Red ginseng polysaccharide attenuates sepsis-induced acute lung injury via suppressing oxidative stress-mediated ER stress through activation of Nrf2/AMPK pathways

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The present study elucidates the protective efficacy of red ginseng polysaccharide (RGP) against septic-associated acute lung injury (ALI), a critical condition exacerbated by oxidative stress and endoplasmic reticulum (ER) stress. Utilizing lipopolysaccharide (LPS)-induced mouse and cellular models, we assessed lung pathology through histological staining, injury scoring, and lung wet-to-dry ratios along with inflammatory cytokine levels. Cell viability and apoptosis were quantified using cell counting kit-8 and TUNEL assays, respectively, while fluorescence labeling was employed to gauge reactive oxygen species (ROS) and mitochondrial membrane potential (MMP). Our findings indicated that RGP markedly attenuated LPS-induced lung damage, inflammation, oxidative injury, ER stress, and apoptotic processes. Mechanistic insights revealed that RGP exerted its protective effects by activating the nuclear factor erythroid-2-related factor 2 (Nrf2)/adenosine monophosphate-activated protein kinase (AMPK) pathway in LPS-stressed lung tissues. Inhibition of Nrf2 or AMPK abrogated RGP’s benefits on apoptosis, ROS production, and MMP preservation in murine lung type II epithelial (MLE-12) cells, underscoring the Nrf2/AMPK-mediated mechanism of RGP’s action against LPS-induced ALI. These results underscore the potential of RGP as a novel therapeutic agent for sepsis-associated ALI.

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