROUND: The objective of this study was to investigate the protective effects of molecular hydrogen, a novel and selective antioxidant, on steroid-induced osteonecrosis (ON) in a rabbit model. METHODS: Sixty rabbits were randomly divided into two groups (model group and hydrogen group). Osteonecrosis was induced according to an established protocol of steroid-induced ON. Rabbits in the hydrogen group were treated with intraperitoneal injections of molecular hydrogen at 10 ml/kg body weight for seven consecutive days. Plasma levels of total cholesterol, triglycerides, soluble thrombomodulin(sTM), glutathione(GSH) and malondialdehyde(MDA) were measured before and after steroid administration. The presence or absence of ON was examined histopathologically. Oxidative injury and vascular injury were assessed in vivo by immunohistochemical staining of 8-hydoxy-2-deoxyguanosine(8-OHdG) and MDA, and ink artery infusion angiography. The terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assays were performed to measure apoptosis. RESULTS: The incidence of steroid-induced ON was significantly lower in hydrogen group (28.6%) than that in model group (68.0%). No statistically differences were observed on the levels of total cholesterol and triglycerides. Oxidative injury, vascular injury and apoptosis were attenuated in the hydrogen group compared with those in the model group in vivo. CONCLUSIONS: These results suggested that molecular hydrogen prevents steroid-induced osteonecrosis in rabbits by suppressing oxidative injury, vascular injury and apoptosis.
Source & links
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