Title:The Jiangtang Tongmai Prescription Inhibits Inflammation and Fibrosis
of Lung Fibroblast Autophagy Induced by Hyperglycemia by Regulating
CAV1 Expression
Volume: 24
Issue: 6
Author(s): Nian Ding, Yanbo Fan and Chenghong Zheng*
Affiliation:
- Department of Endocrinology, Wuhan Hospital of Traditional Chinese Medicine, Wuhan,
Hubei 430014, P.R. China
Keywords:
Jiangtang tongmai prescription, CAV1, diabetic lung injury, autophagy, fibrosis, inflammation.
Abstract:
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.
