Reduction of photodynamic damage of blood vessels in the protected region by(–)-epigallocatechin gallate

Photodynamic therapy(PDT)has been increasingly used in the clinical treatment of neoplastic,inflammatory and infectious skin diseases.However,the generation of reactive oxygen species(ROS)may induce undesired side effects in normal tissue surrounding the treatment lesion,which is a big challenge for the clinical application of PDT.To date,(–)-Epigallocatechin gallate(EGCG)has been widely proposed as an antiangiogenic and antitumor agent for the protection of normal tissue from ROS-mediated oxidative damage.This study evaluates the regulation ability of EGCG for photodynamic damage of blood vessels during hematoporphyrin monomethyl ether(Hemoporfin)-mediated PDT.The quenching rate constants of EGCG for the triplet-state Hemoporfin and photosensitized 1O2 generation are determined to be 6.8×10^(8)M^(−1)S^(−1),respectively.The vasoconstriction of blood vessels in the protected region treated with EGCG hydrogel after PDT is lower than that of the control region treated with pure hydrogel,suggesting an efficiently reduced photodamage of Hemoporfin for blood vessels treated with EGCG.This study indicates that EGCG is an efficient quencher for triplet-state Hemoporfin and 1O2,and EGCG could be potentially used to reduce the undesired photodamage of normal tissue in clinical PDT.

微波辅助合成Ni-gallate(镍基没食子酸金属有机框架)用于CO_(2)吸附的性能研究

CO_(2)排放导致的一系列环境问题,引起广泛关注,金属有机框架(MOFs)因其超高的孔隙率比表面积,被认为是捕集CO_(2)的理想材料。采用微波辅助合成Ni-gallate(镍基没食子酸金属有机框架),并借助扫描电子显微镜(SEM)、傅里叶变换红外光谱(FT-IR)、X射线衍射(XRD)等表征手段进行分析。结果表明:相较于传统水热合成,微波辅助合成的材料有着较高的结晶度和规则的尺寸形貌,在25℃时表现出更高的CO_(2)吸附量(3.82mmol/g)。结合微波辅助合成快速高效的优点,通过相转化法和聚酰亚胺复合得到的聚合物材料,不仅具有良好的CO_(2)吸附性能,而且有着优异的机械和热稳定性,有进一步发展成为工业CO_(2)捕集材料的潜力。

Therapeutic effects of epigallocatechin and epigallocatechin gallate on the allergic reaction ofα_(s1)-casein sensitized mice

To investigate the anti-α_(s1)-casein allergy mechanism of two tea-derived polyphenols,epigallocatechin(EGC)and epigallocatechin gallate(EGCG),BALB/c mice were sensitized and challenged withα_(s1)-casein and nutritional intervention was given by EGC and EGCG during the sensitization provocation phase.The main evaluation indexes used were levels of mast cell proteases,histamine,and specific antibody immunoglobulin E(IgE),as well as cytokine secretion and pathological observation.The results showed that both EGC and EGCG significantly reduced levels of mast cell protease,histamine,specific IgE antibodies,and Th2 cytokines in allergic mice.The histopathology results showed that both EGC and EGCG markedly reduced the degree of lesions in the intestine,thymus,spleen,and lung.The conclusions from this study can provide a theoretical basis for the mechanism by which tea polyphenols regulate food allergens.

Effect of epigallocatechin gallate in green tea on preventing lens opacity and αB-crystallin aggregation in rat model of diabetes

