Journal of Traditional Chinese Medicine ›› 2026, Vol. 46 ›› Issue (4): 779-787.DOI: 10.19852/j.cnki.jtcm.2026.04.001
• Original Articles • Next Articles
Paeonol’s protective effects on H9C2 cells against hypoxia/ reoxygenation injury through the hypoxia-inducible factor 1-alpha/B-cell lymphoma-2/adenovirus E1B 19 kDa interacting protein 3 signaling pathway
ZHAO Chengguo, YIN Meifang, ZHOU Menghan, QIN Shuzhi(
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College of Life Science ,Zhuhai College of Science and Technology Zhuhai 519041, China
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Received:2025-08-19Accepted:2026-01-30Online:2026-08-15Published:2026-08-08 -
Contact:Prof. QIN Shuzhi, College of Life Science, Zhuhai College of Science and Technology, Zhuhai 519041, China. qsz@zcst.edu.cn, Telephone: +86-13631282998
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Supported by:Characteristic Innovation Project of Ordinary Colleges and Universities in Guangdong: Exploring the Mechanism of Paeoniflorin Against Myocardial Ischemia-reperfusion Injury Based on the Phosphatase and Tensin Homolog-induced Putative Kinase 1/Parkin Signaling Pathway(2018KTSCX307);Research Capacity Enhancement Project for Key Construction Disciplines of Guangdong Province: Study on the Pharmacological Effects and Molecular Mechanisms of Traditional Chinese Medicine Against Atherosclerosis Based on the Theory of "Li Shi Hua Zhuo"(2025ZDJS115);Tri-level Talents Development Project of Zhuhai College of Science and Technology
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ZHAO Chengguo, YIN Meifang, ZHOU Menghan, QIN Shuzhi. Paeonol’s protective effects on H9C2 cells against hypoxia/ reoxygenation injury through the hypoxia-inducible factor 1-alpha/B-cell lymphoma-2/adenovirus E1B 19 kDa interacting protein 3 signaling pathway[J]. Journal of Traditional Chinese Medicine, 2026, 46(4): 779-787.
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Figure 1 Impact of PAE on cell viability in H9C2 cells A: the cytotoxic effect of PAE at different concentrations (0, 1, 5, 10, 20, 40, 80, 160 μmol/L) on H9C2 cells was assessed by CCK8; B: effect of PAE on H/R-impaired cell viability was also tested by CCK8. Control group: cells were treated with vehicle; H/R + PAE: cells were treated with 12 h-hypoxia/12 h-reoxygenation and various concentrations (0, 1, 5, 10, 20, 40, 80, 160 μmol/L) of PAE. PAE: paeonol; CCK8: cell counting kit-8; H/R: hypoxia/reoxygenation. Statistical analyses were measured using unpaired t test (A) and one-way analysis of variance (B). Data are presented as mean ± standard error of the mean (n = 5). aP < 0.01, vs Control group; bP < 0.01, vs H/R group.
Figure 1 Impact of PAE on cell viability in H9C2 cells A: the cytotoxic effect of PAE at different concentrations (0, 1, 5, 10, 20, 40, 80, 160 μmol/L) on H9C2 cells was assessed by CCK8; B: effect of PAE on H/R-impaired cell viability was also tested by CCK8. Control group: cells were treated with vehicle; H/R + PAE: cells were treated with 12 h-hypoxia/12 h-reoxygenation and various concentrations (0, 1, 5, 10, 20, 40, 80, 160 μmol/L) of PAE. PAE: paeonol; CCK8: cell counting kit-8; H/R: hypoxia/reoxygenation. Statistical analyses were measured using unpaired t test (A) and one-way analysis of variance (B). Data are presented as mean ± standard error of the mean (n = 5). aP < 0.01, vs Control group; bP < 0.01, vs H/R group.
Figure 2 Effect of PAE on apoptosis in H/R-injured H9C2 cells A: the apoptosis rate of H9C2 cells was measured via flow cytometry. B: apoptosis rate of quantitative analysis; C: expression of cleaved caspase-3 was surveyed via Western blot; D: cleaved caspase-3 level of quantitative analysis; E: expression of Bax/Bcl-2 ratio was surveyed via Western blot; F: the Bax/Bcl-2 ratio of quantitative analysis; G: the ROS content in H9C2 cells was detected via flow cytometry; A1, G1: Control group; A2, G2: H/R group; A3, G3: H/R + PAE group; A4, G4: PAE group; H: ROS content of quantitative analysis. Control group: cells were treated with vehicle; H/R group: cells were treated with 12 h-hypoxia/12 h-reoxygenation; H/R+PAE group: cells were treated with 12 h-hypoxia/12 h-reoxygenation and 10 μmol/L Paeonol; PAE group: cells were treated with 10 μmol/L Paeonol. PAE: paeonol; H/R: hypoxia/reoxygenation; Bax: B-cell lymphoma 2-associated X protein; Bcl-2: B-cell lymphoma 2; ROS: reactive oxygen species. Statistical analyses were measured using one-way analysis of variance. Data are presented as mean ± standard error of the mean (n = 3). aP < 0.01 vs Control group; bP < 0.01 vs H/R group.
