Curcumin in gastric cancer treatment:A commentary on mechanistic insights and future directions

The study by Yang et al presents a comprehensive investigation into the thera-peutic potential of curcumin for gastric cancer(GC).Using network pharma-cology,the researchers identified 48 curcumin-related genes,31 of which overlap with GC targets.Key genes,including ESR1,EGFR,CYP3A4,MAPK14,CYP1A2,and CYP2B6,are linked to poor survival in GC patients.Molecular docking con-firmed strong binding affinity of curcumin to these genes.In vitro experiments demonstrated that curcumin effectively inhibits the growth and proliferation of BGC-823,suggesting its therapeutic potential in GC through multiple targets and pathways.

Antioxidant activity of curcumine as protector on methylmercury inducedpancreas damage in mice

Curcumin has been reported to have a strong antioxidant activity. In recent years, use of antioxidant in reducing heavy metal toxicities has been increased worldwide. In this study, we investigated the protective effects of curcumin on methylmercury-induced pancreas damage in mice. Briefly, 50 male mice were divided into five groups as follows: negative control(mice were given daily with aquadest); positive control(mice were orally given 2 mg/kg BW methylmercury daily for 35 d); and the treatment groups(mice were orally adminstered with curcumin 100 mg; 200 mg; 400 mg/kg BW daily for 35 d, and from 5th day, animals were given 2 mg/kg BW methylmercury daily 1 h after curcumin administration for 30 d). On day 35, levels of glucose, insulin, MDA, SOD and GPx were measured. Pancreas also was fixed in 10% neutral buffered formalin solution for histopathological examination. The results revealed that methylmercury toxicity induced a significant increase in the levels of glucose and MDA. Moreover, a significant decrease in insulin, SOD and GPx levels was observed, and pancreas tissues showed degeneration and necrotic changes in the islets of Langerhans. Treatment with curcumin(400 mg/kg BW but not 200 mg/kg BW and 100 mg/kg BW) significantly(P<0.05) decreased glucose and MDA levels in pancreas in mercury-induced mice. Treatment with curcumin 400 mg/kg BW also significantly increased insulin, SOD and GPx levels and reversed the histopathological damage in methylmercury-induced mice. Taken together, curcumin could be a potent natural herbal product, which had pancreas protective effect against methylmercury-induced pancreas damage in mice.

A DNA tetrahedron-based ferroptosis-suppressing nanoparticle: superior delivery of curcumin and alleviation of diabetic osteoporosis

Diabetic osteoporosis(DOP)is a significant complication that poses continuous threat to the bone health of patients with diabetes;however,currently,there are no effective treatment strategies.In patients with diabetes,the increased levels of ferroptosis affect the osteogenic commitment and differentiation of bone mesenchymal stem cells(BMSCs),leading to significant skeletal changes.To address this issue,we aimed to target ferroptosis and propose a novel therapeutic approach for the treatment of DOP.We synthesized ferroptosis-suppressing nanoparticles,which could deliver curcumin,a natural compound,to the bone marrow using tetrahedral framework nucleic acid(tFNA).This delivery system demonstrated excellent curcumin bioavailability and stability,as well as synergistic properties with tFNA.Both in vitro and in vivo experiments revealed that nanoparticles could enhance mitochondrial function by activating the nuclear factor E2-related factor 2(NRF2)/glutathione peroxidase 4(GPX4)pathway,inhibiting ferroptosis,promoting the osteogenic differentiation of BMSCs in the diabetic microenvironment,reducing trabecular loss,and increasing bone formation.These findings suggest that curcumin-containing DNA tetrahedron-based ferroptosissuppressing nanoparticles have a promising potential for the treatment of DOP and other ferroptosis-related diseases.

Use of curcumin and its nanopreparations in the treatment of inflammatory bowel disease

Inflammatory bowel disease(IBD)is a nonspecific inflammatory disease of the intestine that includes Crohn’s disease and ulcerative colitis.Because IBD is difficult to heal and easily relapses,it could worsen patient quality of life and increase economic burdens.Curcumin(CUR)is a bioactive component derived from the rhizome of turmeric(Curcuma longa).Many basic and clinical studies have shown that CUR can efficiently treat IBD by decreasing the activity of proinflammatory cytokines by communicating with transcription factors and signaling molecules.However,due to the limitations of being almost insoluble in aqueous solutions and having low oral bioavailability,it is important to select appropriate pharmaceutical preparations.

