Effects of gallic acid on hemodynamic parameters and infarct size after ischemia-reperfusion in isolated rat hearts with alloxan-induced diabetes

Ramezani-Aliakbari, Fatemeh; Badavi, Mohammad; Dianat, Mahin; Mard, Seyyed Ali; Ahangarpour, Akram

doi:10.1016/j.biopha.2017.10.014

Cited by 15 publications

(11 citation statements)

References 41 publications

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“…Similarly, Ramezani-Aliakbari et al . reported that gallic acid improved left ventricular dysfunction in a rat model of alloxan-induced diabetes mellitus 25 . Advanced glycation end products (AGEs) are implicated in cardiovascular diseases in diabetics.…”

Section: Discussionmentioning

confidence: 96%

Gallic acid improves cardiac dysfunction and fibrosis in pressure overload-induced heart failure

Jin

Sun

Ryu

et al. 2018

Sci Rep

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Gallic acid is a trihydroxybenzoic acid found in tea leaves and some plants. Here, we report the effect of gallic acid on cardiac dysfunction and fibrosis in a mouse model of pressure overload-induced heart failure and in primary rat cardiac fibroblasts, and compare the effects of gallic acid with those of drugs used in clinics. Gallic acid reduces cardiac hypertrophy, dysfunction, and fibrosis induced by transverse aortic constriction (TAC) stimuli in vivo and transforming growth factor β1 (TGF-β1) in vitro. It decreases left ventricular end-diastolic and end-systolic diameter, and recovers the reduced fractional shortening in TAC. In addition, it suppresses the expression of atrial natriuretic peptide, brain natriuretic peptide, skeletal α-actin, and β-myosin heavy chain. Administration of gallic acid decreases perivascular fibrosis, as determined by Trichrome II Blue staining, and reduces the expression of collagen type I and connective tissue growth factor. However, administration of losartan, carvedilol, and furosemide does not reduce cardiac dysfunction and fibrosis in TAC. Moreover, treatment with gallic acid inhibits fibrosis-related genes and deposition of collagen type I in TGF-β1-treated cardiac fibroblasts. These results suggest that gallic acid is a therapeutic agent for cardiac dysfunction and fibrosis in chronic heart failure.

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Section: Discussionmentioning

confidence: 96%

Gallic acid improves cardiac dysfunction and fibrosis in pressure overload-induced heart failure

Jin

Sun

Ryu

et al. 2018

Sci Rep

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“…Our study showed that the main component of BC is gallic acid, which could account for the antiarrhythmic and antinecroptotic effects. Gallic acid was reported to protect I/R‐caused infarct size and arrhythmias in diabetes rats . However, the detail underlying mechanisms were still unknown.…”

Section: Discussionmentioning

confidence: 99%

Cardiac protection of Bauhinia championii against reperfusion injury

Chen

Chung

et al. 2020

Environmental Toxicology

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This study aims to investigate the protective effects of the Bauhinia championii (BC) against ischemia/reperfusion (I/R)-induced injury in an isolated heart model.Langendorff-perfused C57BL/6JNarl mice hearts were performed with 30 minutes ischemia and 60 minutes reperfusion by left anterior descending artery ligation.Before reperfusion, boiling water extracts of BC (10 mg/L) was pretreated for 15 minutes. During reperfusion, BC significantly decreased the occurrence of ventricular arrhythmias by lead II electrocardiogram (ECG). Electrophysiological effect of BC was further determined in isolated ventricular myocytes by whole-cell patch clamp technique. The underlying mechanism may result from its Na + channel blocking activity characterized with reduced rise slope of action potential and Na + current density.Moreover, BC dramatically reduced I/R-caused infarct size, which was accessed by 2,3,5-triphenyltetrazolium chloride (TTC) assay. Since BC decreased I/R-induced myoglobin release and oxidation of Ca 2+ -calmodulin-dependent protein kinase, inhibition of myocardial necroptosis may account for the protective effects of BC on myocytes lose. This study indicated that BC may prevent I/R induced ventricular arrhythmias and myocyte death by blocking Na + channels and decreasing necroptosis, respectively. Since most of the available antiarrhythmic remedies have unwanted adverse actions, BC could be a novel candidate for the treatment of myocardial infarction and ventricular arrhythmia. K E Y W O R D S arrhythmias, Bauhinia championii, ischemia/reperfusion, sodium current

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“…Although ZXC is a complex system, benefits for ischemia/reperfusion (I/R) of its major active ingredients have been reported. As a bioactive compound, gallic acid prevented rats from hepatic ischemia and reperfusion injury (Bayramoglu et al, 2015; Ramezani-Aliakbari et al, 2017). Glycyrrhetinic acid could decrease histopathologyical damage and apoptosis in brain tissue injured by I/R damage in C57BL/J6 mouse (Oztanir et al, 2014) and play neuroprotective effects in PC12 cells (Tzu-Chien et al, 2009).…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective Effects and Mechanisms of Zhenlong Xingnao Capsule in In Vivo and In Vitro Models of Hypoxia

et al. 2019

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Zhenlong Xingnao Capsule (ZXC) is a Tibetan medicine used to treat ischemic stroke. In this study, we determined the in vitro and in vivo effects of ZXC on reactive oxygen species (ROS) in a mouse BV-2 microglial cell hypoxia-reoxygenation and rat middle cerebral artery occlusion infarction models. We aimed to clarify the role of ZXC in cerebral ischemia protection; reveal amino acid neurotransmitter changes in the frontal cortex after drug intervention; determine mRNA and protein expression changes in Bcl-2, Bax, caspase-3, P38, and nuclear factor (NF)-кB in the frontal cortex and changes in antioxidant indices in the brain; and elucidate the mechanisms underlying ZXC action. After hypoxia-reoxygenation, ROS levels were significantly increased in BV-2 cells, and their levels decreased after treatment with ZXC. ZXC had protective effects on ischemic/anoxic injury in vitro and in vivo by downregulating the expressions of caspase-3 and NF-кB mRNA during ischemia and reperfusion and that of p38 and caspase-3 during acute ischemia and reperfusion as well as the steady-state levels of excitatory amino acids/inhibitory amino acids and by improving the total antioxidant capacity and total superoxide dismutase activities during ischemia. These findings provide new molecular evidence for the mechanisms underlying ZXC action.

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Effects of gallic acid on hemodynamic parameters and infarct size after ischemia-reperfusion in isolated rat hearts with alloxan-induced diabetes

Cited by 15 publications

References 41 publications

Gallic acid improves cardiac dysfunction and fibrosis in pressure overload-induced heart failure

Gallic acid improves cardiac dysfunction and fibrosis in pressure overload-induced heart failure

Cardiac protection of Bauhinia championii against reperfusion injury

Neuroprotective Effects and Mechanisms of Zhenlong Xingnao Capsule in In Vivo and In Vitro Models of Hypoxia

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