Protective Effects Of Epicatechin Research Articles

Preventive and Therapeutic Effects of Epicatechin on Acetaminophen-Induced Liver Injury in Mice

Background: Nowadays, the use of over-the-counter drugs such as acetaminophen (APAP) may cause severe liver injury, which can occur not only in high doses but also in therapeutic doses due to nutritional deficiency, alcoholism, or using cytochrome p450 inducers. Objectives: In this study, the protective effect of epicatechin (EPC) was evaluated against APAP-induced hepatotoxicity to find an effective and inexpensive therapy. Methods: The animals were divided into preventive and therapeutic groups. In the preventive study, the animals received EPC (25, 50, and 100 mg/kg/day) for five days, and the last dose was administered 1 hour before APAP (400 mg/kg). In the therapeutic groups, the animals received EPC just before and 2 hours after the APAP injection. All the animals were killed, and blood and liver samples were taken for further analysis. The liver pathology, enzymes, and oxidant, antioxidant, inflammatory, and anti-inflammatory factors were evaluated. Results: EPC significantly decreased the serum activity level of the liver biomarkers ALT and AST in the APAP-treated mice. Furthermore, the hepatic levels of thiobarbituric acid-reactive substances were noticeably lowered, and the levels of total thiol and catalase activity increased significantly with EPC. Histopathological results were strongly consistent with those of the biochemical estimations. The most effective dose was observed at EPC 100 mg/kg, and the therapeutic groups showed better results than the preventive groups. Conclusions: EPC attenuated the liver toxicity in the mice by suppressing oxidative stress and can be considered a preventive and therapeutic agent for inhibiting and resolving the liver damage induced by APAP.

Current update on the protective effect of epicatechin in neurodegenerative diseases.

Current update on the protective effect of epicatechin in neurodegenerative diseases.

Protective effect of epicatechin in diabetic-induced peripheral neuropathy: A review

Protective effect of epicatechin in diabetic-induced peripheral neuropathy: A review

Low dose exposure of patulin and protective effect of epicatechin on blood cells in vitro

In the present study, we aimed to assess antioxidant status in erythrocytes in vitro after patulin (PAT) and epicatechin exposure by measuring antioxidant enzymes (superoxide-dismutase – SOD, glutathione peroxidase – GPx and catalase – CAT) and parameters associated with oxidative stress (malondialdehyde – MDA and ROS). We also investigated the effect of PAT on viability and count of lymphocytes and lymphocyte subpopulations in rabbit blood in vitro. Whole blood of rabbits was used for analysis of antioxidant changes in rabbit erythrocytes after epicatechin and PAT treatment (separately or in combination, at concentrations of 0.2; 2; 20; 200 µg mL–1 of epicatechin and 0.5; 5; 10 µg mL–1 of PAT). Whole blood of rabbits was also used for analysis of count and viability of lymphocytes after PAT treatment at concentrations of 10; 25 and 50 µg mL–1. Results from our experiment confirmed the ability of epicatechin to protect cells against oxidative stress and lipoperoxidation. Our findings indicate that mycotoxin PAT in low concentrations did not affect the activity of antioxidant enzymes in erythrocytes of rabbits significantly. Only slight non-significant changes in lymphocytes count after treatment with low doses of PAT in rabbit blood were observed.

Protective effects of epicatechin on the oxidation and N-nitrosamine formation of oxidatively stressed myofibrillar protein

ABSTRACT The present study investigated the protective effects of the polyphenol epicatechin on the protein structural changes, gel properties and N-nitrosodiethylamine (NDEA) formation of oxidatively stressed myofibrillar protein (MP). Results showed that oxidation treatments to MP significantly increased their carbonyl content and surface hydrophobicity as compared to the control groups (p < 0.05). Epicatechin inhibited protein carbonyl content and surface hydrophobicity, especially treated with 2 mM epicatechin. Under oxidative conditions, the fluorescence intensity of tryptophan gradually decreased with the increase of epicatechin concentrations from 0 to 2 mM. The storage modulus (G’) was increased gradually after oxidation and epicatechin treatment. Epicatechin reduced the loss of P 22 and water holding capacity (WHC), promoted the hydration of the proteins. Under oxidative conditions, epicatechin had a concentration dependent effect on the formation of NDEA; low concentrations of epicatechin promoted NDEA formation, while high concentrations inhibited NDEA production. In conclusion, an appropriate quantity of polyphenols can inhibit the oxidation of MP and formation of N-nitrosamines.

Protective effect of Epicatechin on APAP-induced acute liver injury of mice through anti-inflammation and apoptosis inhibition

Epicatechin (EC) is the most effective compound in Euonymus alatus (Thunb.)Sieb, and possesses a series of benefits, including anti-inflammatory, antioxidant, antiobesity and anticancer effects. In this study, we investigated the protective effects of EC in Acetaminophen(N-acetyl-p-aminophenol, APAP)-induced acute liver injury in C57BL/6J mice and explored the possible mechanisms involved in these effects.