Role of CD36 in central nervous system diseases

CD36 is a highly glycosylated integral membrane protein that belongs to the scavenger receptor class B family and regulates the pathological progress of metabolic diseases.CD36 was recently found to be widely expressed in various cell types in the nervous system,including endothelial cells,pericytes,astrocytes,and microglia.CD36 mediates a number of regulatory processes,such as endothelial dysfunction,oxidative stress,mitochondrial dysfunction,and inflammatory responses,which are involved in many central nervous system diseases,such as stroke,Alzheimer’s disease,Parkinson’s disease,and spinal cord injury.CD36 antagonists can suppress CD36 expression or prevent CD36 binding to its ligand,thereby achieving inhibition of CD36-mediated pathways or functions.Here,we reviewed the mechanisms of action of CD36 antagonists,such as Salvianolic acid B,tanshinone IIA,curcumin,sulfosuccinimidyl oleate,antioxidants,and small-molecule compounds.Moreover,we predicted the structures of binding sites between CD36 and antagonists.These sites can provide targets for more efficient and safer CD36 antagonists for the treatment of central nervous system diseases.

Curcumin inhibits the growth and invasion of gastric cancer by regulating long noncoding RNA AC022424.2

BACKGROUND Gastric cancer,characterized by a multifactorial etiology and high heterogeneity,continues to confound researchers in terms of its pathogenesis.Curcumin,a natural anticancer agent,exhibits therapeutic promise in gastric cancer.Its effects include promoting cell apoptosis,curtailing tumor angiogenesis,and enhancing sensitivity to radiation and chemotherapy.Long noncoding RNAs(lncRNAs)have garnered significant attention as biomarkers for early screening,diagnosis,treatment,and drug response because of their remarkable specificity and sensitivity.Recent investigations have revealed an association between aberrant lncRNA expression and early diagnosis,clinical staging,metastasis,drug sensitivity,and prognosis in gastric cancer.A profound understanding of the intricate mechanisms through which lncRNAs influence gastric cancer develop-ment can provide novel insights for precision treatment and tailored management of patients with gastric cancer.This study aimed to unravel the potential of curcumin in suppressing the malignant behavior of gastric cancer cells by upregu-lating specific lncRNAs and modulating gastric cancer onset and progression.AIM To identify lncRNAs associated with curcumin treatment and investigate the role of lncRNA AC022424.2 in the effects of curcumin on gastric cancer cell apoptosis,proliferation,and invasion.Furthermore,these findings were validated in clinical samples.METHODS The study employed CCK-8 assays to assess the impact of curcumin on gastric cancer cell proliferation,flow cytometry to investigate its effects on apoptosis,and scratch and Transwell assays to evaluate its influence on the migration and invasion of BGC-823 and MGC-803 cells.Western blotting was used to gauge changes in the protein expression levels of CDK6,CDK4,Bax,Bcl-2,caspase-3,P65,and the PI3K/Akt/mTOR pathway in gastric cancer cell lines after curcumin treatment.Differential expression of lncRNAs before and after curcumin treatment was assessed using lncRNA sequencing and validated using quantitative reverse transcription polymerase chain reaction(qRT-PCR)in BGC-823 and MGC-803 cells.AC022424.2-1 knockdown BGC-823 and MGC-803 cells were generated to scrutinize the impact of lncRNA AC022424.2 on apoptosis,proliferation,migration,and invasion of gastric cancer cells.Western blotting was performed to ascertain changes in the expression of proteins implicated in the PI3K/Akt/mTOR and NF-κB signaling pathways.RT-PCR was employed to measure lncRNA AC022424.2 expression in clinical gastric cancer tissues and to correlate its expression with clinical pathological characteristics.RESULTS Curcumin induced apoptosis and hindered proliferation,migration,and invasion of gastric cancer cells in a dose-and time-dependent manner.LncRNA AC022424.2 was upregulated after curcumin treatment,and its knockdown enhanced cancer cell aggressiveness.LncRNA AC022424.2 may have affected cancer cells via the PI3K/Akt/mTOR and NF-κB signaling pathways.LncRNA AC022424.2 downregulation was correlated with lymph node metastasis,making it a potential diagnostic and prognostic marker.CONCLUSION Curcumin has potential anticancer effects on gastric cancer cells by regulating lncRNA AC022424.2.This lncRNA plays a significant role in cancer cell behavior and may have clinical implications in diagnosis and prognosis evaluation.The results of this study enhance our understanding of gastric cancer development and precision treatment.

