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Cecal Ligation and Puncture-induced Sepsis as a Model To Study Autophagy in Mice
Published on: February 9, 2014
Andrographolide Attenuates Sepsis-Induced Acute Lung Injury via Peroxisome Proliferator-Activated Receptor Gamma in a
Lokesh V Thimmana1,2, Hari Prakash Kalla1, Kumarla Kaluva Ruhinaz1
1Department of Zoology, Yogi Vemana University, Kadapa, India.
Introduction:
Sepsis-induced acute lung injury (ALI) is a life-threatening complication marked by intense inflammation, oxidative stress, and respiratory failure, with no effective targeted treatments available. This study aims to explore the protective effects of andrographolide (AGL) against sepsis-induced ALI and uncover its underlying mechanisms, focusing on the modulation of peroxisome proliferator-activated receptor gamma (PPARγ) as a potential therapeutic pathway.
Methods:
A murine model of ALI was established using cecal ligation and puncture (CLP). AGL was administered to evaluate its effects on pulmonary inflammation and oxidative stress. Neutrophil and macrophage infiltration, pulmonary edema, and levels of malondialdehyde and nitrite were measured in bronchoalveolar lavage (BAL) fluid and lung tissue, along with the expression of PPARγ and the activities of antioxidant enzymes superoxide dismutase (SOD) and catalase. The involvement of PPARγ was further confirmed using GW9662, a selective PPARγ antagonist.
Results:
AGL treatment significantly attenuated neutrophil and macrophage infiltration, reduced pulmonary edema and inflammation, and decreased nitrite levels in BAL. Additionally, AGL upregulated PPARγ expression and enhanced SOD and catalase activity. These protective effects were significantly reversed by co-administration of GW9662, indicating a PPARγ-dependent mechanism.
Discussion:
The present study demonstrated that AGL exerts significant protective effects against CLP-induced ALI, primarily through modulation of inflammatory and oxidative pathways.
Conclusion:
AGL's ability to upregulate PPARγ and enhance SOD and catalase activity further supports its mechanistic role in mitigating lung damage. The reversal of AGL protective effects by GW9662 confirms its PPARγ-dependent mechanism, highlighting its potential as a targeted protective treatment for sepsis-induced ALI.