AIM:To evaluate the effect of epigallocatechin gallate(EGCG) in preventing lens opacity and the aggregation of lens αB-crystallin in model rats of diabetes mellitus(DM).METHODS:This experimental study included Wistar rats for DM as in vivo models and divided into 5 groups.The treatment groups were administered EGCG by orally for 20d and were then assessed for their degree of lens opacity with binocular microscope and lens αB-crystallin expression from Western blot analyze.RESULTS:Pearson correlation test and regression analysis on EGCG exposure and final random blood sugar(RBS) obtained a significance level of P<0.05.EGCG exposure can significantly lower RBS with an R~2 of 0.5634(56.34%).The same analysis on EGCG exposure and the degree of lens opacity obtained a significance level of P<0.05 and increased exposure to EGCG can significantly lower the degree of lens opacity with an R~2 of 0.8577(85.77%).Correlation analysis between EGCG and the expression of lens αB-crystallin can be concluded that the higher the EGCG exposure administered,the higher the native lens αB-crystallin expression and the lower the aggregate lens αB-crystallin expression.There was also significant effect in which every 1 mg/kg body weight dose of EGCG can increase the native lens αB-crystallin expression by 0.0063 and decrease the aggregate lens αB-crystallin expression by 0.0076.CONCLUSION:The administration of EGCG at a dose of 300,600,and 1200 mg shows a significant effect on preventing lens opacity and aggregation of αB-crystallin in diabetic rat models and this research could be a biomolecular prevention of cataract.

Structural shift of gut microbiota during chemopreventive effects of epigallocatechin gallate on colorectal carcinogenesis in mice

AIM To investigate the effect of epigallocatechin gallate(EGCG) on structural changes of gut microbiota in colorectal carcinogenesis.METHODS An azoxymethane(AOM)/dextran sodium sulfate(DSS)-induced colitis mouse model was established. Fortytwo female FVB/N mice were randomly divided into the following three groups: group 1(10 mice, negative control) was treated with vehicle, group 2(16 mice, positive control) was treated with AOM plus vehicle, and group 3(16 mice, EG) was treated with AOM plus EGCG. For aberrant crypt foci(ACF) evaluation, the colons were rapidly took out after sacrifice, rinsed with saline, opened longitudinally, laid flat on a polystyrene board, and fixed with 10% buffered formaldehyde solution before being stained with 0.2% methylene blue in saline. For tumor evaluation, the colon was macroscopically inspected and photographed, then the total number of tumors was enumerated and tumor size measured. For histological examination, the fixed tissues were paraffin-embedded and sectioned at 5 mm thickness. Microbial genomic DNA was extracted from fecal and intestinal content samples using a commercial kit. The V4 hypervariable regions of 16 S r RNA were PCR-amplified with the barcoded fusion primers. Using the best hit classification option, the sequences from each sample were aligned to the RDP 16 S r RNA training set to classify the taxonomic abundance in QIIME. Statistical analyses were then performed.RESULTS Treatment of mice with 1% EGCG caused a significant decrease in the mean number of ACF per mouse, when compared with the model mice treated with AOM/DSS(5.38 ± 4.24 vs 13.13 ± 3.02, P < 0.01). Compared with the positive control group, 1% EGCG treatment dependently decreased tumor load per mouse by 85%(33.96 ± 6.10 vs 2.96 ± 2.86, respectively, P < 0.01). All revealed that EGCG could inhibit colon carcinogenesis by decreasing the number of precancerous lesions as well as solid tumors, with reduced tumor load and delayed histological progression of CRC. During the cancerization, the diversity of gut microbiota increased, potential carcinogenic bacteria such as Bacteroides were enriched, and the abundance of butyrate-producing bacteria(Clostridiaceae, Ruminococcus, etc.) decreased continuously. In contrast, the structure of gut microbiota was relatively stable during the intervention of EGCG on colon carcinogenesis. Enrichment of probiotics(Bifidobacterium, Lactobacillu, etc.) might be a potential mechanism for EGCG's effects on tumor suppression. Via bioinformatics analysis, principal coordinate analysis and cluster analysis of the tumor formation process, we found that the diversity of gut microbiota increased in the tumor model group while that in the EGCG interfered group(EG) remained relatively stable.CONCLUSION Gut microbiota imbalance might be a potential mechanism for the prevention of malignant transformation by EGCG, which is significant for diagnosis, treatment, prognosis evaluation, and prevention of colorectal cancer.