The protective effect of epicatechin on experimental ulcerative colitis in mice is mediated by increasing antioxidation and by the inhibition of NF-κB pathway.

Ulcerative colitis (UC) is a chronic inflammatory intestinal disease. It is necessary to find out new effective drugs for UC. In our study epicatechin extracted from grape seed by our institute for the first time could treat UC effectively. Then anti-UC mechanisms of epicatechin were elucidated in vivo and in vitro. Dextran sulfate sodium (DSS)-induced acute UC mice model was used to evaluate the activity of epicatechin and its properties against UC. Then its anti-inflammatory and antioxidant effects were evaluated as follows: the concentrations of TNF-α and IL-6 in the colon supernatants were determined by ELISA. NO and MPO were assayed by Griess method and commercial kit respectively. NF-κB were determined by NF-κB-Dependent Reporter Gene Expression Assay and Western Blotting respectively. Antioxidant factors such as SOD, MDA, GSH-Px and CAT were also measured in colon tissues and cell supernatant stimulated by LPS respectively. In C57BL/6J mice model with DSS-induced UC, epicatechin was able to decrease the disease activity index and colon macroscopic damage index scores, reduce body weight loss, and significantly relieve colon contracture and crypt damage. TNF-α, IL-6, NO, MPO and MDA were reduced in the mice administered epicatechin, whereas antioxidant enzymes showed increased activity in epicatechin-treated mice and cell line respectively. Furthermore, inhibition effect on NF-κB activation by epicatechin were demonstrated in vivo and in vitro. Epicatechin has inhibitory effect on DSS-induced acute UC. This effect is mainly due to its antioxidant effect and the inhibition of inflammatory molecules related to NF-κB pathway.

Cocoa flavonoids protect hepatic cells against high-glucose-induced oxidative stress: relevance of MAPKs.

Oxidative stress plays a main role in the pathogenesis of type 2 diabetes mellitus. Cocoa and (-)-epicatechin (EC), a main cocoa flavanol, have been suggested to exert beneficial effects in type 2 diabetes mellitus because of their protective effects against oxidative stress and insulin-like properties. In this study, the protective effect of EC and a cocoa phenolic extract (CPE) against oxidative stress induced by a high-glucose challenge, which causes insulin resistance, was investigated on hepatic HepG2 cells. Oxidative status, phosphorylated mitogen-activated protein kinases (MAPKs), nuclear factor E2 related factor 2 (Nrf2) and p-(Ser)-IRS-1 expression, and glucose uptake were evaluated. EC and CPE regulated antioxidant enzymes and activated extracellular-regulated kinase and Nrf2. EC and CPE pre-treatment prevented high-glucose-induced antioxidant defences and p-MAPKs, and maintained Nrf2 stimulation. The presence of selective MAPK inhibitors induced changes in redox status, glucose uptake, p-(Ser)- and total IRS-1 levels that were observed in CPE-mediated protection. EC and CPE recovered redox status of insulin-resistant HepG2 cells, suggesting that the functionality in EC- and CPE-treated cells was protected against high-glucose-induced oxidative insult. CPE beneficial effects on redox balance and insulin resistance were mediated by targeting MAPKs.

Intravenous (−)-epicatechin reduces myocardial ischemic injury by protecting mitochondrial function

BackgroundTargeting the mitochondria during ischemia/reperfusion (IR) can confer cardioprotection leading to improved clinical outcomes. The cardioprotective potential of (−)-epicatechin (EPI) during IR via modulation of mitochondrial function was evaluated. Methods and resultsIschemia was induced in rats via a 45min occlusion of the left anterior descending coronary artery followed by 1h, 48h, or 3week reperfusion. EPI (10mg/kg) was administered IV 15min prior to reperfusion for the single dose group and again 12h later for the double dose group. Controls received water. Experiments also utilized cultured neonatal rat ventricular myocytes (NRVM) and myoblasts. A single dose of EPI reduced infarct size by 27% at 48h and 28% at 3week. Double dose treatment further decreased infarct size by 80% at 48h, and 52% by 3weeks. The protective effect of EPI on mitochondrial function was evident after 1h of reperfusion when mitochondria demonstrated less respiratory inhibition, lower mitochondrial Ca2+ load, and a preserved pool of NADH that correlated with higher tissue ATP levels. Mechanistic studies in NRVM revealed that EPI acutely stimulated maximal rates of respiration, an effect that was blocked by inhibitors of the mitochondrial pyruvate carrier, nitric oxide synthase, or soluble guanylyl cyclase. In myoblasts, knockdown of components of the mitochondrial pyruvate carrier blocked EPI-induced respiratory stimulation. ConclusionsIV EPI confers cardioprotection via preservation of mitochondrial function potentially through enhanced substrate provision. These provocative results document a novel mechanism of a natural product with potential clinical utility.

