In vivo and in vitro anti-inflammatory effects of ethanol fraction from Periploca forrestii Schltr.

Li Dong; Yun Zhang; Xia Wang; Yong-xi Dong; Lin Zheng; Yong-jun Li; Jing-man Ni

doi:10.1007/s11655-017-2803-3

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In vivo and in vitro anti-inflammatory effects of ethanol fraction from Periploca forrestii Schltr.

OriginalPaper | Updated：2021-08-27

- In vivo and in vitro anti-inflammatory effects of ethanol fraction from Periploca forrestii Schltr.
- In vivo and in vitro anti-inflammatory effects of ethanol fraction from Periploca forrestii Schltr.
- 中国结合医学杂志（英文版） 2017年23卷第7期页码：528-534
- Affiliations：
  
  1. Key Laboratory of Preclinical Study for New Drugs of Gansu Province, School of Basic Medical Sciences, Lanzhou University,Lanzhou,China
  2. Engineering Research Center for the Development and Application of Ethnic Medicine and Chinese Medicine (Ministry of Education), Guizhou Medical University,Guiyang,China
- Author bio：
- Funds：
  
  Supported by the National Natural Science Foundation of China (No. 81460641, No. 81660691)
- DOI：10.1007/s11655-017-2803-3
  中图分类号：
- 纸质出版日期：2017，
  
  网络出版日期：2017-3-10，
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Dong, L., Zhang, Y., Wang, X. et al. , In vivo and in vitro anti-inflammatory effects of ethanol fraction from Periploca forrestii Schltr.., Chin. J. Integr. Med. 23, 528–534 (2017). https://doi.org/10.1007/s11655-017-2803-3

Li Dong, Yun Zhang, Xia Wang, et al. In vivo and in vitro anti-inflammatory effects of ethanol fraction from Periploca forrestii Schltr.[J]. Chinese Journal of Integrative Medicine, 2017,23(7):528-534.
Dong, L., Zhang, Y., Wang, X. et al. , In vivo and in vitro anti-inflammatory effects of ethanol fraction from Periploca forrestii Schltr.., Chin. J. Integr. Med. 23, 528–534 (2017). https://doi.org/10.1007/s11655-017-2803-3 DOI：

Li Dong, Yun Zhang, Xia Wang, et al. In vivo and in vitro anti-inflammatory effects of ethanol fraction from Periploca forrestii Schltr.[J]. Chinese Journal of Integrative Medicine, 2017,23(7):528-534. DOI： 10.1007/s11655-017-2803-3.

摘要

To determine the anti-inflflammatory effects of an ethanol fraction of Periploca forrestii Schltr. (EFPF) and to investigate the potential mechanisms underlying in vivo and in vitro models. The antiinflflammatory effects of EFPF were evaluated using the xylene-induced mouse ear edema and carrageenan-induced rat paw edema models in vivo. In vitro

RAW264.7 cells were exposed to 0–800 μg/mL EFPF and the cell viability was determined by 3-(4

5-dimethylthiazol-2-yl)-2

5-diphenyltetrazolium bromide (MTT) assay. Then cells were treated with different concentrations of EFPF (100–400 μg/mL) and stimulated with lipopolysaccharide (LPS

1 μg/mL) for 24 h. The supernatant was analyzed for nitric oxide (NO) using the Griess reagent

and the levels of inflflammatory mediators and cytokines were determined using enzyme-linked immunosorbent assays for prostaglandin E2 (PGE2)

tumor necrosis factor α (TNF-α)

interleukin (IL) 6

and IL-10. The protein expressions of inducible NO synthase (iNOS)

cyclooxygenase-2 (COX-2)

nuclear factor κB (NF-κB)

and mitogen-activated protein kinases (MAPKs) including extracellular signal-regulated kinase (ERK)

c-Jun N-terminal kinase (JNK)

and p38 MAPK were examined by Western blot. Compared with the control group

EFPF signifificantly reduced mouse ear edema and rat paw edema rate (P<0.05 or P<0.01). Compared with the LPS group

EFPF signifificantly inhibited the LPS-stimulated production of NO

PGE2

TNF-α and IL-6 (P<0.05 or P<0.01)

and increased the IL-10 production (P<0.05). EFPF also signifificantly inhibited LPS-induced protein expressions of iNOS and COX-2

suppressed the phosphorylation and degradation of inhibitor of NF-κB-α

decreased p65 level

and inhibited the phosphorylation of p38

ERK1/2 and JNK P<0.05 or P<0.01). EFPF exerted anti-inflflammatory effect by reducing protein expressions of iNOS and COX-2 and the production of the inflflammation factors

including TNF-α

IL-6

NO and PGE2

mainly through inhibition of LPS-mediated stimulation of NF-κB and MAPK signaling pathways.

Abstract

RAW264.7 cells were exposed to 0–800 μg/mL EFPF and the cell viability was determined by 3-(4

5-dimethylthiazol-2-yl)-2

5-diphenyltetrazolium bromide (MTT) assay. Then cells were treated with different concentrations of EFPF (100–400 μg/mL) and stimulated with lipopolysaccharide (LPS

1 μg/mL) for 24 h. The supernatant was analyzed for nitric oxide (NO) using the Griess reagent

and the levels of inflflammatory mediators and cytokines were determined using enzyme-linked immunosorbent assays for prostaglandin E2 (PGE2)

tumor necrosis factor α (TNF-α)

interleukin (IL) 6

and IL-10. The protein expressions of inducible NO synthase (iNOS)

cyclooxygenase-2 (COX-2)

nuclear factor κB (NF-κB)

and mitogen-activated protein kinases (MAPKs) including extracellular signal-regulated kinase (ERK)

c-Jun N-terminal kinase (JNK)

and p38 MAPK were examined by Western blot. Compared with the control group

EFPF signifificantly reduced mouse ear edema and rat paw edema rate (P<0.05 or P<0.01). Compared with the LPS group

EFPF signifificantly inhibited the LPS-stimulated production of NO

PGE2

TNF-α and IL-6 (P<0.05 or P<0.01)

and increased the IL-10 production (P<0.05). EFPF also signifificantly inhibited LPS-induced protein expressions of iNOS and COX-2

suppressed the phosphorylation and degradation of inhibitor of NF-κB-α

decreased p65 level

and inhibited the phosphorylation of p38

ERK1/2 and JNK P<0.05 or P<0.01). EFPF exerted anti-inflflammatory effect by reducing protein expressions of iNOS and COX-2 and the production of the inflflammation factors

including TNF-α

IL-6

NO and PGE2

mainly through inhibition of LPS-mediated stimulation of NF-κB and MAPK signaling pathways.

关键词

Periploca forrestii Schltr.anti-inflflammatory effectmitogen-activated protein kinasenuclear factor κB

Keywords

Periploca forrestii Schltr.anti-inflflammatory effectmitogen-activated protein kinasenuclear factor κB

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