Effect of Propyl Gallate on Activity of Cyclooxygenase 1 and 2 in Mice's Peritoneal Macrophages*

Objective: To investigate the effect of Red Peony 801 (propyl gallate,PrG) on cyclooxygenase (COX) activity in murine peritoneal macrophages. Methods: A screening model for COX inhibitors in vitro based on murine peritoneal macrophages was used. COX-1 activity was reflected by the level of 6-ketoprostaglandin F1α(6-keto-PGF1α) in supernatants of cultured macrophages which were stimulated with calcium ionophore A23187 for a short-term, while COX-2 activity was reflected by the level of prostaglandin E2 (PGE2) in supernatants of cultured macrophages which were stimulated with lipopolysaccharide (LPS) for a long-term. Results: PrG did not affect A23187-induced, COX-1-derived 6-keto-PGF1α synthesis at the concentrations of 1×10-5, 5×10-6 mol/L (P>0.05), but enhanced 6-keto-PGF1α synthesis at the concentrations of 1×10-6, 5×10-7, 1×10-7 mol/L (P<0.01) in vitro, and showed a good dose-dependent manner. It inhibited LPS-induced, COX-2-derived PGE2 synthesis at the concentrations of 1×10-5,1×10-6 mol/L (P< 0. 05). Conclusion: Within the range of 1×10-5 to 1×10-7 mol/L, PrG activated COX-1 at lower concentrations and inhibited COX-2 at higher concentrations in murine peritoneal macrophages.

Does combined therapy of curcumin and epigallocatechin gallate have a synergistic neuroprotective effect against spinal cord injury？

Systematic inflammatory response after spinal cord injury （SCI） is one of the factors leading to lesion development and a profound degree of functional loss. Anti-inflammatory compounds, such as curcumin and epigallocatechin gallate （EGCG） are known for their neuroprotective effects. In this study, we investigated the effect of combined therapy of curcumin and EGCG in a rat model of acute SCI induced by balloon compression. Immediately after SCI, rats received curcumin, EGCG, curcumin ＋ EGCG or saline [daily intraperitoneal doses （curcumin, 6 mg/kg; EGCG 17 mg/kg）] and weekly intramuscular doses （curcumin,60 mg/kg; EGCG 17 mg/kg）] for 28 days. Rats were evaluated using behavioral tests （the Basso, Beattie, and Bresnahan （BBB） open-field locomotor test, flat beam test）. Spinal cord tissue was analyzed using histological methods （Luxol Blue-cresyl violet staining） and mmunohistochemistry （anti-glial fibrillary acidic protein, anti-growth associated protein 43）. Cytokine levels （interleukin-1β, interleukin-4, interleukin-2,interleukin-6, macrophage inflammatory protein 1-alpha, and RANTES） were measured using Luminex assay. Quantitative polymerase chain reaction was performed to determine the relative expression of genes （Sort1, Fgf2, Irf5, Mrc1, Olig2, Casp3, Gap43, Gfap, Vegf, NfκB, Cntf） related to regenerative processes in injured spinal cord. We found that all treatments displayed significant behavioral recovery, with no obvious synergistic effect after combined therapy of curcumin and ECGC. Curcumin and EGCG alone or in combination increased axonal sprouting, decreased glial scar formation, and altered the levels of macrophage inflammatory protein 1-alpha, interleukin-1β, interleukin-4 and interleukin-6 cytokines. These results imply that although the expected synergistic response of this combined therapy was less obvious, aspects of tissue regeneration and immune responses in severe SCI were evident.

