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 a...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.展开更多
Lipophilic tea polyphenols (LTP) were prepared by catalytic esterifieation of green tea polyphenols (GRIP) with hexadeeanoyl chloride. A novel long-chain aeyl-derivative of epigalloeateehin-3-o-gallate(EGCG) was first...Lipophilic tea polyphenols (LTP) were prepared by catalytic esterifieation of green tea polyphenols (GRIP) with hexadeeanoyl chloride. A novel long-chain aeyl-derivative of epigalloeateehin-3-o-gallate(EGCG) was first isolated from purification of LTP by high-speed eountereurrent ehromatography (HSCCC)using a solvent system composed of n-hexane-ethyl acetate-methanol-water ( 1 : 1 : 1 : 1, v/v) . The moleeularstructure of the acyl-derivative, Epigallocatechin-3-O-gallate-4'-O-hexadeeanate , was elucidated by meansof elemental analysis, IR, 1H-NMR and MS spectra.展开更多
Objective:To investigate the effect of epigallocatechin-3-gallate(EGCG)on endothelial dysfunction in spontaneously hypertensive rats(SHR).Methods:Wistar-Kyoto(WKY)rats and SHR were divided into four groups;WKY control...Objective:To investigate the effect of epigallocatechin-3-gallate(EGCG)on endothelial dysfunction in spontaneously hypertensive rats(SHR).Methods:Wistar-Kyoto(WKY)rats and SHR were divided into four groups;WKY control,SHR control and SHR treated with EGCG(50 mg/kg/day)or losartan(10 mg/kg/day).The treatment was given daily for 4 weeks by oral gavage and the blood pressure was monitored by tail-cuff method every 3 days.Acetylcholineinduced endothelium-dependent relaxations were assessed in isolated phenylephrine-precontracted aortic rings at the end of treatment.The vascular levels of reactive oxygen species,nitric oxide,tetrahydrobiopterin,and cyclic guanosine monophosphate were also measured.Moreover,the expression of angiotensinⅡtype 1(AT_(1))receptor protein was determined.Results:The systolic blood pressure was significantly decreased in SHR treated with EGCG.The impaired endothelium-dependent relaxation was significantly improved in aortic ring isolated from the EGCG-treated SHR group.EGCG also significantly increased the levels of nitric oxide,tetrahydrobiopterin,and cyclic guanosine monophosphate,while decreasing the level of reactive oxygen species and the protein expression of AT_(1)receptor in SHR.Conclusions:EGCG attenuates endothelial dysfunction in SHR by decreasing oxidative stress and increasing vascular nitric oxide bioavailability,which may be modulated partly by inhibition of vascular AT_(1)receptors.An increase in endothelium-dependent relaxation may contribute to a decrease in blood pressure in hypertensive animals.展开更多
Alzheimer's disease(AD)shows cognitive impairments in clinic,which is multifactorial with different etiopathogenic mechanisms such as A|3 deposition,neuroinflammation and neuronal dystrophy involved.Therefore,mult...Alzheimer's disease(AD)shows cognitive impairments in clinic,which is multifactorial with different etiopathogenic mechanisms such as A|3 deposition,neuroinflammation and neuronal dystrophy involved.Therefore,multi-targets drugs with neuroprotective,anti-amyloidogenic and anti-inflammatory properties will be effective in AD treatment.Epigallocatechin-3-gallate(EGCG)possesses a broad spectrum of pharmacological activities in the prevention and treatment of multiple neurodegenerative diseases.In the present study,we showed that oral administration of EGCG(50 mg/kg)for 4 months significantly attenuated the cognitive deficits in APP/PS1 transgenic mice,which served as AD model.Moreover,EGCG induced an improvement in dendritic integrity and expression levels of synaptic proteins in the brain of APP/PS 1 mice.And EGCG exerted obvious anti-inflammatory effects,which was manifested by alleviating microglia activation,decreasing pro-inflammatory cytokine(IL-β)and increasing anti-inflammatory cytokines(IL-10,IL-β).Furthermore,p-amyloid(AP)plaques were markedly reduced in the hippocampus of 6-month old APP/PS 1 mice after EGCG treatment.In conclusion,these findings indicate that EGCG improves AD-like cognitive impairments through neuroprotective,anti-amyloidogenic and anti-inflammatory effects,thus is a promising therapeutic can didate for AD.展开更多
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 inj...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.展开更多
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...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.展开更多
