Why the study?
This study explored the activity of sinapic acid against doxorubicin-induced cardiotoxicity and sought to reveal its underlying mechanisms.
Does sinapic acid ameliorate doxorubicin-induced cardiotoxicity in a rat model?
Does sinapic acid ameliorate doxorubicin-induced cardiotoxicity in a rat model?
Sinapic acid demonstrates cardioprotective effects against doxorubicin-induced cardiotoxicity in rats by reducing oxidative stress, inflammation, and apoptosis.
Hypothesis-generating for salvianolic acid in doxorubicin cardiotoxicity; human trials needed before any clinical consideration.
In the present study, we explored SA’s activity against DOX‐induced cardiotoxicity and revealed its underlying mechanisms. Male Wistar rats (weight, 190‐210g; n = 6) were randomly divided into four groups: group I, normal control; group II, DOX 15 mg/kg via intraperitoneal (ip) route; group III, administered DOX+SA 20 mg/kg; and group IV, administered DOX+captopril (CAP 30 mg/kg). SA and CAP were administered orally for seven days, and DOX (15 mg/kg) was injected intraperitoneally an hour before SA treatment on the fifth day. Forty‐eight hours after DOX administration, animals were anesthetized and sacrificed for molecular and histology experiments. SA significantly mitigated the myocardial effects of DOX, and following daily administration, it reduced serum levels of lactate dehydrogenase (LDH) and creatine kinase isoenzyme‐MB to near normal values. Levels of oxidative stress markers, glutathione‐peroxidase, superoxide dismutase, and catalase, in the cardiac tissue were significantly increased, whereas malondialdehyde levels decreased after SA treatment in DOX‐administered rats. Furthermore, DOX caused an inflammatory reaction by elevating the levels of proinflammatory cytokines, tumor necrosis factor‐ α (TNF‐ α ), interleukin‐1 β (IL‐1 β ), and endothelin‐ (ET‐) 1, as well as nuclear factor kappa‐B (NF‐ κ B) expression. Daily administration of SA significantly repressed TNF‐ α , IL‐1 β , ET‐1, and NF‐ κ B levels. caspase‐3 and Bax expression, bcl‐2‐like protein and caspase‐3 activities and levels. Overall, we found that SA could inhibit DOX‐induced cardiotoxicity by inhibiting oxidative stress, inflammation, and apoptotic damage.
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Jardan et al. (2020) studied this question.
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