Open Access

Honokiol inhibits endoplasmic reticulum stress‑associated lipopolysaccharide-induced inflammation and apoptosis in bovine endometrial epithelial cells

  • Authors:
    • Wenshu Chen
    • Jieli Wu
    • Sisi Zhan
    • Xiaojie Lu
  • View Affiliations

  • Published online on: October 22, 2021     https://doi.org/10.3892/etm.2021.10911
  • Article Number: 1476
  • Copyright: © Chen et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

Honokiol (HKL) has been previously reported to exert anti-inflammatory effects in numerous diseases. However, the role of HKL in endometritis remains unclear. The present study aimed to explore and elucidate the role of HKL in a lipopolysaccharide (LPS)-induced in vitro model of endometritis. Bovine endometrial epithelial cells (bEECs) were pre-treated with HKL at doses of 1, 10 and 20 µM, followed by 1 µg/ml LPS. MTT assay was then used to detect cell viability. ELISA was utilized to measure the levels of the proinflammatory cytokines TNF-α, IL-1β and IL-6 in bEECs culture supernatants. Reverse transcription-quantitative PCR was further performed to examine the mRNA expression levels of these cytokines. Cell apoptosis was observed by TUNEL staining and the levels of Bcl-2, Bax, cleaved caspase 3 and cleaved caspase 9 were assayed by western blotting. Western blotting was also performed to detect the expression levels of endoplasmic reticulum (ER) stress-related proteins activating transcription factor 6, CCAAT-enhancer-binding protein homologous protein, inositol-requiring enzyme 1 and cleaved caspase 12 in bEECs. LPS treatment reduced cell viability and HKL treatment improved the viability of bEECs after LPS treatment. The LPS-induced inflammatory response and apoptosis in bEECs were also inhibited by HKL treatment. Additionally, the increased expression of ER stress-related proteins induced by LPS was reversed by HKL treatment. Following stimulation with the ER stress inducer tunicamycin, it was revealed that HKL attenuated ER stress and inhibited LPS-induced inflammatory response and apoptosis in bEECs. In summary, HKL inhibited ER stress associated with LPS-induced inflammation and apoptosis in bEECs, providing evidence that HKL can serve to be a novel agent for the treatment of endometritis.
View Figures
View References

Related Articles

Journal Cover

December-2021
Volume 22 Issue 6

Print ISSN: 1792-0981
Online ISSN:1792-1015

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Chen W, Wu J, Zhan S and Lu X: Honokiol inhibits endoplasmic reticulum stress‑associated lipopolysaccharide-induced inflammation and apoptosis in bovine endometrial epithelial cells. Exp Ther Med 22: 1476, 2021
APA
Chen, W., Wu, J., Zhan, S., & Lu, X. (2021). Honokiol inhibits endoplasmic reticulum stress‑associated lipopolysaccharide-induced inflammation and apoptosis in bovine endometrial epithelial cells. Experimental and Therapeutic Medicine, 22, 1476. https://doi.org/10.3892/etm.2021.10911
MLA
Chen, W., Wu, J., Zhan, S., Lu, X."Honokiol inhibits endoplasmic reticulum stress‑associated lipopolysaccharide-induced inflammation and apoptosis in bovine endometrial epithelial cells". Experimental and Therapeutic Medicine 22.6 (2021): 1476.
Chicago
Chen, W., Wu, J., Zhan, S., Lu, X."Honokiol inhibits endoplasmic reticulum stress‑associated lipopolysaccharide-induced inflammation and apoptosis in bovine endometrial epithelial cells". Experimental and Therapeutic Medicine 22, no. 6 (2021): 1476. https://doi.org/10.3892/etm.2021.10911