1. Academic Validation
  2. Protective effects of esculentic acid against endotoxic shock in Kunming mice

Protective effects of esculentic acid against endotoxic shock in Kunming mice

  • Int Immunopharmacol. 2014 Nov;23(1):229-35. doi: 10.1016/j.intimp.2014.08.022.
Xiaofeng Niu 1 Qingli Mu 2 Weifeng Li 3 Huan Yao 2 Huani Li 2 Yongmei Li 2 Hua Hu 2 Huimin Huang 2
Affiliations

Affiliations

  • 1 School of Pharmacy, Xi'an Jiaotong University, Xi'an 710061, P.R. China. Electronic address: niuxf@mail.xjtu.edu.cn.
  • 2 School of Pharmacy, Xi'an Jiaotong University, Xi'an 710061, P.R. China.
  • 3 School of Pharmacy, Xi'an Jiaotong University, Xi'an 710061, P.R. China. Electronic address: liwf@mail.xjtu.edu.cn.
Abstract

Esculentic acid (EA), a triterpene compound extracted from the root of Phytolacca esculenta (the Chinese name Shang Lu), has been widely used to therapy a variety of inflammatory diseases such as rheumatoid arthritis, edema, hepatitis and bronchitis. The present study was designed to investigate the protective effects of EA against LPS-induced endotoxic shock by the intraperitoneal injection of EA (1, 5 and 10 mg/kg) prior to LPS stimulation (1 mg/kg, i.p.). We examined the effects of EA on the survival rate of mice, inflammatory cytokine and pro-inflammatory mediator production, histopathological changes and protein expression of COX-2 in tissue sections from lung, liver and kidney. The results indicate that EA not only increases the survival rate of mice, but decreases the levels of TNF-α, IL-6, NO and PGE2 in serum or tissues, histopathological changes and COX-2 protein expression also. Furthermore, EA also increases the levels of anti-inflammatory cytokine IL-10 in serum. Overall, these data suggest that the protective effects of EA against LPS-induced endotoxic shock may be mediated, at least in part, by regulation the release of inflammatory cytokines and mediators, and protein expression of COX-2 in mice.

Keywords

Cyclooxygenase-2; Endotoxic shock; Esculentic acid; Inflammatory cytokines; Pro-inflammatory mediators.

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