Unveiling the emerging role of curcumin to alleviate ochratoxin A-induced muscle toxicity in grass carp(Ctenopharyngodon idella):in vitro and in vivo studies

Background Ochratoxin A(OTA),a globally abundant and extremely hazardous pollutant,is a significant source of contamination in aquafeeds and is responsible for severe food pollution.The developmental toxicity of OTA and the potential relieving strategy of natural products remain unclear.This study screened the substance curcumin(Cur),which had the best effect in alleviating OTA inhibition of myoblast proliferation,from 96 natural products and investigated its effect and mechanism in reducing OTA myotoxicity in vivo and in vitro.Methods A total of 720 healthy juvenile grass carp,with an initial average body weight of 11.06±0.05 g,were randomly assigned into 4 groups:the control group(without OTA and Cur),1.2 mg/kg OTA group,400 mg/kg Cur group,and 1.2 mg/kg OTA+400 mg/kg Cur group.Each treatment consisted of 3 replicates(180 fish)for 60 d.Results Firstly,we cultured,purified,and identified myoblasts using the tissue block culture method.Through preliminary screening and re-screening of 96 substances,we examined cell proliferation-related indicators such as cell viability and ultimately found that Cur had the best effect.Secondly,Cur could alleviate OTA-inhibited myoblast differentiation and myofibrillar development-related proteins(Myo G and MYHC)in vivo and in vitro and improve the growth performance of grass carp.Then,Cur could also promote the expression of OTA-inhibited protein synthesis-related proteins(S6K1 and TOR),which was related to the activation of the AKT/TOR signaling pathway.Finally,Cur could downregulate the expression of OTA-enhanced protein degradation-related genes(murf1,foxo3a,and ub),which was related to the inhibition of the Fox O3a signaling pathway.Conclusions In summary,our data demonstrated the effectiveness of Cur in alleviating OTA myotoxicity in vivo and in vitro.This study confirms the rapidity,feasibility,and effectiveness of establishing a natural product screening method targeting myoblasts to alleviate fungal toxin toxicity.

Facile in situ synthesis and characterization of Fe@Si/zeolite Na composites with magnetic core–shell structures from natural materials for enhanced curcumin loading capacity

Curcumin is a natural polyphenol that is used in various traditional medicines.However,its inherent properties,such as its rapid degradation and metabolism,low bioavailability,and short half-life,are serious problems that must be resolved.To this end,a drug carrier incorporating natural magnetic cores in a zeolite framework was developed and applied to the loading of curcumin in ethanol solutions.In this system,curcumin is encapsulated in a zeolite Na(ZNA)magnetic core–shell structure(Fe@Si/ZNA),which can be easily synthesized using an in situ method.Synthesis of Fe_(3)O_(4) nanoparticles was carried out from natural materials using a co-precipitation method.Analysis of the prepared magnetic core–shell structures and composites was carried out using vibrating-sample magnetometery,Fourier transform infrared spectroscopy,transmission electron microscopy,and x-ray diffraction.The cumulative loading of curcumin in the ZNA composite with 9%nanoparticles was found to reach 90.70%with a relatively long half-life of 32.49 min.Stability tests of curcumin loading in the composite showed that adding magnetic particles to the zeolite framework also increased the stability of the composite structure.Adsorption kinetics and isotherm studies also found that the system follows the pseudo-second-order and Langmuir isotherm models.

