The clinical efficacy and mechanism of Shenfu injection combined with azithromycin on infantile mycoplasma pneumonia
- Author:
Jun ZHANG
1
Author Information
- Publication Type:Journal Article
- Keywords: Azithromycin; Infantile mycoplasma pneumonia; MiR-181a; Shenfu injection; T cell subset
- From: Journal of Xi'an Jiaotong University(Medical Sciences) 2019;40(6):1012-1017
- CountryChina
- Language:Chinese
- Abstract: Objective: To evaluate the clinical efficacy and molecular mechanism of Shenfu combined with azithromycin on infantile mycoplasma pneumonia. Methods: Totally 80 children with mycoplasma pneumonia treated in Children's Hospital Affiliated to Soochow University from June 2016 to June 2017 were selected and randomly divided into two groups with 40 in each. Azithromycin was provided in both groups. Shenfu was administered in the observation group. The clinical efficacy, immunological functions and miR-181a level, and related molecular markers of all the subjects were observed. Lentivirus was used to transfer miR-181a into human T lymphocytes to observe its effects on lymphocyte proliferation, cytokine secretion level and related signaling pathways. Results: Compared with the normal group after treatment, the clinical efficacy, T lymphocyte subset proportion and inflammation cytokines were significantly increased (P<0.05), and the time of clinical symptoms remission was significantly decreased in the observation group after treatment (P<0.05). In addition, the content of miR-181a (9.3±5.3) in lymphocytes of the observation group after treatment was significantly lower than that (12.2±4.5) of the control group after treatment (P<0.05). In vitro assay revealed that miR-181a was significantly decreased lymphocyte proliferation and the ability of secretory cytokine. Luciferase reporter assay demonstrated that miR-181a could inhibit KRAS, NRAS and MAPK1 expressions, thus down-regulating P-AKT and P-MEK phosphorylation. Conclusion: Shenfu combined with azithromycin can effectively improve immunity functions and its mechanism might be related to the level of miR-181a in lymphocytes.
