Butorphanol alleviates lipopolysaccharide‑induced inflammation and apoptosis of cardiomyocytes via activation of the κ‑opioid receptor
- Weiqing Tang
- Liu Luo
- Baoji Hu
- Mingzhi Zheng
Affiliations: Department of Anesthesiology, Shanghai Pudong Hospital, Fudan University Pudong Medical Center, Shanghai 201399, P.R. China, Department of Anesthesiology, The Affiliated Zhuzhou Hospital of Xiangya School of Medicine, Central South University, Zhuzhou Central Hospital, Zhuzhou, Hunan 412000, P.R. China
- Published online on: September 2, 2021 https://doi.org/10.3892/etm.2021.10683
Copyright: © Tang
et al. This is an open access article distributed under the
terms of Creative
Commons Attribution License.
Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )
This article is mentioned in:
Sepsis‑induced myocardial dysfunction is a leading cause of the high mortality rates associated with sepsis. The aim of the present study was to investigate the effect of butorphanol on sepsis‑induced cardiomyocyte dysfunction. Lipopolysaccharide (LPS) was used to induce H9C2 cardiomyocytes to establish an in vitro sepsis model. The effect of butorphanol on the viability of LPS‑induced H9C2 cells was analyzed using a Cell Counting Kit‑8 assay. The levels of tumor necrosis factor‑α, interleukin (IL)‑1β and IL‑6 were detected using ELISA. Western blotting was used to analyze the expression levels of inflammation‑and apoptosis‑related proteins. Cell apoptosis was measured using a TUNEL assay. The expression levels of κ‑opioid receptor (KOR) were analyzed using reverse transcription‑quantitative PCR analysis and western blotting. Following LPS induction, the levels of inflammatory cytokines and proapoptotic proteins were found to be upregulated in H9C2 cells, while butorphanol treatment downregulated these levels. The expression levels of KOR were also upregulated following butorphanol treatment in LPS‑induced H9C2 cells. Addition of the KOR inhibitor, nor‑binaltorphimine, alleviated the inhibitory effects of butorphanol on inflammation and apoptosis in LPS‑induced H9C2 cells. In conclusion, the findings of the present study provided evidence indicating that butorphanol may alleviate LPS‑induced inflammation and apoptosis in cardiomyocytes by upregulating KOR expression, which may provide a novel insight into the potential therapeutic effects of butorphanol and its underlying mechanism of action.