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ZHENG Ming-xing, LIU Xiao-dong, FAN Shi-cheng. et al. Expression of Nerve Growth Factor and Type 3 of Acid Sensitive Ion Channels in Rat Model of Type Ⅲ Prostatitis[J]. Journal of Sichuan University (Medical Sciences), 2018, 49(1): 39-43.
Citation: ZHENG Ming-xing, LIU Xiao-dong, FAN Shi-cheng. et al. Expression of Nerve Growth Factor and Type 3 of Acid Sensitive Ion Channels in Rat Model of Type Ⅲ Prostatitis[J]. Journal of Sichuan University (Medical Sciences), 2018, 49(1): 39-43.

Expression of Nerve Growth Factor and Type 3 of Acid Sensitive Ion Channels in Rat Model of Type Ⅲ Prostatitis

  • Objective To investigate the expressions of nerve growth factor(NGF)and acid-sensing ion channel 3 (ASIC3) in prostatic tissue of experimental rats with type Ⅲ prostatitis. Methods Thirty SD rats were randomly allocated into control group and experimental group. The rats in control group were subjected to pelvic and bilateral scapular subcutaneous injections of 0.9% sodium chloride, while the rats in experimental group were given pelvic and bilateral scapular subcutaneous injections of mixed suspension of complete Freund’s adjuvant and prostatic tissue to induce autoimmune prostatitis (EAP).Tactile allodynia was quantified using Von-Frey as a measure of pelvic pain behavior. This measurement was performed on 0th, 5th, 10th, 20th, 30th and 40th day in the two groups. After that, the prostate samples were collected and processed for HE staining, while the expressions of NGF and ASIC3 were measured by immunohistochemistry and Western blot. Results Von-Frey filaments measurement showed that pelvis pain in EAP group was significantly more obvious than that in control group. HE staining found lymphocytes and neutrophils infiltrated in the prostate of EAP rats, but no inflammatory cells in the prostate of control group rats. The expressions of NGF and ASIC3 were significantly increased in EAP group when compared with control group (P<0.01). Conclusion The expressions of NGF and ASIC3 in the prostate with EAP were significantly increased, which may be the important mediators of chronic pelvic pain.
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