The Jiangtang Tongmai Prescription inhibits inflammation and fibrosis of lung fibroblast autophagy induced by hyperglycemia by regulating CAV1 expression
Chenghong Zheng, Nian Ding, Yanbo Fan- Immunology and Allergy
- Endocrinology, Diabetes and Metabolism
Objective:
The lung is one of the target organs of diabetes. This study aimed to probe the protective mechanism of Jiangtang Tongmai Prescription (JTTMP) against diabetic lung injury.
Methods:
JTTMP-containing serum was collected, and a high glucose and high-fat diabetic cell model was established. The cells were treated with a drug-containing serum or a CAV1-associated vector. Transfection efficiency was measured by qRT-PCR and western blot, the cell proliferative capacity was tested by CCK-8 assay, and the expression of autophagosome marker LC3B was measured by immunophluorescence assay. Expression levels of the autophagy markers LC3B, p62, and Beclin-1, and the expression levels of the fibrosis markers α-SMA, FN-1, and TGF-β1 were determined by western blot, and the levels of inflammatory factors TNF-α and IL-1β in the supernatants were assessed by ELISA.
Results:
In high glucose and high fat-induced MRC-5 cells, JTTMP-containing serum impeded the abnormal cell proliferation and the expression levels of autophagy markers, fibrosis markers, as well as inflammatory factors. CAV1 expression was decreased in MRC-5 cells treated with JTTMP-containing serum. In MRC-5 cells upon transfection with the CAV1 overexpression vector and treatment with JTTMP-containing serum, increased cell proliferation, increased LC3B, p62, Beclin-1, α-SMA, FN-1, and TGF-β1, TNF-α, and IL-1β levels were found compared with cells treated with JTTMP-containing serum alone.
Conclusion:
This study suggests that JTTMP suppresses CAV1 expression to attenuate diabetic lung injury by reducing abnormal proliferation and autophagy, and reducing levels of fibrosis and inflammation.