Liposomal chrysin attenuates hepatic ischaemia-reperfusion injury: possible mechanism via inhibiting NLRP3 inflammasome
| Autor: | Bin Wang, Lidan Zhang, Zizuo Zhao, Rui Huang, Hong-Tao Tie, Xujie Jiang, Weiwei Li |
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| Rok vydání: | 2021 |
| Předmět: |
Male
Inflammasomes Pharmaceutical Science Apoptosis Absorption (skin) Pharmacology chemistry.chemical_compound Mice NLR Family Pyrin Domain-Containing 3 Protein medicine Animals Chrysin Particle Size Liver injury chemistry.chemical_classification Flavonoids Reactive oxygen species Liver Diseases Inflammasome medicine.disease Malondialdehyde Bioavailability Mice Inbred C57BL Disease Models Animal chemistry Reperfusion Injury Liposomes Reactive Oxygen Species medicine.drug |
| Zdroj: | The Journal of pharmacy and pharmacology. 74(2) |
| ISSN: | 2042-7158 |
| Popis: | Objectives The chrysin has properties of low aqueous solubility, bioavailability and absorption, and its effect on hepatic ischaemia-reperfusion (HIR) remains unclear. Thus, we prepared a liposomal chrysin (LC) and explored its effect and potential mechanism on HIR. Methods A thin-film dispersion method was used to prepare LC, and a mouse HIR model was used. Mice were pre-treated with LC (100 mg/kg) or placebo by gavage feeding at 16.5 h, 8.5 h, 0.5 h before modelling. Results The average particle sizes, polydispersity index, zeta potential, encapsulation efficiency and drug loading of LC were 129 ± 13.53 nm, 0.265 ± 0.021, −34.46 ± 4.14 mV, 95.03 ± 2.17%, 16.4 ± 0.8%. The concentration of chrysin in plasma and liver tissue by LC administration increased 2.54 times and 1.45 times. LC pre-treatment reduced HIR-induced liver injury and inhibited cell apoptosis. Besides, LC pre-treatment decreased reactive oxygen species and malondialdehyde and inhibited the inflammation response indicated by lower IL-6, TNF-α, infiltration of neutrophils. Further, LC pre-treatment significantly decreased NLRP3 activation, evidenced by reduced cleaved caspase-3, NLRP3, ASC, cleaved caspase-1 and IL-1β expression. Conclusions LC has good biocompatibility, and it could attenuate HIR-induced injury. Its mechanism was associated with NLRP3 inflammasome inhibition, and LC might be an effective drug for treating and preventing HIR-induced injury. |
| Databáze: | OpenAIRE |
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