Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2021 Apr 1:2021:6662261.
doi: 10.1155/2021/6662261. eCollection 2021.

Dahuang Zhechong Pills Suppress Silicosis Fibrosis Progression via p38 MAPK/TGF- β 1/Smad Pathway In Vitro

Affiliations

Dahuang Zhechong Pills Suppress Silicosis Fibrosis Progression via p38 MAPK/TGF- β 1/Smad Pathway In Vitro

Li-Juan Wu et al. Evid Based Complement Alternat Med. .

Abstract

Background: Dahuang Zhechong pills (DHZCP) is a classic Chinese medicinal prescription in "Treatise on Cold Pathogenic and Miscellaneous Diseases (Shanghan Zabing Lun)," and it has the function of tonifying blood, nourishing Yin, and removing blood stasis. Previous studies have shown that DHZCP could alleviate SiO2 induced pulmonary fibrosis in mice. This study aims to further explore the preventive and therapeutic effects of DHZCP against silicosis fibrosis and the underlying mechanisms in vitro.

Methods: We used the experimental model of SiO2-induced MH-S cells to evaluate the therapeutic potential of DHZCP. MH-S cells induced by SiO2 were intervened with the drug-containing serum of DHZCP, and the effects of drug-containing serum of DHZCP on the MH-S cells were detected by CCK8, ELISA, flow cytometry, western blot, and immunofluorescence.

Results: DHZCP improved cell viability by reducing apoptosis. It also decreased the levels of TNF-α, IL-1β, IL-6 in the supernatant of MH-S cells induced by SiO2, inhibited the expression of p38 MAPK, blocked the activation of NF-κB, and controlled the upstream inflammatory response by multiple _targeting. Concomitantly, we observed upregulation of Smad7 and a marked decline in TGF-β1, α-SMA, Smad2, Smad3 expression in MH-S cells treated with DHZCP.

Conclusion: To sum up, we conclude that DHZCP protects against SiO2-induced silicosis by reducing the persistent irritation of inflammation, regulating the p38 MAPK/TGF-β1/Smad pathway.

PubMed Disclaimer

Conflict of interest statement

The authors declare no conflicts of interest.

Figures

Figure 1
Figure 1
Representative chromatograms of reference standard solution and DMS sample. (a) Representative chromatograms of the five compounds in reference standard solution. From top to bottom: amygdalin (500 ng/mL), baicalin (500 ng/mL), catalpol (500 ng/mL), emodin (500 ng/mL), paeoniflorin (500 ng/mL). (b) Representative chromatograms of the five compounds in the DMS sample. From top to bottom: amygdalin, baicalin, catalpol, emodin, paeoniflorin.
Figure 2
Figure 2
DHZCP inhibits apoptosis in MH-S after SiO2 exposure. (a) Two dimensional scatter diagram of 5 groups. (b) Repeat the experiment 3 times and count the total apoptosis rate (%). n = 3, ∗∗∗P < 0.001 VS the NC group, ###P < 0.001 vs. the MC group.
Figure 3
Figure 3
DHZCP regulates the protein expression of the p38 MAPK/TGF-β1/Smad pathway in MH-S cells induced by SiO2. (a) Representative western blot bands of p38 MAPK, p-p38, NF-κB p65, p-p65, TGF-β1, α-SMA, Smad2, Smad3 and Smad7. (b) Quantitation of p38 MAPK, p-p38, NF-κB p65, p-p65, TGF-β1, α-SMA, Smad2, Smad3, and Smad7 in MH-S. The experiment was repeated three times. n = 3. P < 0.05 and ∗∗∗P < 0.001 VS the NC group, #P < 0.05, ##P < 0.01 , and ###P < 0.001 VS the MC group.
Figure 4
Figure 4
DHZCP regulates the protein average optical of p38 MAPK/TGF-β1/Smad pathway in MH-S cells induced by SiO2. Representative immunofluorescence staining of p38 MAPK, NF-κB p65, TGF-β1, α-SMA, Smad2, Smad3, and Smad7 (red) in MH-S. Nuclei were stained with DAPI (the blue mark in the pictures); Scale bar = 20 μm.

Similar articles

Cited by

References

    1. Guo J., Yang Z., Jia Q., Bo C., Shao H., Zhang Z. Pirfenidone inhibits epithelial-mesenchymal transition and pulmonary fibrosis in the rat silicosis model. Toxicology Letters. 2019;300:59–66. doi: 10.1016/j.toxlet.2018.10.019. - DOI - PubMed
    1. Zhang B. N., Xu H., Gao X. M., Zhang G. Z., Zhang X., Yang F. Protective effect of angiotensin (1–7) on silicotic fibrosis in rats. Biomedical and Environmental Sciences: BES. 2019;32(6):419–426. doi: 10.3967/bes2019.057. - DOI - PubMed
    1. Chen S., Yuan J., Yao S., et al. Lipopolysaccharides may aggravate apoptosis through accumulation of autophagosomes in alveolar macrophages of human silicosis. Autophagy. 2015;11(12):2346–2357. doi: 10.1080/15548627.2015.1109765. - DOI - PMC - PubMed
    1. Hoy R. F., Chambers D. C. Silica‐related diseases in the modern world. Allergy. 2020;75(11):2805–2817. doi: 10.1111/all.14202. - DOI - PubMed
    1. Xu T., Yan W., Wu Q., et al. MiR-326 inhibits inflammation and promotes autophagy in silica-induced pulmonary fibrosis through _targeting TNFSF14 and PTBP1. Chemical Research in Toxicology. 2019;32(11):2192–2203. doi: 10.1021/acs.chemrestox.9b00194. - DOI - PubMed

LinkOut - more resources

  NODES
twitter 2