Kong Dejia, Fu Ping, Zhang Qin, Ma Xian, Jiang Ping
Department of Chinese Gynecology, Hangzhou Women's Hospital, Hangzhou, Zhejiang 310008, P.R. China.
Department of Chinese Gynecology, The Affiliated Guang-Xing Hospital of Zhejiang Traditional Chinese Medicine University, Hangzhou, Zhejiang 310007, P.R. China.
Exp Ther Med. 2019 Jun;17(6):4687-4692. doi: 10.3892/etm.2019.7498. Epub 2019 Apr 17.
Asiatic acid (AA) is one of the major components of the Chinese herb and exerts a variety of pharmacological activities. However, the pharmacological effects of AA on pelvic inflammatory disease (PID) remain unknown. The purpose of the present study was to investigate the therapeutic efficacy and potential mechanisms of AA on PID in rats. A total of 75 female Sprague Dawley rats were randomly divided into the following five groups: A control group; a PID group; a PID + AA 5 mg/kg group; a PID + AA 35 mg/kg group; and a PID + AA 75 mg/kg group. Changes in cytokine and chemokine levels, myeloperoxidase (MPO) activity, nucleotide-binding domain-like receptor protein 3 (NLRP3) inflammasome and nuclear factor-κB (NF-κB) activation, oxidative stress and cleaved caspase-3 were measured. AA treatment significantly decreased the excessive production of cytokines and chemokines and suppressed MPO activity and the activation of NLRP3 inflammasome, NF-κB and caspase-3, as well as oxidative stress. These results suggest that AA exhibits potent anti-inflammatory and antioxidant effects in rats with pathogen-induced PID and that the mechanism of these anti-inflammatory effects may be associated with the suppression of NLRP3 inflammasome activation and the NF-κB pathway.
齐墩果酸(AA)是中药的主要成分之一,具有多种药理活性。然而,AA对盆腔炎(PID)的药理作用尚不清楚。本研究的目的是探讨AA对大鼠PID的治疗效果及潜在机制。将75只雌性Sprague Dawley大鼠随机分为以下五组:对照组;PID组;PID + AA 5 mg/kg组;PID + AA 35 mg/kg组;以及PID + AA 75 mg/kg组。检测细胞因子和趋化因子水平、髓过氧化物酶(MPO)活性、核苷酸结合寡聚化结构域样受体蛋白3(NLRP3)炎性小体和核因子-κB(NF-κB)的激活、氧化应激和裂解的半胱天冬酶-3的变化。AA治疗显著降低了细胞因子和趋化因子的过量产生,并抑制了MPO活性以及NLRP3炎性小体、NF-κB和半胱天冬酶-3的激活以及氧化应激。这些结果表明,AA在病原体诱导的大鼠PID中表现出强大的抗炎和抗氧化作用,并且这些抗炎作用的机制可能与抑制NLRP3炎性小体激活和NF-κB途径有关。