Scholarlink

<p>Cervical cancer remains a major cause of mortality among women worldwide. Natural products provide anticancer leads with comparatively low toxicity. Bavachinin, a flavanone from <i>Psoralea corylifolia</i>, has documented bioactivities, yet its mechanisms in cervical cancer remain unclear. To determine whether bavachinin suppresses HeLa cell survival by inducing oxidative-stress–driven mitochondrial apoptosis and by downregulating NF-κB-regulated inflammatory signaling. Cytotoxicity across 5–40&#xa0;µM was quantified by MTT. Oxidative stress and antioxidant status were assessed by TBARS and reduced glutathione (GSH). Apoptotic indices were evaluated by intracellular ROS generation, loss of mitochondrial membrane potential (ΔΨm), lactate dehydrogenase (LDH) release, AO/PI staining, Annexin V/PI flow cytometry, and DNA damage analyses. mRNA levels of NF-κB p65, TNF-α, IL-6, Bcl-2, and Bax <b>were</b> measured by quantitative RT-PCR. One-way ANOVA analyzed data with appropriate post hoc testing. Bavachinin decreased cervical cancer cell viability and induced apoptosis in a dose-dependent manner. Treatment increased ROS and TBARS, depleted GSH, disrupted mitochondrial membrane potential (ΔΨm), and elevated LDH release, accompanied by AO/PI-defined apoptotic morphology and DNA fragmentation. Annexin V/PI flow cytometry analysis in SiHa cervical cancer cells confirmed a dose-dependent increase in apoptotic cell populations following bavachinin treatment. Transcriptionally, NF-κB p65, TNF-α, IL-6, and Bcl-2 were downregulated, whereas Bax expression was increased, indicating modulation of apoptosis-associated and inflammatory signaling pathways. Bavachinin exhibited anti-inflammatory and pro-apoptotic activities against HeLa cells, likely through oxidative stress-associated apoptosis and modulation of NF-κB-associated inflammatory gene expression. These findings support further mechanistic validation and in vivo evaluation of bavachinin as a potential therapeutic candidate for cervical cancer.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Bavachinin induces oxidative stress-associated apoptosis and modulates NF-κB-associated inflammatory gene expression in cervical cancer cells

  • 期刊论文

  • 发表日期：

    2026年7月14日

查看全文
  • Yu Wang,
  • Xiaofeng Gui

摘要

Cervical cancer remains a major cause of mortality among women worldwide. Natural products provide anticancer leads with comparatively low toxicity. Bavachinin, a flavanone from Psoralea corylifolia, has documented bioactivities, yet its mechanisms in cervical cancer remain unclear. To determine whether bavachinin suppresses HeLa cell survival by inducing oxidative-stress–driven mitochondrial apoptosis and by downregulating NF-κB-regulated inflammatory signaling. Cytotoxicity across 5–40 µM was quantified by MTT. Oxidative stress and antioxidant status were assessed by TBARS and reduced glutathione (GSH). Apoptotic indices were evaluated by intracellular ROS generation, loss of mitochondrial membrane potential (ΔΨm), lactate dehydrogenase (LDH) release, AO/PI staining, Annexin V/PI flow cytometry, and DNA damage analyses. mRNA levels of NF-κB p65, TNF-α, IL-6, Bcl-2, and Bax were measured by quantitative RT-PCR. One-way ANOVA analyzed data with appropriate post hoc testing. Bavachinin decreased cervical cancer cell viability and induced apoptosis in a dose-dependent manner. Treatment increased ROS and TBARS, depleted GSH, disrupted mitochondrial membrane potential (ΔΨm), and elevated LDH release, accompanied by AO/PI-defined apoptotic morphology and DNA fragmentation. Annexin V/PI flow cytometry analysis in SiHa cervical cancer cells confirmed a dose-dependent increase in apoptotic cell populations following bavachinin treatment. Transcriptionally, NF-κB p65, TNF-α, IL-6, and Bcl-2 were downregulated, whereas Bax expression was increased, indicating modulation of apoptosis-associated and inflammatory signaling pathways. Bavachinin exhibited anti-inflammatory and pro-apoptotic activities against HeLa cells, likely through oxidative stress-associated apoptosis and modulation of NF-κB-associated inflammatory gene expression. These findings support further mechanistic validation and in vivo evaluation of bavachinin as a potential therapeutic candidate for cervical cancer.