Figure 2 Effect of PAE on apoptosis in H/R-injured H9C2 cells A: the apoptosis rate of H9C2 cells was measured via flow cytometry. B: apoptosis rate of quantitative analysis; C: expression of cleaved caspase-3 was surveyed via Western blot; D: cleaved caspase-3 level of quantitative analysis; E: expression of Bax/Bcl-2 ratio was surveyed via Western blot; F: the Bax/Bcl-2 ratio of quantitative analysis; G: the ROS content in H9C2 cells was detected via flow cytometry; A1, G1: Control group; A2, G2: H/R group; A3, G3: H/R + PAE group; A4, G4: PAE group; H: ROS content of quantitative analysis. Control group: cells were treated with vehicle; H/R group: cells were treated with 12 h-hypoxia/12 h-reoxygenation; H/R+PAE group: cells were treated with 12 h-hypoxia/12 h-reoxygenation and 10 μmol/L Paeonol; PAE group: cells were treated with 10 μmol/L Paeonol. PAE: paeonol; H/R: hypoxia/reoxygenation; Bax: B-cell lymphoma 2-associated X protein; Bcl-2: B-cell lymphoma 2; ROS: reactive oxygen species. Statistical analyses were measured using one-way analysis of variance. Data are presented as mean ± standard error of the mean (n = 3). aP < 0.01 vs Control group; bP < 0.01 vs H/R group.
Figure 3 Effect of PAE and 3-MA on the autophagy flux and apoptosis induced by H/R injury in H9C2 cells A: the viability of PAE and 3-MA on H9C2 cells was measured by CCK8; B: the apoptosis rate of PAE and 3-MA on H9C2 cells was tested by flow cytometry; B1: Control group; B2: PAE group; B3: 3-MA group; B4: H/R group; B5: H/R + PAE group; B6: H/R + 3-MA group; B7: H/R + PAE + 3-MA group; C: apoptosis rate of quantitative analysis. Control group: cells were treated with vehicle; PAE group: cells were treated with 10 μmol/L Paeonol; 3-MA group: cells were treated with 5 mmol/L 3-Methyladenine; H/R group: cells were treated with 12 h-hypoxia/12 h-reoxygenation; H/R + PAE group: cells were treated with 12 h-hypoxia/12 h-reoxygenation and 10 μmol/L Paeonol; H/R + 3-MA group: cells were treated with 12 h-hypoxia/12 h-reoxygenation and 5 mmol/L 3-Methyladenine; H/R + PAE + 3-MA group: cells were treated with 12 h-hypoxia/12 h-reoxygenation, 10 μmol/L Paeonol and 5 mmol/L 3-Methyladenine. PAE: paeonol; H/R: hypoxia/reoxygenation; CCK8: cell counting kit-8; 3-MA: 3-methyladenine. Statistical analyses were measured using one-way analysis of variance. Data are presented as mean ± standard error of the mean (n = 3). aP < 0.01, vs Control group; bP <0.01, vs H/R group; cP < 0.01, vs H/R + PAE group.
Figure 3 Effect of PAE and 3-MA on the autophagy flux and apoptosis induced by H/R injury in H9C2 cells A: the viability of PAE and 3-MA on H9C2 cells was measured by CCK8; B: the apoptosis rate of PAE and 3-MA on H9C2 cells was tested by flow cytometry; B1: Control group; B2: PAE group; B3: 3-MA group; B4: H/R group; B5: H/R + PAE group; B6: H/R + 3-MA group; B7: H/R + PAE + 3-MA group; C: apoptosis rate of quantitative analysis. Control group: cells were treated with vehicle; PAE group: cells were treated with 10 μmol/L Paeonol; 3-MA group: cells were treated with 5 mmol/L 3-Methyladenine; H/R group: cells were treated with 12 h-hypoxia/12 h-reoxygenation; H/R + PAE group: cells were treated with 12 h-hypoxia/12 h-reoxygenation and 10 μmol/L Paeonol; H/R + 3-MA group: cells were treated with 12 h-hypoxia/12 h-reoxygenation and 5 mmol/L 3-Methyladenine; H/R + PAE + 3-MA group: cells were treated with 12 h-hypoxia/12 h-reoxygenation, 10 μmol/L Paeonol and 5 mmol/L 3-Methyladenine. PAE: paeonol; H/R: hypoxia/reoxygenation; CCK8: cell counting kit-8; 3-MA: 3-methyladenine. Statistical analyses were measured using one-way analysis of variance. Data are presented as mean ± standard error of the mean (n = 3). aP < 0.01, vs Control group; bP <0.01, vs H/R group; cP < 0.01, vs H/R + PAE group.
