Hydrogen Therapy Reduces Nerve Pain by Repairing Cell Cleanup Process
- Authors
- Huixing Wang, Xiaodong Huo, Hongguang Chen, Bo Li, Jingzhi Liu, Wenting Ma, Xiaojuan Wang, Keliang Xie, Yonghao Yu, Kemei Shi
- Journal
- BioMed Research International
- Year
- 2018
- DOI
- 10.1155/2018/4670834
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Neuropathic Pain
- Body System
- Nervous System
TL;DR
Hydrogen-rich saline (HRS) may help reduce chronic nerve pain by boosting the cell's waste disposal system through a specific cellular pathway.
Key Finding
Hydrogen-rich saline reduced nerve pain in rats by activating cellular autophagy (a cleanup process inside cells) through the HIF-1α molecular pathway in the spinal cord.
Summary
Researchers tested whether hydrogen-rich saline could reduce nerve pain in rats with a specific type of injury-induced chronic pain. They found that hydrogen-rich saline reduced pain sensitivity and activated autophagy (a cellular cleanup process) in the spinal cord through a specific molecular pathway called HIF-1α. When they blocked this pathway, the pain-relieving effects disappeared, suggesting this mechanism is important for how hydrogen-rich saline works.
Practical Takeaway
This animal study suggests hydrogen-rich saline may help with nerve pain by triggering a cellular repair process, but it was conducted only in rats and does not yet indicate whether this would work in humans. Much more research, including human trials, would be needed before any health claims could be made.
Abstract
Background Neuropathic pain is a chronic and intractable pain, with very few effective analgesics. It involves an impaired cell autophagy process. Hydrogen-rich saline (HRS) reportedly reduces allodynia and hyperalgesia in a neuropathic pain model; however, it is unknown whether these effects involve autophagy induction. Methods We investigated the relationship between HRS and cell autophagy in a neuropathic pain model generated by chronic constriction injury (CCI) in Sprague–Dawley rats. Rats received an intraperitoneal injection of HRS (10 mL/kg daily, from 1 day before until 14 days after CCI), 3MA (autophagy inhibitor), 2ME2 (HIF-1α inhibitor), or EDHB (HIF-1α agonist). The mechanical withdrawal threshold (MWT) and thermal withdrawal latency (TWL) were tested 1 day before and 1, 3, 7, 10, and 14 days after the operation. HIF-1α and cell autophagy markers in the spinal cord were evaluated by western blotting and real-time PCR assays at 14 days after CCI. Autophagosomes with double membranes were identified by transmission electron microscopy. Results CCI caused behavioral hypersensitivity to mechanical and thermal stimulation in the hind-paw of the injured side. HRS improved MWT and TWL, activated autophagy, and increased autophagosomes and autolysosomes in CCI rats. 3-MA aggravated hyperalgesia and allodynia and suppressed autophagy, while EDHB attenuated hyperalgesia and activated the autophagy procedure and the HIF-1α downstream target gene BNIP3. HIF-1α inhibitors reversed the regulatory effects of HRS on autophagy in CCI rats at 14 days after spinal cord injury. Conclusion HRS reduced mechanical hyperalgesia and activation of cell autophagy in neuropathic pain through a HIF1-dependent pathway.