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<p>Cerebral ischemia-reperfusion (I/R) injury triggers a systemic inflammatory response and a catastrophic respiratory burst of reactive oxygen species, resulting in widespread multi-organ damage. This study evaluated the phytochemical profile of <i>Tridax procumbens</i> ethanol extract (TP) and validated its multi-target, systemic organoprotective efficacy against cerebral I/R-induced cardiohepatorenal oxidative injury. TP constituents were identified using LC-MS profiling. Its in-vitro antioxidant metrics were quantified via DPPH, reducing power, and H<sub>2</sub>O<sub>2</sub> scavenging assays. For in-vivo assessment, Wistar rats were subjected to 30&#xa0;min of global cerebral ischemia via bilateral common carotid artery occlusion (BCCAO), followed by reperfusion. TP (20–80&#xa0;mg/kg, i.p.) and quercetin (20&#xa0;mg/kg, i.p.) was administered immediately at reperfusion. After 24&#xa0;h, malondialdehyde (MDA) and reduced glutathione (GSH) were mapped across the heart, liver, and kidneys, alongside brain histopathology. LC-MS profiling identified 10 major phenolics and flavonoids, notably luteolin (37.32%), kaempferol (21.41%), and resveratrol (14.65%). In vitro, TP demonstrated significant antioxidant prowess, achieving 56.8% DPPH inhibition (50&#xa0;µg/mL) and 86.98% H<sub>2</sub>O<sub>2</sub> scavenging (10&#xa0;µg/mL). In vivo, BCCAO caused severe cerebral injury and a systemic surge in lipid peroxidation paired with systemic GSH depletion. TP treatment significantly (<i>P</i> &lt; 0.05) minimized multi-organ MDA accumulation, dose-dependently restored endogenous GSH pools across all harvested peripheral tissues, and preserved neuro-architectural integrity while reversing cerebral necrosis. TP exerts powerful multi-systemic protection by mitigating distant-organ oxidative bankruptcy and neuro-structural collapse, showcasing its potential as a natural therapeutic compound for complex vascular injuries.</p>

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Phytochemical profiling and systemic organoprotection of Tridax procumbens against cerebral ischemia-reperfusion injury

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月6日

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  • Adewunmi Rofiat Funmilola,
  • Ahmed-Oke Maryam Opeyemi,
  • Alhassan Maina Abdullahi,
  • Pedro Shamsudeen,
  • Yesufu Hassan Braimah,
  • Bababe Abdulkadir

摘要

Cerebral ischemia-reperfusion (I/R) injury triggers a systemic inflammatory response and a catastrophic respiratory burst of reactive oxygen species, resulting in widespread multi-organ damage. This study evaluated the phytochemical profile of Tridax procumbens ethanol extract (TP) and validated its multi-target, systemic organoprotective efficacy against cerebral I/R-induced cardiohepatorenal oxidative injury. TP constituents were identified using LC-MS profiling. Its in-vitro antioxidant metrics were quantified via DPPH, reducing power, and H2O2 scavenging assays. For in-vivo assessment, Wistar rats were subjected to 30 min of global cerebral ischemia via bilateral common carotid artery occlusion (BCCAO), followed by reperfusion. TP (20–80 mg/kg, i.p.) and quercetin (20 mg/kg, i.p.) was administered immediately at reperfusion. After 24 h, malondialdehyde (MDA) and reduced glutathione (GSH) were mapped across the heart, liver, and kidneys, alongside brain histopathology. LC-MS profiling identified 10 major phenolics and flavonoids, notably luteolin (37.32%), kaempferol (21.41%), and resveratrol (14.65%). In vitro, TP demonstrated significant antioxidant prowess, achieving 56.8% DPPH inhibition (50 µg/mL) and 86.98% H2O2 scavenging (10 µg/mL). In vivo, BCCAO caused severe cerebral injury and a systemic surge in lipid peroxidation paired with systemic GSH depletion. TP treatment significantly (P < 0.05) minimized multi-organ MDA accumulation, dose-dependently restored endogenous GSH pools across all harvested peripheral tissues, and preserved neuro-architectural integrity while reversing cerebral necrosis. TP exerts powerful multi-systemic protection by mitigating distant-organ oxidative bankruptcy and neuro-structural collapse, showcasing its potential as a natural therapeutic compound for complex vascular injuries.