3,4-Dihydroxyphenylethanol ameliorates lipopolysaccharide-induced septic cardiac injury in a murine model

被引:7
|
作者
Zhang, Lu [2 ]
Wen, Kun [2 ]
Zhang, Zhiqiang [2 ]
Ma, Chengen [2 ]
Zheng, Ni [1 ]
机构
[1] Shandong First Med Univ, Dept Clin Lab, Shandong Prov Hosp, 324 Jingwu Weiqi Rd, Jinan 250021, Shandong, Peoples R China
[2] Shandong Univ, Hosp 2, Dept Intens Care Unit, Jinan 250033, Shandong, Peoples R China
来源
OPEN LIFE SCIENCES | 2021年 / 16卷 / 01期
关键词
DOPET; sepsis; LPS; cardiac damage; inflammation; apoptosis; INDUCED CARDIOTOXICITY; INFLAMMATORY RESPONSE; OXIDATIVE STRESS; SEPSIS; DYSFUNCTION; ACTIVATION; APOPTOSIS; EXTRACT;
D O I
10.1515/biol-2021-0125
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
3,4-Dihydroxyphenylethanol (DOPET) is a polyphenol found in olive oil. The present study evaluated the protective role of DOPET on LPS provoked septic cardiac injury in a murine model. Four groups were used in the study (n = 3): control, LPS, DOPET alone, and DOPET + LPS. LPS (15 mg/kg; i.p.); they were used to induce cardiac sepsis. The cardiac markers like LDH, CK-MB, and troponin-T, as well as inflammatory cytokines like TNF-alpha and IL-6 were measured in the serum. The antioxidants and oxidative stress parameters were measured in cardiac tissues. RT-PCR and western blot methods were done to evaluate the expression of inflammatory mediators and apoptotic markers. DOPET significantly decreased the cardiac markers (LDH, CK-MB, and troponin-T) and TNF-alpha and IL-6 level in the serum. DOPET effectively reduced the levels of MDA and NO in LPS intoxicated rats. DOPET also increased the levels of antioxidants like SOD, CAT, GPx, and GSH in LPS intoxicated rats. The mRNA levels of TNF-alpha, IL-6, and NF-kappa B were significantly downregulated by DOPET in cardiac tissues of LPS rats. The protein expression of Bcl-2 was upregulated, and Bax and caspase-3 were downregulated by DOPET. DOPET effectively attenuates LPS-induced cardiac dysfunction through its antioxidant, anti-inflammatory, and anti-apoptotic mechanisms.
引用
收藏
页码:1313 / 1320
页数:8
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