Conclusion
In conclusion, it was demonstrated that EA alleviated CP-induced pain, which was partly achieved by the downregulation of inflammation, oxidative stress, and spinal cord glial activation.
Methods
Rats were castrated and treated with beta-estradiol for 28 days for CP modeling, and EA was initiated one week after. Following three weeks of treatment, pain-related behavioral testing, mechanical withdrawal threshold, and potential histopathological mechanisms were examined.
Purpose
Chronic prostatitis (CP) is a common urinary disease characterized by a complex sequence of symptoms including prostatodynia, which
Results
EA treatment produced a significant antinociceptive effect, effectively increasing the pain threshold of CP rats, and the biochemical results revealed significantly lowered prostatic specific antigen levels. Histopathological results also demonstrated that EA exerted protective properties on prostate morphological changes, as well as decreased inflammation cytokines and oxidative stress molecular expressions in prostate tissue. Furthermore, EA alleviated microglial and astrocyte activation in the dorsal horn of the spinal cord, decreasing CXC motif ligand 1 expressions in activated spinal astrocytes.