A recent scientific study has found that molecular hydrogen may have protective effects against steroid-induced osteonecrosis (ON) in rabbits. The study, which was conducted on 60 rabbits, found that those treated with intraperitoneal injections of molecular hydrogen at 10 ml/kg body weight for seven consecutive days had a significantly lower incidence of steroid-induced ON compared to a control group.
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The study found that molecular hydrogen prevents steroid-induced osteonecrosis by suppressing oxidative injury, vascular injury, and apoptosis. Oxidative injury is caused by an imbalance between the production of reactive oxygen species (ROS) and the body’s ability to detoxify them. Vascular injury is damage to the blood vessels and Apoptosis is a type of programmed cell death.
Osteonecrosis is a debilitating bone disease that occurs when the blood supply to the bone is disrupted. This leads to bone death and can cause severe pain and disability. Steroid-induced osteonecrosis is a common complication of long-term steroid use, and currently, there is no effective treatment for this condition.
The study found that molecular hydrogen was able to reduce the levels of ROS in the body, thereby reducing oxidative stress. It also reduces vascular injury and apoptosis. This suggests that molecular hydrogen may be a useful tool in the fight against steroid-induced osteonecrosis.
In conclusion, this study found that molecular hydrogen may have protective effects against steroid-induced osteonecrosis in rabbits. The study found that molecular hydrogen prevents steroid-induced osteonecrosis by suppressing oxidative injury, vascular injury, and apoptosis. These results suggest that molecular hydrogen may be a useful tool in the fight against this debilitating bone disease. However, more research is needed to confirm these findings and to explore the potential use of molecular hydrogen as a treatment for osteonecrosis in humans.
Li, J., et al., Protective effects of molecular hydrogen on steroid-induced osteonecrosis in rabbits via reducing oxidative stress and apoptosis. BMC Musculoskelet Disord, 2017. 18(1): p. 58.