» Articles » PMID: 38356488

Chlorogenic Acid Inhibits Progressive Pulmonary Fibrosis in a Diabetic Rat Model

Overview
Authors
Affiliations
Soon will be listed here.
Abstract

Background: Chlorogenic acid (CGA) is known to have antifibrotic and hypoglycemic effects and may play a role in preventing diabetes-induced pulmonary fibrosis. This study aimed to determine the effect and optimum dose of CGA on diabetes-induced pulmonary fibrosis.

Methods: Thirty Wistar rats (two-month-old, 150-200 grams) were randomly divided into six groups, namely control, six weeks diabetes mellitus (DM1), eight weeks DM (DM2), and three DM2 groups (CGA1, CGA2, and CGA3) who received CGA doses of 12.5, 25, and 50 mg/Kg BW, respectively. After six weeks, CGA was administered intraperitoneally for 14 consecutive days. Lung tissues were taken for TGF-β1, CTGF, SMAD7, Collagen-1, and α-SMA mRNA expression analysis and paraffin embedding. Data were analyzed using one-way ANOVA and the Kruskal-Wallis test. P<0.05 was considered statistically significant.

Results: TGF-β1 expression in the CGA1 group (1.01±0.10) was lower than the DM1 (1.33±0.25, P=0.05) and DM2 (1.33±0.20, P=0.021) groups. α-SMA expression in the CGA1 group (median 0.60, IQR: 0.34-0.64) was lower than the DM1 (median 0.44, IQR: 0.42-0.80) and DM2 (median 0.76, IQR: 0.66-1.10) groups. Collagen-1 expression in the CGA1 group (0.75±0.13) was lower than the DM1 (P=0.24) and DM2 (P=0.26) groups, but not statistically significant. CTGF expression in CGA groups was lower than the DM groups (P=0.088), but not statistically significant. There was an increase in SMAD7 expression in CGA groups (P=0.286). Histological analysis showed fibrosis improvement in the CGA1 group compared to the DM groups.

Conclusion: CGA (12.5 mg/Kg BW) inhibited the expression of profibrotic factors and increased antifibrotic factors in DM-induced rats.

References
1.
Rout-Pitt N, Farrow N, Parsons D, Donnelley M . Epithelial mesenchymal transition (EMT): a universal process in lung diseases with implications for cystic fibrosis pathophysiology. Respir Res. 2018; 19(1):136. PMC: 6052671. DOI: 10.1186/s12931-018-0834-8. View

2.
Wang D, Ma Y, Tong X, Zhang Y, Fan H . Diabetes Mellitus Contributes to Idiopathic Pulmonary Fibrosis: A Review From Clinical Appearance to Possible Pathogenesis. Front Public Health. 2020; 8:196. PMC: 7285959. DOI: 10.3389/fpubh.2020.00196. View

3.
Upadhyay S, Dixit M . Role of Polyphenols and Other Phytochemicals on Molecular Signaling. Oxid Med Cell Longev. 2015; 2015:504253. PMC: 4477245. DOI: 10.1155/2015/504253. View

4.
Bai L, Zhang L, Pan T, Wang W, Wang D, Turner C . Idiopathic pulmonary fibrosis and diabetes mellitus: a meta-analysis and systematic review. Respir Res. 2021; 22(1):175. PMC: 8188656. DOI: 10.1186/s12931-021-01760-6. View

5.
Bagdas D, Etoz B, Inan Ozturkoglu S, Cinkilic N, Ozyigit M, Gul Z . Effects of systemic chlorogenic acid on random-pattern dorsal skin flap survival in diabetic rats. Biol Pharm Bull. 2014; 37(3):361-70. DOI: 10.1248/bpb.b13-00635. View