Abstract Title:

Crocin protects cardiomyocytes against LPS-Induced inflammation.

Abstract Source:

Pharmacol Rep. 2019 Nov ;71(6):1228-1234. Epub 2019 Jul 30. PMID: 32002862

Abstract Author(s):

Vafa Baradaran Rahim, Mohammad Taghi Khammar, Hassan Rakhshandeh, Alireza Samzadeh-Kermani, Azar Hosseini, Vahid Reza Askari

Article Affiliation:

Vafa Baradaran Rahim


BACKGROUND: Sepsis causes organ dysfunctions via elevation of oxidative stress and inflammation. Lipopolysaccharide (LPS) is the major surface molecule of most gram-negative bacteria and routinely used as a sepsis model in investigation studies. Crocin is an active compound of saffron which has different pharmacological properties such as anti-oxidant and anti-inflammatory. In this research, the protective effect of crocin was evaluated against LPS-induced toxicity in the embryonic cardiomyocyte cell line (H9c2).

METHODS: The cells were pre-treated with different concentration of crocin ( 10,20 and 40μM) for 24 h, and then LPS was added (10μg/ml) for another 24 h. Afterward, the percentage of cell viability and the levels of inflammatory cytokines (TNF-α, PGE, IL-1β, and IL-6), gene expression levels (TNF-α, COX-2, IL-1β, IL-6, and iNOS), and the level of nitric oxide (NO) and thiol were measured.

RESULTS: Our results showed that LPS reduced cell viability, increased the levels of cytokines, gene- expression, nitric oxide, and thiol. Crocin attenuated the LPS-induced toxicity in H9c2 cells via reducing the levels of inflammatory factors (TNF-α, PGE, IL-1β, and IL-6, p<0.001), gene expression (TNF-α, COX-2, IL-1β, IL-6, and iNOS, p<0.001 ), and NO (p<0.001 ), whereas increased the level of thiol content (p<0.001 ).

CONCLUSION: The observed results revealed that crocin has preventive effects on the LPS induced sepsis and its cardiac toxicity in-vitro model. Probably, these findings are related to anti-inflammatory and antioxidant properties of crocin. However, performing further animal studies are necessary to support the therapeutic effects of crocin in septic shock cardiac dysfunction.

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