Curcumin delivery nanoparticles based on Maillard reaction of Haematococcus pluvialis protein/galactose for alleviating acute alcoholic liver damage

The aim of this study is to investigate the feasibility of Maillard reaction products of Haematococcus pluvialis protein and galactose(HPP-GAL)for improving the bioactivities of curcumin(CUR)for alleviating alcoholic liver damage.CUR was embedded into HPP-GAL nanoparticles by the self-assembly of hydrogen bonding and hydrophobic interaction with the particle size around 200 nm.HPP-GAL enhanced the encapsulation efficiency and loading amount of CUR with the value of(89.21±0.33)%and(0.500±0.004)%,respectively.The stabilities of CUR under strong acid,salt ion stability and ultraviolet irradiation conditions were improved by the encapsulation.HPP-GAL-CUR nanoparticles exhibited excellent concentration-dependent in vitro antioxidant activities including DPPH and ABTS scavenging rates,and better protective effect on CUR against gastric acid environment as well as longer release of CUR in simulated intestinal fluid.In addition,the HPPGAL-CUR delivery system possessed liver targeting property due to the existence of GAL,which could effectively alleviate the alcohol-induced liver damage and the inflammation indexes by inhibiting the oxidative stress.Therefore,HPP-GAL-CUR nanoparticles might be a potential candidate system for the prevention of alcoholic liver damage in the future.

Complexation process and binding parameters of curcumin and short amylose with V7-type helix structure

Pre-formed V7-type short amylose(SA)could interact with curcumin to form inclusion complex(IC)thereby to improve the stability of curcumin.However,the complexation mechanism of V7-type SA and curcumin is not clear,which limit the improvement of inclusion efficiency.To obtain a starch nanocarrier with high loading capacity,the encapsulation process and interaction parameters of V7-type SA-curcumin IC was studied.The analysis results demonstrated that stoichiometric ratio value of the SA-curcumin complex was around 1.V7-type SA performed excellently in the delivery of curcumin attributing to their high loading capacity(over 20%).It was found that curcumin could enter into the pre-formed helical cavity of SA to form an IC.The conformation change of SA caused the reduction in the interaction ratio in the last 20 ns of simulation.However,SA and curcumin always remained complexation status during the simulation.Hydrogen bonds(H-bonds)and hydrophobic interaction were the most critical acting forces involved in the formation and stability of V7-type SA-curcumin complex.Molecular docking presented that H-bonds interaction between curcumin ligand and V7-type SA chain(O3 at the 25th glucose unit,and O6 at the 17th and 20th glucose units)were found.Furthermore,the hydrophobic interactions were discovered between curcumin ligand and SA chain(18th,19th,21st,22nd and 23rd glucose units).

Curcumin for gastric cancer:Mechanism prediction via network pharmacology,docking,and in vitro experiments

BACKGROUND Curcumin originates from the natural herb turmeric,and its antitumor effects have been known about for a long time.However,the mechanism by which curcumin affects gastric cancer(GC)has not been elucidated.AIM To elucidate the potential mechanisms of curcumin in the treatment of GC.METHODS Network pharmacological approaches were used to perform network analysis of Curcumin.We first analyzed Lipinski’s Rule of Five for the use of Curcumin.Curcumin latent targets were predicted using the PharmMapper,SwissTargetPrediction and DrugBank network databases.GC disease targets were mined through the GeneCard,OMIM,DrugBank and TTD network databases.Then,GO enrichment,KEGG enrichment,protein-protein interaction(PPI),and overall survival analyses were performed.The results were further verified through molecular docking,differential expression analysis and cell experiments.RESULTS We identified a total of 48 curcumin-related genes with 31 overlapping GC-related targets.The intersection targets between curcumin and GC have been enriched in 81 GO biological processes and 22 significant pathways.Following PPI analysis,6 hub targets were identified,namely,estrogen receptor 1(ESR1),epidermal growth factor receptor(EGFR),cytochrome P450 family 3 subfamily A member 4(CYP3A4),mitogen-activated protein kinase 14(MAPK-14),cytochrome P450 family 1 subfamily A member 2(CYP1A2),and cytochrome p450 family 2 subfamily B member 6(CYP2B6).These factors are correlated with decreased survival rates among patients diagnosed with GC.Molecular docking analysis further substantiated the strong binding interactions between Curcumin and the hub target genes.The experimental findings demonstrated that curcumin not only effectively inhibits the growth of BGC-823 cells but also suppresses their proliferation.mRNA levels of hub targets CYP3A4,MAPK14,CYP1A2,and CYP2B6 in BGC-823 cells were significantly increased in each dose group.CONCLUSION Curcumin can play an anti-GC role through a variety of targets,pathways and biological processes.

