In vitro and in vivo antiseptic activities of caffeoylquinic acid

Yanfeng Liu,Kai Li,Zhaojie Li,Xin Shang,Mingzhi Long

doi:10.4314/tjpr.v17i8.27

Abstract

Purpose: To evaluate the antiseptic effect of caffeoylquinic acid (CA) in in vivo and in vitro models.Methods: In vivo sepsis was produced in rats via cecal ligation and puncture (CLP) method. Four groups of rats were used: control group, untreated CLP group, and two CA groups treated with caffeoylquinic acid (50 and 100 mg/kg, p.o.) for 30 days before the induction of sepsis. Following the induction of sepsis, histological assessment of lung tissue was carried out using hematoxylin and eosin, and isolectin B4 staining. In addition, in vitro tests were performed on RAW264.7 cells in which inflammation and oxidative stress were induced by lipopolysaccharide (LPS).Results: Treatment with CA significantly (p < 0.05) enhanced the survival of lung cells, relative to the CLP group. Lung histopathology revealed that pretreatment with CA did not attenuate the increased infiltration of macrophages in the alveoli. Results from in vitro studies showed that CA attenuated LPS-induced nitric oxide (NO) levels, but had no significant effect on the level of LPS-induced pro-inflammatory cytokines in RAW264.7 cells (p < 0.05).Conclusion: These results reveal that CA attenuates NO and TNF-α levels in LPS-stimulated macrophages, thereby decreasing inflammation-associated sepsis. Thus, CA may have beneficial effects on lung injury as a result of its antioxidant and anti-inflammatory activities.Keywords: Caffeoylquinic acid, Sepsis, Oxidative stress, Cytokines, Cecalligation, Puncture

Highlights

Sepsis is an inflammation that occurs due to microbial infection
It was observed that the cecal ligation and puncture (CLP) group showed infiltration of interstitial zone, and increased inflammation that caused enhancement of thickness of the alveolar septa (Figure 1b)
The result of this study reveals that treatment of RAW264.7 cells with caffeoylquinic acid (CA) in presence of LPS did not alter the level of tumor necrosis factor α (TNF-α) and thereby produces its anti-inflammatory property in septic shock condition

Summary

INTRODUCTION

Sepsis is an inflammation that occurs due to microbial infection. It is one of the major causes of death [1]. Studies have shown that LPS promotes sepsis condition in infection caused by gram negative bacteria by stimulating inflammation in macrophages. All of the animals received volume resuscitation with both intravenous and intraperitoneal saline (4 mL/100 g of body weight) Thereafter, they were placed in cages and allowed free access to normal standard chow and water. The tissue sections were rinsed with PBS, and incubated with 3,3-diaminobenzidine (DAB) substrate for 5 min for the visualization of sites containing macrophage-bound peroxidase-lectin conjugates. They were thereafter mounted in EntellanNeu after counterstaining with thionine. Griess reagent was added a to equal amount of cell culture and the resultant solution was incubated at room temperature for 10 min. The absorbance of the solution was read at 540 nm in an ELISA test reader

RESULTS

DISCUSSION

Conflict of interest