Abstract
Tannic acid (TA) belongs to a class of complex water-soluble polyphenolic derivatives that show anticarcinogenic, antiinflammatory, antioxidant, and scavenging activities. Here, we investigate the protective effects of TA against isoproterenol (ISO)-induced myocardial fibrosis (MF) in mice. Mice received TA and ISO dosing and were sacrificed 48 h later. The activities of creatine kinase (CK), creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH), and mitochondria enzymes were measured. Cardiac histopathology was done using H&E, Sirius red, and Masson’s Trichrome staining. Immunohistochemical staining was applied to indicate changes in B-cell lymphoma-2 (Bcl-2), Bcl-2-associated X protein (Bax), and basic fibroblast growth factor (bFGF) protein expressions in cardiac tissue. RT-PCR was used to measure the expression of atrial and brain natriuretic peptides (ANP and BNP, respectively), c-fos, and c-jun. Western blotting was used to measure the expression of nuclear factor-κB (NF-κB) p65, phosphorylated NF-κB p65), toll-like receptor 4 (TLR4), p38, phosphorylated p38, Bax, Bcl-2, and caspase-3. Compared to the ISO group, the TA group had reduced levels of TLR4, p38, p-p38, NF-κB (p65), p-NF-κB (p-p65), caspase-3, Bax, and Bcl-2, as well as CK, CK-MB, and LDH. These results indicate that TA protects against ISO-induced MF, possibly through its ability to suppress the TLR4-mediated NF-κB signaling pathway.
Highlights
Despite increasing mean lifespan and living standards, cardiovascular disease (CVD) remains a major cause of death (Oka et al, 2014)
To investigate whether Tannic acid (TA) has inhibitory effects on ISOinduced Myocardial fibrosis (MF), we studied inflammation and apoptosis-associated MF mediators, such as TLR4, p38, p-p38, nuclear factor kB (NF-kB) (p65), p-NF-kB (p65), B-cell lymphoma-2 (Bcl-2), and Bcl-2-associated protein (Bax)
The data are expressed as the mean ± standard error of the mean, and the differences between the groups were quantified by analysis of variance (ANOVA) or Dunnett's T-test
Summary
Despite increasing mean lifespan and living standards, cardiovascular disease (CVD) remains a major cause of death (Oka et al, 2014). Myocardial fibrosis (MF) is an important pathological change that eventually leads to heart failure. MF typically results from the continuous progression of CVD (e.g., myocardial infarction and hypertension) (Wu et al, 2009; Duygu et al, 2013). MF is a key pathological feature of Protective Effects of Tannic Acid myocardial remodeling and an important cause of CVD formation. MF manifests mainly as excessive collagen fiber deposition in cardiac muscle tissue, a significant increase in collagen content, an imbalance in the proportion of collagen types (increased proportions of I/III), and disorganized collagen arrangements. The mechanism underlying MF remains unclear (Elliott et al, 2000)
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