Comparison of the impact of epigallocatechin gallate and ellagic acid in an experimental cataract model induced by sodium selenite

AIM：To compare the potential protective effects of epigallocatechin gallate（EGCG） and ellagic acid（EA） in an experimental cataract model.●METHODS：Twenty-eight Spraque-Dawley rat pups were assigned into four groups.All the rats,except for those in the control group,were injected subcutaneously sodium selenite to induce experimental cataract on the postpartum ninth day,and between 10 th and 14 th days.Rats in the sham,EGCG,and EA groups were intraperitoneally administered 50 mg/（kg·d） saline solution,50 mg/（kg·d） EGCG and 200 mg/（kg·d） EA,respectively.The reduced glutathione（GSH） and malondialdehyde（MDA） levels,total antioxidant status（TAS） and total oxidant status（TOS） in lens supernatants were measured.RESULTS：The mean cataract gradings in EGCG and EA groups were found to be significantly lower than that in sham group（P〈0.001）.The mean GSH levels and TASs in EGCG and EA groups were significantly higher than that in sham group while mean MDA levels and TOSs in EGCG and EA groups were significantly lower than that in the sham group（P〈0.001）.CONCLUSION：EGCG and EA have protective effects on cataract development via the inhibition of oxidative stress.

Epigallocatechin gallate content change of the fresh tea leaf homogenates extracted by different methods in extraction and preservation

The fresh leaves of China green tea, Camellia sinensis, were collected from Fuyang, Zhejiang Province, China, in April. The tea polyphenols was extracted by four different methods （homogenized with distilled water at room temperature, homogenized with 0.3% citric acid （w/v） at room temperature, 5- min boiling and homogenized with distilled water at room temperature, homogenized with 85℃ distilled water）, and after preserving at room temperature, the change of the Epigallocatechin gallate （EGCG） contents of the extracts was investigated. Results indicated that the EGCG content of homogenate extracted with 85℃ distilled water was the highest before the extract was preserved, followed by that of the extract homogenized with 0.3% citric acid at room temperature. During preservation, EGCG content changed obviously. The EGCG contents of homogenates extracted with distilled water at room temperature and 85℃ distilled water declined quickly and separately reduced to 21.52% and 54.6% of their initial contents after preservation for 12 h. The EGCG contents extracted by 0.3% citric acid （w/v） solvent at room temperature and 5- min boiling/homogenized with distilled water at room temperature declined relatively slowly ,and separately reduced to 76.9% and 85.16% of their initial contents after preservation for 12 h. It was also found that the citric acid can prevent the degradation of EGCG and the extract solution color is light green

Development of Doped Lanthanum Gallate Solid Electrolytes

Development of the doped lanthanum gallate solid electrolytes in the recent years was reviewed. The structure and oxygen ion transference mechanism were discussed. Effects of alkali earths, transition metals, and impurities on electrical conductivity of the doped lanthanum gallates were also discussed. The applications of doped lanthanum gallate were described. The current problems and corresponding strategies were explored.

Epigallocatechin gallate inhibits HBV DNA synthesis in a viral replication-inducible cell line

AIM:To analyze the antiviral mechanism of Epigallocatechin gallate(EGCG)against hepatitis B virus(HBV) replication.METHODS:In this research,the HBV-replicating cell line HepG2.117 was used to investigate the antiviral mechanism of EGCG.Cytotoxicity of EGCG was analyzed by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay.Hepatitis B virus e antigen(HBeAg)and hepatitis B virus surface antigen(HBsAg)in the supernatant were detected by enzyme-linked immunosorbent assay.Precore mRNA and pregenomic RNA(pgRNA) levels were determined by semi-quantitative reverse transcription polymerase chain reaction(PCR)assay.The effect of EGCG on HBV core promoter activity was measured by dual luciferase reporter assay.HBV covalently closed circular DNA and replicative intermediates of DNA were quantified by real-time PCR assay.RESULTS:When HepG2.117 cells were grown in the presence of EGCG,the expression of HBeAg was suppressed,however,the expression of HBsAg was not affected.HBV precore mRNA level was also downregulated by EGCG,while the transcription of precore mRNA was not impaired.The synthesis of both HBV covalently closed circular DNA and replicative intermediates of DNA were reduced by EGCG treatment to a similar extent,however,HBV pgRNA transcripted from chromosome-integrated HBV genome was not affected by EGCG treatment,indicating that EGCG targets only replicative intermediates of DNA synthesis.CONCLUSION:In HepG2.117 cells,EGCG inhibits HBV replication by impairing HBV replicative intermediates of DNA synthesis and such inhibition results in reduced production of HBV covalently closed circular DNA.

