Immunity, inflammation and disease · 2026
Baicalin as a Regulator of Peroxisome Proliferator-Activated Receptor Gamma: Alleviating Sepsis-Induced Liver Injury by Inhibiting the Cluster of Differentiation 14/Nuclear Factor Kappa B Signaling Pathway.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Wang Hui, Guo Mengmeng, Zeng Xueling, Hu Yuqi, Ma Jiawei, Chang Yufei
Аннотация
BACKGROUND: Sepsis frequently results in multiple organ failure, with the liver particularly susceptible to sepsis-induced damage. The flavonoid baicalin (BA), derived from Scutellaria baicalensis, presents anti-inflammatory properties, yet its effects on liver injury in sepsis through the Cluster of Differentiation 14 (CD14)/Nuclear Factor kappa B (NF-κB) pathway remain underexplored.
METHODS: Alpha Mouse Liver 12 (AML12) cells were intervened with different concentrations of BA and subsequently challenged with lipopolysaccharide (LPS) to induce inflammation. Cell viability, apoptosis, inflammatory cytokine production, and signaling pathway activation were tested by Cell Counting Kit 8 (CCK8), flow cytometry, quantitative real-time PCR (qRT-PCR) and western blotting, respectively. And immunofluorescence was employed to visualize nuclear ectopic location of NF-κB in cells. Additionally, the impact of peroxisome proliferator-activated receptor gamma (PPARγ) silencing for BA's function was explored using small interfering RNA (siRNA) techniques.
RESULTS: BA significantly improved viability and decreased apoptosis in LPS-treated cells. It also downregulated tumor necrosis factor alpha (TNF-α), interleukin-1 beta (IL-1β) and IL-6, upregulated PPARγ, and diminished CD14 and phosphorylated inhibitor of kappa B alpha (p-IKBα)/IKBα levels. Silencing PPARγ reversed the protective effects of BA, underscoring the importance of PPARγ in BA's mechanism of action.
CONCLUSION: BA alleviates sepsis-induced liver injury through activating PPARγ and inhibiting CD14/NF-κB pathway, highlighting its potential as a new approach to treatment sepsis.
METHODS: Alpha Mouse Liver 12 (AML12) cells were intervened with different concentrations of BA and subsequently challenged with lipopolysaccharide (LPS) to induce inflammation. Cell viability, apoptosis, inflammatory cytokine production, and signaling pathway activation were tested by Cell Counting Kit 8 (CCK8), flow cytometry, quantitative real-time PCR (qRT-PCR) and western blotting, respectively. And immunofluorescence was employed to visualize nuclear ectopic location of NF-κB in cells. Additionally, the impact of peroxisome proliferator-activated receptor gamma (PPARγ) silencing for BA's function was explored using small interfering RNA (siRNA) techniques.
RESULTS: BA significantly improved viability and decreased apoptosis in LPS-treated cells. It also downregulated tumor necrosis factor alpha (TNF-α), interleukin-1 beta (IL-1β) and IL-6, upregulated PPARγ, and diminished CD14 and phosphorylated inhibitor of kappa B alpha (p-IKBα)/IKBα levels. Silencing PPARγ reversed the protective effects of BA, underscoring the importance of PPARγ in BA's mechanism of action.
CONCLUSION: BA alleviates sepsis-induced liver injury through activating PPARγ and inhibiting CD14/NF-κB pathway, highlighting its potential as a new approach to treatment sepsis.