AIM:To investigate the mechanism underlying the anti-inflammatory effects of epigallocatechin-3-gallate(EGCG)in lipopolysaccharide(LPS)-stimulated human retinal endothelial cells(HRECs).METHODS:HRECspre-treatedwithEGC...AIM:To investigate the mechanism underlying the anti-inflammatory effects of epigallocatechin-3-gallate(EGCG)in lipopolysaccharide(LPS)-stimulated human retinal endothelial cells(HRECs).METHODS:HRECspre-treatedwithEGCG(0-100μmol/L)were stimulated with LPS(250 ng/mL).Levels of tumor necrosis factor alpha(TNF-α),vascular endothelial growth factor(VEGF),monocyte chemotactic protein-1(MCP-1)and nitric oxide(NO)in the supernatants were determined by enzyme-linked immunosorbent assay(ELISA)and Griess assay.The protein expression of phosphorylated extracellular signal-regulated kinase(ERK)1/2 and p38 mitogen-activated protein kinases(p38)were determined by Western blot analysis.RESULTS:EGCG pre-treatment significantly inhibited the secretion of TNF-α,VEGF,MCP-1 and NO in LPSstimulated HRECs.Moreover,EGCG effectively attenuated LPS-induced activation and phosphorylation of ERK1/2 and p38 in HRECs in a dose-dependent manner.CONCLUSION:EGCG exhibited inhibitory effects on LPS-induced pro-inflammatory cytokines production by modulating ERK1/2 and p38 pathways in HRECs,suggesting EGCG as a potential candidate for antiinflammatory intervention.展开更多
Traumatic spinal cord injury （SCI） causes motor paralysis, sensory anesthesia and autonomic dysfunction below the le- sion site and additionally some SCI patients refer neuropathic pain together with these signs and...Traumatic spinal cord injury （SCI） causes motor paralysis, sensory anesthesia and autonomic dysfunction below the le- sion site and additionally some SCI patients refer neuropathic pain together with these signs and symptoms. Clinical and experimental studies have revealed the main pathological changes of injured spinal cord implicated in all these signs and symptoms, including neuropathic pain. After few hours of traumatic SCI, it is usual to observe broken blood brain barrier with plasma and blood cells extravasation, cell necrosis, disruption of ascending and descending spinal cord pathways and increased potassium and glutamate. Glutamate contributes to excitotoxicity of neurons whereas potassium facilitates ectopic depolarization of survival neurons and activation of resident microglia.展开更多
基金the support of the National Natural Science Foundation of China(NSFC Nos.61722508 and 11305020)Nanophotonics and Biophotonics Key Laboratory of Jilin Province,P.R.China(20140622009JC)and(14GH005).
文摘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.
文摘Lipophilic tea polyphenols (LTP) were prepared by catalytic esterifieation of green tea polyphenols (GRIP) with hexadeeanoyl chloride. A novel long-chain aeyl-derivative of epigalloeateehin-3-o-gallate(EGCG) was first isolated from purification of LTP by high-speed eountereurrent ehromatography (HSCCC)using a solvent system composed of n-hexane-ethyl acetate-methanol-water ( 1 : 1 : 1 : 1, v/v) . The moleeularstructure of the acyl-derivative, Epigallocatechin-3-O-gallate-4'-O-hexadeeanate , was elucidated by meansof elemental analysis, IR, 1H-NMR and MS spectra.
基金funded by the Universiti Tunku Abdul Rahman Research fund(IPSR/RMC/UTARRF/2019-C2/L08)。
文摘Objective:To investigate the effect of epigallocatechin-3-gallate(EGCG)on endothelial dysfunction in spontaneously hypertensive rats(SHR).Methods:Wistar-Kyoto(WKY)rats and SHR were divided into four groups;WKY control,SHR control and SHR treated with EGCG(50 mg/kg/day)or losartan(10 mg/kg/day).The treatment was given daily for 4 weeks by oral gavage and the blood pressure was monitored by tail-cuff method every 3 days.Acetylcholineinduced endothelium-dependent relaxations were assessed in isolated phenylephrine-precontracted aortic rings at the end of treatment.The vascular levels of reactive oxygen species,nitric oxide,tetrahydrobiopterin,and cyclic guanosine monophosphate were also measured.Moreover,the expression of angiotensinⅡtype 1(AT_(1))receptor protein was determined.Results:The systolic blood pressure was significantly decreased in SHR treated with EGCG.The impaired endothelium-dependent relaxation was significantly improved in aortic ring isolated from the EGCG-treated SHR group.EGCG also significantly increased the levels of nitric oxide,tetrahydrobiopterin,and cyclic guanosine monophosphate,while decreasing the level of reactive oxygen species and the protein expression of AT_(1)receptor in SHR.Conclusions:EGCG attenuates endothelial dysfunction in SHR by decreasing oxidative stress and increasing vascular nitric oxide bioavailability,which may be modulated partly by inhibition of vascular AT_(1)receptors.An increase in endothelium-dependent relaxation may contribute to a decrease in blood pressure in hypertensive animals.