Preparation of chitosan-Epigallocatechin-3-O-gallate nanoparticles and their inhibitory effect on the growth of breast cancer cells

In this paper,we prepared the nanoparticle drug carrier system between nanoparticles chitosan and Epigallocatechin-3 O-gallate(EGCG)for breast cancer cell inhibiting application.For this drug carrier system,chitosan acts as a carrier and EGOG as a drug.Which were systematically characterized and thoroughly evaluated in terms of their inhibition rate and biocompatibility.We also did a cell scratch test and the result indicated that the chitosan EGCG nanoparticles have inhibitory effect on the growth of breast cancer cells.The inhibition rate could reach up to 21.91%.This work revealed that the modification of nanopartidles paved a way for specific biomedical applications.

Thermally Reversible,Self-Healing Polyurethane Based on Propyl Gallate and Polyurethane Prepolymers with Varied Isocyanate Content

Thermosetting polyurethanes are widely used in various fields owing to their excellent elasticity,strength and solvent resistance.Three environmental friendly propyl gallate-based self-healing polyurethanes were prepared from polyurethane prepolymers with varying isocyanate content.The thermal stabilities of the polyurethanes were tested using thermogravimetric analysis.Their self-healing and mechanical properties were analyzed using a universal testing machine and dynamic thermomechanical analysis.The polyurethanes were found with high self-healing ability and excellent mechanical properties due to the absence of phenolic carbamate.These qualities improved with increased isocyanate content and the prolonged selfhealing time.We found,therefore,that the propyl gallate-based polyurethane has potential for use in industrial applications as self-healing materials.

Epigallocatechin gallate inhibits dimethylhydrazine-induced colorectal cancer in rats

BACKGROUND Epigallocatechin gallate(EGCG)is a polyhydroxy phenolic compound extracted from tea and its antitumor effect has received widespread attention.We explored the inhibitory effect of EGCG on dimethylhydrazine(DMH)-induced colorectal cancer(CRC)using a rat model,predicted the interaction between EGCG and CRC target genes using a database,and explained the EGCG associated target pathways and mechanisms in CRC.AIM To understand the inhibitory mechanisms of EGCG on CRC cell proliferation and identify its pharmacological targets by network pharmacology analysis.METHODS DMH(40 mg/kg,s.c.,twice weekly for eight weeks)was used to induce CRC in rats.After model establishment,the rats were administered with EGCG(50,100,or 200 mg/kg,p.o.,once daily for eight weeks)and killed 12 and 20 wk after the start of the experiment.Formation of aberrant crypt foci and tumor was studied by histological analysis.Using network pharmacology analysis,candidate and collective targets of EGCG and CRC were identified,and Gene ontology(GO)and Kyoto Encyclopedia of Genes and Genomes analyses were used to predict the pathways altered by EGCG.RESULTS At week 12,high-dose EGCG treatment significantly reduced the tumor formation rate,total number of tumors,cancerous and non-cancerous tumors,tumor volume,ascites formation,and aberrant crypt foci count.At week 20,all three doses of EGCG were effective.Seventy-eight collective targets of EGCG and CRC were identified,of which 28 genes were dysregulated in CRC.Kyoto Encyclopedia of Genes and Genomes and GO analyses showed that the dysregulated genes were enriched in hsa05210(CRC),hsa04115(p53 signaling pathway),and hsa04151(PI3K-Akt signaling pathway),GO:0043124(negative regulation of I-kappaB kinase/NF-kappaB signaling pathway),GO:0043409(negative regulation of mitogen-activated protein kinase cascade),and GO:2001244(positive regulation of intrinsic apoptotic signaling pathway)respectively.CONCLUSION EGCG inhibits the formation of DMH-induced CRC by regulating key pathways involved in tumorigenesis.

