CROCIN SUPPRESSES INFLAMMATORY RESPONSE IN LPS-INDUCED ACUTE LUNG INJURY (ALI) VIA REGULATION OF HMGB1/TLR4 INFLAMMATION PATHWAY.
| Autor: | Ceylan, Tayfun, Akin, Ali Tugrul, Kaymak, Emin, Varinli, Saban, Toluk, Ayse |
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| Předmět: |
ANTI-inflammatory agents
PEARSON correlation (Statistics) ACUTE diseases DATA analysis APOPTOSIS KRUSKAL-Wallis Test LUNG injuries CELLULAR signal transduction RATS GENE expression IMMUNOHISTOCHEMISTRY LIPOPOLYSACCHARIDES ANIMAL experimentation ANTIOXIDANTS HISTOLOGICAL techniques STATISTICS NONOPIOID analgesics INFLAMMATION GRAM-negative bacterial diseases DATA analysis software DNA-binding proteins CELL receptors HEMORRHAGE PHARMACODYNAMICS |
| Zdroj: | Journal of Basic & Clinical Health Sciences; May2024, Vol. 8 Issue 2, p271-278, 8p |
| Abstrakt: | Purpose: The most significant pathogen hypothesized to be causing the formation of Acute lung injury (ALI) in sepsis is thought to be lipopolysaccharide (LPS), a key endotoxin component of gram-negative bacteria. The main objective of this study is to determine possible anti-inflammatory effects of crocin (CRO) which has many biological properties such as anti-inflammatory, antioxidant, and anti-apoptotic in LPSinduced ALI. Material and Methods: 40 Wistar albino rats were divided into four groups: Control (no treatment), CRO (given 50 mg/kg crocin for 9 days), LPS (given 30 mg/kg LPS at 9th day), LPS+CRO (given 50 mg/kg crocin for 9 days and 30 mg/kg LPS at 9th day). After experimental, rats were sacrificed and lungs were extracted. Histological examinations were performed in the lung tissue and the changes in the HMGB1 and TLR4 expressions were determined via immunohistochemical staining. Results: Hemorrhage, HMGB1 and TLR4 expressions significantly increased in the LPS group. However, CRO administrations exerted a strong protective effect on the lungs in terms of these parameters in LPS+CRO group. Conclusion: According to our results, we suggest that CRO can be considered as a protective agent against LPS induced ALI via inhibition of HMGB1/TLR4 pathway-mediated inflammatory response. [ABSTRACT FROM AUTHOR] |
| Databáze: | Complementary Index |
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