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<p>Astragaloside IV (AS-IV), a compound extracted from Radix Astragali, has been shown to have beneficial effects on cardiovascular disease. However, the role of AS-IV in cardiac toxicity caused by arsenic trioxide (ATO) is unknown. The current experiment aimed to explore the protective effects and molecular mechanisms of AS-IV against ATO-induced cardiac toxicity. Rats were administered AS-IV intragastrically (40, 80&#xa0;mg/kg) concurrently with ATO (5&#xa0;mg/kg) infused intraperitoneally over 7&#xa0;days. Electrocardiography, cardiac weight index, and heart morphology changes were observed. Histopathological and cardiac function indices showed that ATO caused severe cardiac damage. It increased MDA levels while reducing SOD and GSH-Px, indicating oxidative damage. Inflammatory markers, including IL-1β and TNF-α, were markedly upregulated. Apoptosis, marked by upregulated Bax and decreased Bcl-2, was enhanced. However, AS-IV treatment significantly suppressed these changes. Moreover, AS-IV treatment resulted in a significant decrease in the protein expression levels of p38MAPK and NF-κB. The findings revealed that AS-IV may inhibit the inflammation, apoptosis, and oxidative stress to exert protective effects on ATO-induced cardiac toxicity in rats through inhibiting the p38MAPK/NF-κB signaling pathway.</p>

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Astragaloside IV attenuates arsenic trioxide-induced cardiac toxicity in rats via the p38 MAPK/NF-κB signaling pathway

  • 期刊论文

  • 发表日期：

    2026年5月1日

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  • Weiyue Jin,
  • Shuling Fei,
  • Jing Li,
  • Yurun Xue,
  • Boli Wang,
  • He Tang,
  • Xue Han,
  • Jie Cheng,
  • Shengjiang Guan

摘要

Astragaloside IV (AS-IV), a compound extracted from Radix Astragali, has been shown to have beneficial effects on cardiovascular disease. However, the role of AS-IV in cardiac toxicity caused by arsenic trioxide (ATO) is unknown. The current experiment aimed to explore the protective effects and molecular mechanisms of AS-IV against ATO-induced cardiac toxicity. Rats were administered AS-IV intragastrically (40, 80 mg/kg) concurrently with ATO (5 mg/kg) infused intraperitoneally over 7 days. Electrocardiography, cardiac weight index, and heart morphology changes were observed. Histopathological and cardiac function indices showed that ATO caused severe cardiac damage. It increased MDA levels while reducing SOD and GSH-Px, indicating oxidative damage. Inflammatory markers, including IL-1β and TNF-α, were markedly upregulated. Apoptosis, marked by upregulated Bax and decreased Bcl-2, was enhanced. However, AS-IV treatment significantly suppressed these changes. Moreover, AS-IV treatment resulted in a significant decrease in the protein expression levels of p38MAPK and NF-κB. The findings revealed that AS-IV may inhibit the inflammation, apoptosis, and oxidative stress to exert protective effects on ATO-induced cardiac toxicity in rats through inhibiting the p38MAPK/NF-κB signaling pathway.