Protective effects of tannic acid on pressure overload-induced cardiac hypertrophy and underlying mechanisms in rats

Chu, Li; Li, Pinya; Song, Tao; Han, Xue; Zhang, Xuan; Song, Qiongtao; Liu, Tao; Zhang, Yuanyuan; Zhang, Jianping

doi:10.1111/jphp.12763

Cited by 16 publications

(14 citation statements)

References 61 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Our previous studies have indicated that TA has beneficial effects on cardiovascular disease (42)(43)(44); moreover, we found that Ta ameliorates aTo-induced nephrotoxicity (45). However, the effects of Ta on aTo-induced cardiotoxicity have not yet been reported.…”

Section: Introductionmentioning

confidence: 79%

Mechanisms underlying the protective effect of tannic acid against arsenic trioxide‑induced cardiotoxicity in rats: Potential involvement of mitochondrial apoptosis

Xue

et al. 2020

Mol Med Rep

Self Cite

View full text Add to dashboard Cite

arsenic trioxide (aTo) is a frontline chemotherapy drug used in the therapy of acute promyelocytic leukemia. However, the clinical use of aTo is hindered by its cardiotoxicity. The present study aimed to observe the potential effects and underlying mechanisms of tannic acid (Ta) against aTo-induced cardiotoxicity. Male rats were intraperitoneally injected with aTo (5 mg/kg/day) to induce cardiotoxicity. Ta (20 and 40 mg/kg/day) was administered to evaluate its cardioprotective efficacy against ATO-induced heart injury in rats. administration of aTo resulted in pathological damage in the heart and increased oxidative stress as well as levels of serum cardiac biomarkers creatine kinase and lactate dehydrogenase and the inflammatory marker NF-κB (p65). conversely, Ta markedly reversed this phenomenon. additionally, Ta treatment caused a notable decrease in the expression levels of cleaved caspase-3/caspase-3, Bax, p53 and Bad, while increasing Bcl-2 expression levels. notably, the application of Ta decreased the expression levels of cytochrome c, second mitochondria-derived activator of caspases and high-temperature requirement a2, which are apoptosis mitochondrial-associated proteins. The present findings indicated that Ta protected against aTo-induced cardiotoxicity, which may be associated with oxidative stress, inflammation and mitochondrial apoptosis.

show abstract

Section: Introductionmentioning

confidence: 79%

Mechanisms underlying the protective effect of tannic acid against arsenic trioxide‑induced cardiotoxicity in rats: Potential involvement of mitochondrial apoptosis

Xue

et al. 2020

Mol Med Rep

Self Cite

View full text Add to dashboard Cite

show abstract

“…TA is a natural polyphenol which has been used to improve human health [45]. TA is reported to alleviate acute lung injury [46], cardiac hypertrophy [47], acute doxorubicin-induced cardiotoxicity [48], and isoproterenol-induced myocardial injury [32]. However, there are no reports on the effects of TA on LPSinduced cardiomyocytes injury.…”

Section: Discussionmentioning

confidence: 99%

Tannic Acid Alleviates Lipopolysaccharide-Induced H9C2 Cell Apoptosis by Suppressing ROS-Mediated ER Stress

Yang

Zhao

Gao

et al. 2021

Preprint

View full text Add to dashboard Cite

Background: Sepsis-induced myocardial dysfunction (SIMD), which is one of the features of multiple organ dysfunction in sepsis with extremely high mortality, is characterized by impaired myocardial compliance. To date, there are few effective treatment options to cure sepsis. Tannic acid (TA) is reportedly protective during sepsis. However, the underlying mechanisms by which TA protects against septic heart injury remains elusive. Methods: We investigated the potential effects and underlying mechanisms of TA in alleviating lipopolysaccharide (LPS)-induced H9C2 cardiomyocyte cell apoptosis. H9C2 cells were treated with LPS (15 μg/mL), TA (10 μM) and TA+LPS. Control cells were treated with media only. Apoptosis was measured using flow cytometry, RT-PCR, and Western blotting analysis. Additionally, laser confocal immunofluorescence analysis detected the production of reactive oxygen species (ROS). Western blot and RT-PCR were employed to detect ER stress-associated functional proteins. Results: The results demonstrated that TA reduced the degree of LPS-induced H9C2 cells injury, including the inhibition of ROS production and endoplasmic reticulum (ER) stress-associated apoptosis. ER stress-associated functional proteins, including ATF6, PERK, IRE1, XBP1s, and CHOP were suppressed in response to TA treatment. Furthermore, the expression levels of ER stress-associated apoptotic proteins, including JNK, Bax, Cyt, Caspase3, Caspase12, and Caspase9 were reduced following treatment with TA. Additionally, the protective effects of TA on LPS-induced H9C2 cells were strengthened following treatment with the ROS inhibitor, N-Acetylcysteine (NAC), which demonstrated that ROS-mediated ER stress-associated apoptosis and TA decreased ROS-mediated ER stress-associated apoptosis. Conclusion: Our findings demonstrated that the protective effects of TA against LPS-induced H9C2 cells apoptosis may be associated with the amelioration of ROS-mediated ER stress. These findings may assist the development of potential novel therapeutic methods to inhibit the progression of myocardial cell injury. (TA alleviates LPS-induced H9C2 cell apoptosis.)

show abstract

“…However, the bioavailability score of TA was lower than that of synthetic small molecule PDI inhibitors due to its larger molecular size. Abdominal, intravenous and even nasal administration of TA still achieved antioxidant, anti‐inflammatory and anti‐apoptotic effects although the absorption rate of TA is low 56,57 . Dissecting the distribution, metabolism of TA via different routes of administration will facilitate translating its protective role into clinical practice.…”

Section: Discussionmentioning

confidence: 99%

Molecular docking‐assisted screening reveals tannic acid as a natural protein disulphide isomerase inhibitor with antiplatelet and antithrombotic activities

Ren

You

et al. 2020

J Cellular Molecular Medi

View full text Add to dashboard Cite

show abstract

Protective effects of tannic acid on pressure overload-induced cardiac hypertrophy and underlying mechanisms in rats

Cited by 16 publications

References 61 publications

Mechanisms underlying the protective effect of tannic acid against arsenic trioxide‑induced cardiotoxicity in rats: Potential involvement of mitochondrial apoptosis

Mechanisms underlying the protective effect of tannic acid against arsenic trioxide‑induced cardiotoxicity in rats: Potential involvement of mitochondrial apoptosis

Tannic Acid Alleviates Lipopolysaccharide-Induced H9C2 Cell Apoptosis by Suppressing ROS-Mediated ER Stress

Molecular docking‐assisted screening reveals tannic acid as a natural protein disulphide isomerase inhibitor with antiplatelet and antithrombotic activities

Contact Info

Product

Resources

About