Pakistan journal of pharmaceutical sciences · 2026
Andrographolide mitigates paraquat-induced pulmonary injury via PI3K/Akt/PPARγ pathway-mediated regulation of EMT and oxidative stress.
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Zhang Degang, Zhao Shengming, Xiao Jiayi, Cai Qinyi, Zhao Bo
Аннотация
BACKGROUND: Paraquat (PQ) poisoning causes acute pulmonary injury via oxidative stress and epithelial-mesenchymal transition (EMT), with limited treatment options.
OBJECTIVES: This study investigated whether andrographolide (Andro) alleviates PQ-induced lung damage and the underlying mechanisms.
METHODS: PQ-induced pulmonary injury was established in C57BL/6J mice. Animals were assigned to Control, Andro, PQ and PQ +Andro groups. Lung pathology, oxidative stress markers (MPO, ROS, MDA, SOD, CAT), EMT markers (E-cadherin, α-SMA), and PI3K/Akt/PPARγ pathway proteins were assessed in vivo and in MLE-12 cells, with PI3K inhibition using LY294002.
RESULTS: Andro significantly improved survival, reduced alveolar injury and collagen deposition, and suppressed oxidative stress by downregulating ROS/MDA/MPO and enhancing SOD/CAT. It suppressed EMT by upregulating E-cadherin and reducing α-SMA. Andro inhibited PI3K/Akt activation and increased PPARγ expression. LY294002 partially reproduced these effects, supporting pathway involvement.
CONCLUSION: Andro mitigates PQ-induced lung damage by limiting oxidative stress and EMT via the PI3K/Akt/PPARγ pathway. These findings provide preclinical evidence for its further investigation as a candidate protective agent.
OBJECTIVES: This study investigated whether andrographolide (Andro) alleviates PQ-induced lung damage and the underlying mechanisms.
METHODS: PQ-induced pulmonary injury was established in C57BL/6J mice. Animals were assigned to Control, Andro, PQ and PQ +Andro groups. Lung pathology, oxidative stress markers (MPO, ROS, MDA, SOD, CAT), EMT markers (E-cadherin, α-SMA), and PI3K/Akt/PPARγ pathway proteins were assessed in vivo and in MLE-12 cells, with PI3K inhibition using LY294002.
RESULTS: Andro significantly improved survival, reduced alveolar injury and collagen deposition, and suppressed oxidative stress by downregulating ROS/MDA/MPO and enhancing SOD/CAT. It suppressed EMT by upregulating E-cadherin and reducing α-SMA. Andro inhibited PI3K/Akt activation and increased PPARγ expression. LY294002 partially reproduced these effects, supporting pathway involvement.
CONCLUSION: Andro mitigates PQ-induced lung damage by limiting oxidative stress and EMT via the PI3K/Akt/PPARγ pathway. These findings provide preclinical evidence for its further investigation as a candidate protective agent.