Yellow Laser Stimulation at GV2 Acupoint Mitigates Apoptosis, Oxidative Stress, Inflammation, and Motor Deficit in Spinal Cord Injury Rats.
Parichat On-Ong-ArjJintanaporn WattanathornSupaporn MuchmapuraWipawee Thukham-MeePublished in: Evidence-based complementary and alternative medicine : eCAM (2018)
Currently, the suppression of oxidative stress and inflammation is considered as the treatment targets of spinal cord injury due to their roles on the hindrance of recovery process. Since laser acupuncture decreased oxidative stress and enhanced the survival of neurons from oxidative stress damage and GV2 stimulation was selected as one stimulated acupoint in order to enhance the recovery of spinal cord injury, we hypothesized that laser acupuncture at GV2 should enhance the recovery of spinal cord injury. To test this hypothesis, male Wistar rats were induced spinal cord injury at T10 level and they were exposed to a 10 minute-stimulation at GV2 by yellow laser. Laser acupuncture was performed at 0.25 and 1, 2, 6, and 12 hours after spinal cord injury. Then, the stimulation was performed once daily for 7 days. Locomotor assessment was carried out on days 3 and 7 after injury. At the end of study period, the densities of polymorphonuclear of leukocyte, Bax, Caspase-3, Bcl-2, and BDNF positive stained cells in ventral horn of spinal cord were determined. Cyclooxygenase-2 (COX-2), interleukin-6 (IL-6), and oxidative stress status was also assessed. The results showed that laser acupuncture at GV2 increased BBB score, gross motor score, and densities of Bcl-2 and BDNF positive stained cells but decreased density with polymorphonuclear leukocyte, the densities of Bax and Caspase-3 positive stained cells, COX-2 level, and oxidative stress status in ventral horn of the lesion spinal cord. The reduction of serum COX-2 was also decreased. Therefore, GV2 stimulation by yellow laser might enhance the recovery of spinal cord via the increase in BDNF and the decrease in inflammation, apoptosis, and oxidative stress status in the lesion spinal cord.
Keyphrases
- oxidative stress
- induced apoptosis
- spinal cord
- spinal cord injury
- neuropathic pain
- diabetic rats
- endoplasmic reticulum stress
- ischemia reperfusion injury
- dna damage
- cell cycle arrest
- cell death
- signaling pathway
- high speed
- heat shock
- cell proliferation
- physical activity
- nitric oxide
- children with cerebral palsy
- heat shock protein