Green tea extract and epigallocatechin 3-gallate reduced labile iron pool and protected oxidative stress in iron-loaded cultured hepatocytes

Cellular and mitochondrial damage can be caused by labile iron pool (LIP) and mediated by reactive oxygen species (ROS). Livers of the thalassemias have highly increased levels of LIP and ROS. Green tea extract (GTE) and epigallocatechin 3-gallatte (EGCG) can potentially protect liver inflammation, fibrosis and cancer due to their anti-oxidative and iron-chelating activities. We studied the effects of GTE and EGCG on intracellular LIP and ROS, and mitochondrial membrane potential (ΔΨm) in mouse hepatocyte and HepG2 cell cultures using specific fluorescent techniques. Treatment with GTE (12.5 - 25 mg/dl) and EGCG (25 - 50 μM) significantly lowered levels of ΔΨm in the mouse hepatocytes;however, combined treatment of 25 μM DFP with GTE and EGCG did not enhance the decrease of hepatic ΔΨm. The results showed that GTE and EGCG effectively removed the intracellular LIP and ROS, and relieved the mitochondria membrane collapse of the liver cells, suggesting a hepatoprotective effect of green tea extract and EGCG in the hepatocytes with iron overload. Their actions might be related to iron-chelating and free radical-scavenging capacities. Whether the effects can improve iron overload and oxidative stress in thalassemia patients remains to be seen upon further examination.

Green tea, epigallocatechin gallate and the prevention of Alzheimer’s disease: clinical evidence

Given its increasing global prevalence,Alzheimer’s disease(AD)has become a major public health challenge worldwide.The symptomatic treatments available for AD have shown no significant efficacy,and no disease-modifying interventions are capable of slowing the progression of the disorder.The potential of lifestyle-related factors,including diet,is increasingly recognized as an important consideration in the primary prevention of AD.Numerous mechanisms potentially underlying neuroprotective effects of bioactive components contained in tea,such as(-)-epigallocatechin-3-gallate,as well as their preventive efficacy against AD,have been elucidated in preclinical studies.However,in contrast to the abundance of mechanistic findings in animals,clinical results demonstrating efficacy in humans are scarce.While epidemiological studies have provided some evidence indicating that green tea consumption is associated with a reduced risk of age-related cognitive decline and AD,a causal relationship cannot be established on the basis of these observations.The clinical evidence regarding preventive or therapeutic effects of green tea and its bioactive components is unsatisfactory.A role of green tea in the prevention of AD cannot be recommended until well-designed,randomized,placebo-controlled clinical trials using standardized formulations confirm the purported beneficial effects of green tea.

Methyl gallate isolated from Mangifera pajang kernel induces proliferation inhibition and apoptosis in MCF-7 breast cancer cells via oxidative stress

Objective:To determine the lead bioactive compound in kernel extract of Mangifera pajang and its anti-cancer activity against human breast cancer cell lines with positive estrogen receptor(MCF-7).Methods:The methanolic extract of dried powder kernel of Mangifera pajang was exposed to column chromatography for isolation.The structural elucidation of the isolated compound was characterized using infrared,nuclear magnetic resonance,mass spectrometry.Furthermore,cytotoxicity,morphological changes,flow cytometry and cell cycle arrest analyses were performed to examine the mechanism of anti-proliferation and apoptosis induced by methyl gallate against MCF-7.Results:One compound was isolated from the methanolic extract of Mangifera pajang kernel and identified as methyl gallate.The flow cytometric results demonstrated induction of apoptosis in MCF-7 cells by three concentrations of methyl gallate.The cell cycle arrest showed a significant(P<0.05)decrease in cell progression at G2/M phase of MCF-7 after treatment with 100μM of methyl gallate.The cell percentage of early and late apoptosis was significant at 10 and 100μM of methyl gallate.Also,methyl gallate treatment induced up-regulation of reactive oxygen species levels in MCF-7 cells with a reduction in superoxide dismutase levels.Conclusions:These findings indicate that isolated methyl gallate from Mangifera pajang kernel extracts induces growth inhibition and apoptosis in MCF-7 cells via up-regulating oxidative stress pathway.

