Sangxingtang inhibits the inflammation of LPS-induced acute lung injury in mice by down-regulating the MAPK/NF-κB pathway.
10.1016/S1875-5364(15)30094-7
- Author:
Tian-Zhu ZHANG
1
,
2
;
Shi-Hai YANG
3
;
Jin-Fu YAO
4
;
Juan DU
5
;
Tian-Hua YAN
6
Author Information
1. School of Pharmaceutical Sciences, Changchun University of Chinese Medicine, Changchun 130117, China
2. College of Chinese Medicinal Materials, Jilin Agricultural University, Changchun 130118, China.
3. College of Chinese Medicinal Materials, Jilin Agricultural University, Changchun 130118, China. Electronic address: zhangtz452@126.com.
4. School of Pharmaceutical Sciences, Changchun University of Chinese Medicine, Changchun 130117, China.
5. School of Life Science, Peking University, Beijing 100871, China.
6. Department of Physiology and Pharmacology, China Pharmaceutical University, Nanjing, 210009, China.
- Publication Type:Journal Article
- Keywords:
Inflammation;
LPS-induced acute lung injury;
MAPK/NF-κB pathway;
Sangxingtang
- MeSH:
Acute Lung Injury;
drug therapy;
enzymology;
genetics;
immunology;
Animals;
Anti-Inflammatory Agents;
administration & dosage;
Down-Regulation;
drug effects;
Drugs, Chinese Herbal;
administration & dosage;
Female;
Humans;
Lipopolysaccharides;
adverse effects;
Mice;
Mice, Inbred BALB C;
Mitogen-Activated Protein Kinases;
genetics;
immunology;
Signal Transduction;
drug effects;
Tumor Necrosis Factor-alpha;
genetics;
immunology
- From:
Chinese Journal of Natural Medicines (English Ed.)
2015;13(12):889-895
- CountryChina
- Language:English
-
Abstract:
In the present study, we investigated anti-inflammatory effects of Sangxingtang (SXT) on acute lung injury using a lipopolysaccharide (LPS)-induced acute lung injury (ALI) mouse model. The cell counting in the bronchoalveolar lavage fluid (BALF) was performed. The degree of lung edema was evaluated by measuring the wet/dry weight (W/D) ratio. The superoxidase dismutase (SOD) and myeloperoxidase (MPO) activities were assayed by SOD and MPO kits, respectively. The levels of inflammatory mediators, including tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6), were assayed by the enzyme-linked immunosorbent assay methods. Pathological changes of lung tissues were observed by Hematoxylin and eosin (HE) staining. The inflammatory signaling pathway-related proteins nuclear factor mitogen activated protein kinases (P38MAPK), extracellular regulated protein kinases (Erk), c-Jun N-terminal kinase (Jnk) and nuclear transcription factor (NF-κB) p65 expressions were measured by Western blotting. Our results showed that the treatment with the SXT markedly attenuated the inflammatory cell numbers in the BALF, decreased the levels of P-P38MAPK, P-Erk, P-Jnk and P-NF-κB p65 and the total protein levels in lungs, improved the SOD activity and inhibited the MPO activity. Histological studies demonstrated that SXT substantially reduced the LPS-induced neutrophils in lung tissues, compared with the untreated LPS group. In conclusion, our results indicated that SXT had protective effects on LPS-induced ALI in mice.
