Tannic acid modulates fibroblast proliferation and differentiation in response to pro‐fibrotic stimuli

Pattarayan, Dhamotharan; Sivanantham, Ayyanar; Bethunaickan, Ramalingam; Palanichamy, Rajaguru; Rajasekaran, Subbiah

doi:10.1002/jcb.26866

Cited by 23 publications

(15 citation statements)

References 41 publications

(96 reference statements)

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“…Increasing the TA content in the hydrogels yielded a small decrease of cell viability from 90% for TAPS2 to 75% for TAPS8 hydrogel, probably due to the dose-dependent inhibition of TA on fibroblast proliferation. 46…”

Section: Resultsmentioning

confidence: 99%

“…Increasing the TA content in the hydrogels yielded a small decrease of cell viability from 90% for TAPS2 to 75% for TAPS8 hydrogel, probably due to the dosedependent inhibition of TA on fibroblast proliferation. 46 Skin compatibility of the polySBMA and TAPS8 hydrogels was evaluated using the irritation test according to the standard protocol. No reaction signs of erythema or edema were observed on the animal skin after treatment (Fig.…”

Section: Cytotoxicity and Skin Compatibilitymentioning

confidence: 99%

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Tannic acid-reinforced zwitterionic hydrogels with multi-functionalities for diabetic wound treatment

Fang

Zeng

et al. 2022

J. Mater. Chem. B

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Section: Resultsmentioning

confidence: 99%

Section: Cytotoxicity and Skin Compatibilitymentioning

confidence: 99%

Tannic acid-reinforced zwitterionic hydrogels with multi-functionalities for diabetic wound treatment

Fang

Zeng

et al. 2022

J. Mater. Chem. B

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“…Tannic acid (TA; chemical structure, C 76 H 52 O 46 ) is a specific type of tannin, which is a water-soluble polyphenol, and is a mixture of five galloyl esters and one glucose (25). Previous studies have indicated that TA possesses anticarcinogenic, antioxidant, antimutagenic, anti-inflammatory, antifibrotic and cardioprotective effects (26)(27)(28)(29)(30). To date, to the best of our knowledge, there are no published scientific reports on the effects of TA on LPS-induced myocardial injury or related ailments.…”

Section: Introductionmentioning

confidence: 99%

Tannic acid alleviates lipopolysaccharide‑induced H9C2 cell apoptosis by suppressing reactive oxygen species‑mediated endoplasmic reticulum stress

et al. 2021

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Sepsis-induced myocardial dysfunction is one of the features of multiple organ dysfunction in sepsis, which is associated with extremely high mortality and is characterized by impaired myocardial compliance. To date, there are few effective treatment options available to cure sepsis. Tannic acid (TA) is reportedly protective during sepsis; however, the underlying mechanisms by which TA protects against septic heart injury remain elusive. The present study 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 medium only. Apoptosis was measured using flow cytometry, reverse transcription-quantitative PCR (RT-qPCR) and western blot analysis. Additionally, the levels of cellular reactive oxygen species (ROS), malondialdehyde and nicotinamide adenine dinucleotide phosphate were evaluated. Western blotting and RT-qPCR were also employed to detect the expression levels of endoplasmic reticulum (ER) stress-associated functional proteins. The present findings demonstrated that TA reduced the degree of LPS-induced H9C2 cell injury, including inhibition of ROS production and ER stress (ERS)-associated apoptosis. ERS-associated functional proteins, including activating transcription factor 6, protein kinase-like ER kinase, inositol-requiring enzyme 1, spliced X box-binding protein 1 and C/EBP-homologous protein were suppressed in response to TA treatment. Furthermore, the expression levels of ERS-associated apoptotic proteins, including c-Jun N-terminal kinase, Bax, cytochrome c, caspase-3, caspase-12 and caspase-9 were reduced following treatment with TA. Additionally, the protective effects of TA on LPS-induced H9C2 cells were partially inhibited following treatment with the ROS inhibitor N-acetylcysteine, which demonstrated that ROS mediated ERS-associated apoptosis and TA was able to decrease ROS-mediated ERS-associated apoptosis. Collectively, the present findings demonstrated that the protective effects of TA against LPS-induced H9C2 cell apoptosis may be associated with the amelioration of ROS-mediated ERS. These findings may assist the development of potential novel therapeutic methods to inhibit the progression of myocardial cell injury.

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“…Tannic acid (TA), a speci c type of tannin, is water-soluble polyphenols with a C 76 H 52 O 46 chemical structure, and is a mixture of ve galloyl esters and one glucose [27]. Previous studies have indicated that TA possesses anticarcinogenic, antioxidant, antimutagenic, anti-in ammatory, anti brotic, and cardioprotective effects [28][29][30][31][32]. To date, there are no published scienti c reports on the effects of TA on LPS-induced myocardial injury or related ailments.…”

Section: Introductionmentioning

confidence: 99%

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

Yang

Zhao

Gao

et al. 2021

Preprint

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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.)

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Tannic acid modulates fibroblast proliferation and differentiation in response to pro‐fibrotic stimuli

Cited by 23 publications

References 41 publications

Tannic acid-reinforced zwitterionic hydrogels with multi-functionalities for diabetic wound treatment

Tannic acid-reinforced zwitterionic hydrogels with multi-functionalities for diabetic wound treatment

Tannic acid alleviates lipopolysaccharide‑induced H9C2 cell apoptosis by suppressing reactive oxygen species‑mediated endoplasmic reticulum stress

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

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