Epicatechin limits renal injury by mitochondrial protection in cisplatin nephropathy

Cisplatin nephropathy can be regarded as a mitochondrial disease. Intervention to halt such deleterious injury is under investigation. Recently, the flavanol (-)-epicatechin emerges as a novel compound to protect the cardiovascular system, owing in part to mitochondrial protection. Here, we have hypothesized that epicatechin prevents the progression of cisplatin-induced kidney injury by protecting mitochondria. Epicatechin was administered 8 h after cisplatin injury was induced in the mouse kidney. Cisplatin significantly induced renal dysfunction and tubular injury along with an increase in oxidative stress. Mitochondrial damages were also evident as a decrease in loss of mitochondrial mass with a reduction in the oxidative phosphorylation complexes and low levels of MnSOD. The renal damages and mitochondrial injuries were significantly prevented by epicatechin treatment. Consistent with these observations, an in vitro study using cultured mouse proximal tubular cells demonstrated that cisplatin-induced mitochondrial injury, as revealed by a decrease in mitochondrial succinate dehydrogenase activity, an induction of cytochrome c release, mitochondrial fragmentation, and a reduction in complex IV protein, was prevented by epicatechin. Such a protective effect of epicatechin might be attributed to decreased oxidative stress and reduced ERK activity. Finally, we confirmed that epicatechin did not perturb the anticancer effect of cisplatin in HeLa cells. In conclusion, epicatechin exhibits protective effects due in part to its ability to prevent the progression of mitochondrial injury in mouse cisplatin nephropathy. Epicatechin may be a novel option to treat renal disorders associated with mitochondrial dysfunction.

Protective effects of epicatechin against the toxic effects of streptozotocin on rat pancreatic islets: in vivo and in vitro.

Green tea catechins have diverse pharmacological effects such as anticarcinogenic and antioxidant activities. To study the protective effects of green tea (-)-epicatechin (EC) against the toxic effects of streptozotocin (STZ), a selective beta cell toxin, on pancreatic islets in vivo and in vitro. Rats were randomly divided into four groups: control, EC (30 mg/kg)-treated, STZ (60 mg/kg)-treated, and EC plus STZ (same doses; EC+STZ)-treated rats. EC was administered twice a day for 6 days, and a single injection of STZ was used. In EC+STZ-treated rats, EC was administered 6 hours prior to STZ since posttreatment with EC had no beneficial effects on fully developed diabetes in our unpublished study. Insulin and insulin mRNA were detected by immunohistochemical analysis and in situ hybridization, respectively, and physiologic parameters including blood glucose concentration were measured daily. Following isolation of the islets, insulin release, nitrite levels, and islet morphology were observed in the four groups: control, EC (0.8 mM)-treated, STZ (5 mM)-treated, and EC+STZ (same doses)-treated islets. In EC+STZ-treated rats, hyperglycemia and weight loss were not observed and islet morphology was well preserved compared with STZ-treated rats. Compared with STZ treatment alone, insulin release was increased and nitrite production was decreased in EC+STZ-treated islets. EC appears to be helpful in protecting pancreatic islets against exposure to STZ in both in vivo and in vitro systems.

Protective Effect of Epicatechin, Epicatechin Gallate, and Quercetin on Lipid Peroxidation in Phospholipid Bilayers

Antioxidative effect of (−)-epicatechin,(−)-epicatechin gallate, and quercetin was examined by measuring the inhibition of lipid peroxidation in large unilamellar liposomes composed of egg yolk phosphatidyicholine (PC). These catechol-type flavonoids were stable in the liposomal suspension. They retarded the accumulation of PC-hydroperoxides depending on their concentrations when the suspension was exposed to an water-soluble radical initiator, 2,2′-azobis(2-amidinopropane)hydrochloride (AAPH). Their inhibitory effects lasted longer than that of α-tocopherol. When each flavonoid and α-tocopherol were mixed in the liposomes, epicatechin and epicatechin gallate disappeared in favor of α-tocopherol. Quercetin also decreased faster than α-tocopherol in the initial stage of incubation. Kinetic studies of the inhibition of radical chain oxidation of methyl linoleate in solution demonstrated that the rate constants for the inhibition of oxidation by these flavonoids ( k inh) were 5-20 times smaller than that by α-tocopherol. It is likely that the flavonoids are localized near the surface of phospholipid bilayers suitable for scavenging aqueous oxygen radicals and thereby they prevent the consumption of lipophilic α-tocopherol. Epicatechin and epicatecin gallate gave smaller k inh values than quercetin. Voltammograms of these compounds showed that electron-donating ability of catechins was lower than that of quercetin. However, antioxidative effects of catechins were comparable to that of quercetin in AAPH-initiated peroxidation of the liposomal suspension. It is concluded that catechins and quercetin serve as powerful antioxidants against lipid peroxidation when phospholipid bilayers are exposed to aqueous oxygen radicals.