ArticleOxidative medicine and cellular longevity2022
The Activation of AMPK/NRF2 Pathway in Lung Epithelial Cells Is Involved in the Protective Effects of Kinsenoside on Lipopolysaccharide-Induced Acute Lung Injury.
Article in Oxidative medicine and cellular longevity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- Macrophage metabolism reprogramming in sepsis: Pathogenesis and therapeutic implications (Review).International journal of molecular medicine · 2026Review
- Luteoloside ameliorates sepsis-induced acute lung injury via AMPK-ULK1 pathway-mediated autophagy.Histology and histopathology · 2025Article
- Mechanisms of alveolar type II epithelial cells' mitochondrial quality control during acute lung injury/acute respiratory distress syndrome: bridging the gap between oxidative stress, inflammation, and fibrosis.Frontiers in physiology · 2025Review
- Targeting the AMPK/Nrf2 Pathway: A Novel Therapeutic Approach for Acute Lung Injury.Journal of inflammation research · 2024Review
- Baicalin Attenuates HInternational journal of molecular sciences · 2023Article
- Article
- Saikosaponin A and Its Epimers Alleviate LPS-Induced Acute Lung Injury in Mice.Molecules (Basel, Switzerland) · 2023Article
- Activation of PPARPPAR research · 2022Article
- Growth Differentiation Factor 7 Prevents Sepsis-Induced Acute Lung Injury in Mice.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Advances in the therapeutic application and pharmacological properties of kinsenoside against inflammation and oxidative stress-induced disorders.Frontiers in pharmacology · 2022Review
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Authors and funding
4 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
The disorder of mitochondrial dynamic equilibrium of lung epithelial cell is one of the critical causes of acute lung injury (ALI). Kinsenoside (Kin) serves as an active small-molecule component derived from traditional medicinal herb displaying multiple pharmacological actions in cancers, hyperglycemia, and liver disease. The objective of this study was to investigate the effects of Kin on lipopolysaccharide- (LPS-) induced ALI and further explore possible molecular mechanisms. Kin was administered orally (100 mg/kg/day) for 7 consecutive days before LPS instillation (5 mg/kg). After 12 hours, pathological injury, inflammatory response, and oxidative stress were detected. The results demonstrated that Kin significantly alleviated lung pathological injury and decreased the infiltration of inflammatory cells and the release of inflammatory mediators in bronchoalveolar lavage fluid (BALF), apart from inhibiting the production of reactive oxygen species (ROS) and lipid peroxidation. Meanwhile, Kin also promoted mitochondrial fusion and restrained mitochondrial fission in mice with ALI. In terms of mechanism, Kin pretreatment increased the phosphorylation of AMP-activated protein kinase (AMPK) and the protein level of nuclear factor erythroid 2-related factor 2 (NRF2). In
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