مختصر البحث:
Aims The study aimed to assess the cardioprotective potential of celastrol against cardiac
injury induced by sepsis via amelioration of IL6, TNF, TLR4, IL10, F2-isoprostane, cardiac
troponin, and CK-MB, as well as at histological level.
Materials…
Aims The study aimed to assess the cardioprotective potential of celastrol against cardiac
injury induced by sepsis via amelioration of IL6, TNF, TLR4, IL10, F2-isoprostane, cardiac
troponin, and CK-MB, as well as at histological level.
Materials & Methods Twenty-four Swiss albino mice aged between 6 and 8 weeks, weighted
between 20 and 30g, were included and were randomly divided into four groups; Sham,
Sepsis (laparotomy with CLP), Vehicle (treated with the equivalent volume of DMSO), and
celastrol (treated with 2mg/kg IP 1hr before CLP) groups. By spectrophotometric assay,
blood samples were then aspirated for cardiac troponin and CK-MB assessment. Part of the
cardiac tissue was used to assess the levels of TNFα, IL6, IL10, F2-Isoprostane, and TLR4
by ELISA method; another part was used to assess the degree of cardiac tissue damage by
histopathological analysis.
Findings Significant cardiac damage was noticed in the sepsis group (p≤0.05) as compared
with the sham group, manifested by a significant elevation in inflammatory markers (TNFα,
IL6, TLR4) and oxidative stress marker (F2-Isoprostane) as well as cardiac troponin and CKMB,
with a significant reduction in IL10. Pretreatment with celastrol resulted in a significant
reduction in TNF, IL6, TLR4, F2-Isoprostane, troponin, and CK-MB with significant elevation
in IL10 compared to the sepsis group. In the same manner, significant histological damage
was encountered in the sepsis group compared to the sham group, while the celastrol-treated
group exhibited minor histological damage compared to the sepsis group.
Conclusion Celastrol has cardio-protective effects against cardiac injury induced by
endotoxemia.