Figure 4 Effect of PAE and siHIF-1α interference on H/R-induced autophagy flux and apoptosis in H9C2 cells A: expression of the HIF-1α was evaluated by Western blot; B: HIF-1α expression of quantitative analysis; C: expression of the BNIP3 was evaluated by Western blot; D: BNIP3 expression of quantitative analysis; E: expression of the LC3 was evaluated by Western blot; F: LC3 expression of quantitative analysis; G: expression of the p62 was evaluated by Western blot; H: p62 expression of quantitative analysis; I: the apoptosis rate of H9C2 cells was measured by flow cytometry; I1: Control group; I2: H/R group; I3: H/R + PAE; I4: H/R + siNC + PAE; I5: H/R + siHIF-1α + PAE; J: apoptosis rate of quantitative analysis. Control group: cells were treated with vehicle; H/R group: cells were treated with 12 h-hypoxia/12 h-reoxygenation; H/R + PAE group: cells were treated with 12 h-hypoxia/12 h-reoxygenation and 10 μmol/L Paeonol; H/R + siNC + PAE: after siNC transfection, cells were treated with 10 μmol/L Paeonol; H/R + siHIF-1α + PAE: after siHIF-1α transfection, cells were treated with 10 μmol/L Paeonol. PAE: paeonol; H/R: hypoxia/reoxygenation; HIF-1α: hypoxia-inducible factor 1-alpha; BNIP3: B-cell lymphoma-2/adenovirus E1B 19 kDa interacting protein 3; LC3: microtubule-associated protein 1 light chain 3; p62: sequestosome-1; siNC: small interfering RNA negative control. Statistical analyses were measured using one-way analysis of variance. Data are presented as mean ± standard error of the mean (n = 3). aP < 0.01 vs Control group; bP < 0.01 vs H/R group; cP < 0.01 vs H/R + siNC + PAE group.
Figure 4 Effect of PAE and siHIF-1α interference on H/R-induced autophagy flux and apoptosis in H9C2 cells A: expression of the HIF-1α was evaluated by Western blot; B: HIF-1α expression of quantitative analysis; C: expression of the BNIP3 was evaluated by Western blot; D: BNIP3 expression of quantitative analysis; E: expression of the LC3 was evaluated by Western blot; F: LC3 expression of quantitative analysis; G: expression of the p62 was evaluated by Western blot; H: p62 expression of quantitative analysis; I: the apoptosis rate of H9C2 cells was measured by flow cytometry; I1: Control group; I2: H/R group; I3: H/R + PAE; I4: H/R + siNC + PAE; I5: H/R + siHIF-1α + PAE; J: apoptosis rate of quantitative analysis. Control group: cells were treated with vehicle; H/R group: cells were treated with 12 h-hypoxia/12 h-reoxygenation; H/R + PAE group: cells were treated with 12 h-hypoxia/12 h-reoxygenation and 10 μmol/L Paeonol; H/R + siNC + PAE: after siNC transfection, cells were treated with 10 μmol/L Paeonol; H/R + siHIF-1α + PAE: after siHIF-1α transfection, cells were treated with 10 μmol/L Paeonol. PAE: paeonol; H/R: hypoxia/reoxygenation; HIF-1α: hypoxia-inducible factor 1-alpha; BNIP3: B-cell lymphoma-2/adenovirus E1B 19 kDa interacting protein 3; LC3: microtubule-associated protein 1 light chain 3; p62: sequestosome-1; siNC: small interfering RNA negative control. Statistical analyses were measured using one-way analysis of variance. Data are presented as mean ± standard error of the mean (n = 3). aP < 0.01 vs Control group; bP < 0.01 vs H/R group; cP < 0.01 vs H/R + siNC + PAE group.
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