Inhibition of Invasion and Up-regulation of E-cadherin Expression in Human Malignant Melanoma Cell Line A375 by(-)-Epigallocatechin-3-gallate

The inhibitory effects of （-）-epigallocatechin-3-gallate （EGCG） on the invasion of human malignant melanoma cell line A375 and the possible molecular mechanisms of this effect were investiaged. A375 cells were pretreated with 20 μg/mL EGCG for 24, 48 and 72 h respectively and the E-cadherin expression was detected by Western blot analysis. A375 cells were also pretreated with different concentrations of EGCG （1, 5, 10 and 20 μg/mL） for 72 h and the expression of E-cadherin was measured by RT-PCR. The adhesion and invasion of A375 cells were tested by cell-matrigel adhesion assay and matrigel invasion assay respectively. The results showed that EGCG could significantly up-regulate the expression of E-cadherin time-and concentration-dependently （both P〈0.05）. Statistical analysis showed that A375 cells invasion was inhibited by EGCG and correlated with the up-regulation of E-cadherin expression. It was suggested that EGCG strongly inhibited invasion of A375 cells, and the inhibition mechanism was possibly associated with the up-regulation of E-cadherin expression.

Neuroprotective effect of epigallocatechin-3-gallate on hemisection-induced spinal cord injury in rats

Epigallocatechin-3-gallate （EGCG）, a naturally occurring compound in green tea, has been widely used as an antioxidant agent. In the present study, model rats with acute spinal cord injury were intraperitoneally injected with 25, 50, and 100 mg/kg EGCG, and spinal cord ultrastructure, oxidative stress reaction, inflammatory factors, and apoptosis-associated gene expression were observed. Results showed that EGCG attenuated neuronal and axonal injury 24 hours post injury. It also decreased serum intedeukin-113, tumor necrosis factor-a, and intercellular adhesion molecule-1 release, and decreased apoptosis-associated gene expression. Furthermore, it increased the level of the superoxide anion （O2-）, superoxide dismutase, and B-cell lymphoma/leukemia-2, and reduced malondialdehyde levels. Furthermore, it reduced the expression of the pro-apoptotic protein Bax. Noticeably, EGCG at the 100 mg/kg dosage exhibited similar effects as methylprednisolone sodium succinate, which has been frequently used for clinical acute spinal cord injury. The results demonstrated that EGCG can significantly inhibit inflammation, suppress oxidation, and reduce apoptosis in acute spinal cord injury.

Protective Effects of Epigallocatechin-3-gallate on Intestinal Ischemia Reperfusion Injury through Enhanced Activation of PI3K/Akt Pathway in Rats

Inflammation plays a critical role in intestinal ischemia reperfusion injury（IRI）. Epigallocatechin-3-gallate（EGCG） has been demonstrated to possess anti-inflammatory effect. This study examined the effect of EGCG on intestinal IRI and explored the possible mechanisms. Male Wistar rats were randomly divided into three groups： sham-operated group（Sham）, IRI control group（IRI） and IRI-EGCG group（EGCG）. Rats in IRI-EGCG group were administered dissolved EGCG in drinking water（0.4 mg/m L） for 14 days prior to IRI induction. A rat model of intestinal IRI was established by ligating the superior mesenteric artery（SMA） for 30 min, followed by reperfusion for 1 h. Intestinal histology, pro-inflammatory cytokines and mediators were examined and the effect of EGCG on PI3K/Akt signalling was assessed. EGCG significantly alleviated the pathological changes of the intestine and suppressed the IRI-induced up-regulation of TNF-α, IL-1 and IL-6 m RNA and protein expression in the serum and intestine. The mechanism might be that EGCG enhanced the activation of PI3K/Akt signalling pathway. In conclusion, the administration of EGCG can significantly mitigate the acute intestinal IRI in rats by enhancing the activation of PI3K/Akt signalling pathway to suppress inflammatory response and might be a promising alternative for the prevention or treatment of intestinal IRI in the clinical practice.