基金the National Natural Science Foundation of China(No.31800851).
文摘Alzheimer's disease(AD)shows cognitive impairments in clinic,which is multifactorial with different etiopathogenic mechanisms such as A|3 deposition,neuroinflammation and neuronal dystrophy involved.Therefore,multi-targets drugs with neuroprotective,anti-amyloidogenic and anti-inflammatory properties will be effective in AD treatment.Epigallocatechin-3-gallate(EGCG)possesses a broad spectrum of pharmacological activities in the prevention and treatment of multiple neurodegenerative diseases.In the present study,we showed that oral administration of EGCG(50 mg/kg)for 4 months significantly attenuated the cognitive deficits in APP/PS1 transgenic mice,which served as AD model.Moreover,EGCG induced an improvement in dendritic integrity and expression levels of synaptic proteins in the brain of APP/PS 1 mice.And EGCG exerted obvious anti-inflammatory effects,which was manifested by alleviating microglia activation,decreasing pro-inflammatory cytokine(IL-β)and increasing anti-inflammatory cytokines(IL-10,IL-β).Furthermore,p-amyloid(AP)plaques were markedly reduced in the hippocampus of 6-month old APP/PS 1 mice after EGCG treatment.In conclusion,these findings indicate that EGCG improves AD-like cognitive impairments through neuroprotective,anti-amyloidogenic and anti-inflammatory effects,thus is a promising therapeutic can didate for AD.
文摘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.
基金supported by grants from the National Natural Science Foundation of China(Nos.81370581,81172827)
文摘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.
基金Supported by Public Technology Application Research Grant of Zhejiang Province(No.2011C33029)Natural Science Foundation of Zhejiang Province,China(No.LY13B020002)
文摘AIM:To investigate the mechanism underlying the anti-inflammatory effects of epigallocatechin-3-gallate(EGCG)in lipopolysaccharide(LPS)-stimulated human retinal endothelial cells(HRECs).METHODS:HRECspre-treatedwithEGCG(0-100μmol/L)were stimulated with LPS(250 ng/mL).Levels of tumor necrosis factor alpha(TNF-α),vascular endothelial growth factor(VEGF),monocyte chemotactic protein-1(MCP-1)and nitric oxide(NO)in the supernatants were determined by enzyme-linked immunosorbent assay(ELISA)and Griess assay.The protein expression of phosphorylated extracellular signal-regulated kinase(ERK)1/2 and p38 mitogen-activated protein kinases(p38)were determined by Western blot analysis.RESULTS:EGCG pre-treatment significantly inhibited the secretion of TNF-α,VEGF,MCP-1 and NO in LPSstimulated HRECs.Moreover,EGCG effectively attenuated LPS-induced activation and phosphorylation of ERK1/2 and p38 in HRECs in a dose-dependent manner.CONCLUSION:EGCG exhibited inhibitory effects on LPS-induced pro-inflammatory cytokines production by modulating ERK1/2 and p38 pathways in HRECs,suggesting EGCG as a potential candidate for antiinflammatory intervention.
基金funded by Accions Singulars de R+D(Sing 12/17)del Vicerectorat de Recerca de la Universitat de Girona,Girona,Spain
文摘Traumatic spinal cord injury （SCI） causes motor paralysis, sensory anesthesia and autonomic dysfunction below the le- sion site and additionally some SCI patients refer neuropathic pain together with these signs and symptoms. Clinical and experimental studies have revealed the main pathological changes of injured spinal cord implicated in all these signs and symptoms, including neuropathic pain. After few hours of traumatic SCI, it is usual to observe broken blood brain barrier with plasma and blood cells extravasation, cell necrosis, disruption of ascending and descending spinal cord pathways and increased potassium and glutamate. Glutamate contributes to excitotoxicity of neurons whereas potassium facilitates ectopic depolarization of survival neurons and activation of resident microglia.