Curcumin inhibits colorectal cancer development by blocking the YAP/TAZ signaling axis

Background:Curcumin is a plant polyphenol with antitumor properties and inhibits the development of colorectal cancer(CRC).However,as the molecular mechanism associated is still unclear,our study aimed to explore the underlying molecular mechanisms by which curcumin inhibits CRC.Methods:HT29 and SW480 cells were treated with curcumin or/and Doxycycline(DOX),and cell viability,colony forming ability,migration and invasion were confirmed by cell counting kit-8(CCK-8),colony forming,Transwell assays.And Yes-associated protein 1(YAP)and PDZ-binding motif(TAZ)signaling-related genes or proteins were analyzed using reverse transcription quantitative real-time PCR(RT-qPCR),western blot,and immunofluorescence assays.Then nude mice xenograft tumor model was constructed,YAP and Ki67 expressions were tested by immunohistochemistry(IHC)staining.Results:In our study,we proved that curcumin significantly inhibited the CRC cell viability,cell migration,and cell invasion abilities.In addition,curcumin inhibited YAP and Transcriptional coactivator with TAZ or the YAP/TAZ signaling axis in CRC cells.Further,in the nude mice model,curcumin treatment significantly decreased the size and weight of xenotransplant tumors.Conclusion:Therefore,curcumin significantly inhibited CRC development and invasion by regulating the YAP/TAZ signaling axis.

Curcuminoids Inhibit Botrytis cinerea and Colletotrichum gloeosporioides

The growth rate method was adopted to measure the inhibitory effect of curcumin,tetrahydrocurcumin,demethoxycurcumin,and bisdemethoxycurcumin on the mycelial growth of Botrytis cinerea and Colletotrichum gloeosporioides.The results showed that the four curcuminoids inhibited the mycelial growth of the two pathogens in a concentration-dependent manner.Bisdemethoxycurcumin at 600 mg/L exerted the strongest inhibitory effect on the mycelial growth of B.cinerea and C.gloeosporioides,with the relative inhibition rates of 98.19%and 100%,respectively;followed by demethoxycurcumin;curcumin exerted the worst inhibitory effect.Toxicity test results also showed that four curcuminoids all had a certain toxicity to B.cinerea and C.gloeosporioides,among which,bisdemethoxycurcumin exhibited the strongest toxicity,with the EC_(50)of 131.125 and 122.235 mg/L,respectively;while curcumin had the lowest toxicity,with the EC_(50)of 273.143 and 194.943 mg/L,respectively.

The Effect of Curcumin on Alzheimer’s Disease

Alzheimer’s disease (AD) is the most prevalent type of dementia, affecting approximately 50 million individuals globally, and projections indicate that this number will increase to 139 million by 2050. It is one of the main factors contributing to cognitive decline in the aging population. Existing treatments do not produce the intended therapeutic benefits;therefore, it is imperative to identify alternative pharmacological and biological techniques. As the precise pathogenic pathways underlying AD remain unknown, existing therapies only address symptoms rather than promote prevention or treatment. Curcumin has attracted increasing attention owing to its distinct molecular structure. It affects antioxidant and inflammatory pathways as well as amyloid aggregation, which is one of the main characteristics of Alzheimer’s disease. Many human ailments have been treated with medicinal plants, owing to their antioxidant properties. Curcumin has been used as a traditional food and medicine in Asia for a long time. Numerous studies have shown that curcumin has several advantageous properties including anti-inflammatory and antioxidant activities. Numerous clinical trials have been conducted to clarify the impact of curcumin on cancers, owing to its documented effects on tumors. Recent findings suggest that curcumin may have therapeutic potential in the pathogenesis of Alzheimer’s disease (AD). The overall memory of patients with AD has improved because of several benefits of curcumin, including decreased beta-amyloid plaques, delayed neuronal degradation, metal chelation, anti-inflammatory and antioxidant effects, and decreased microglial production.

HISP-1 Inhibits HSV-1 Infection in Cultured Vero Cells

Herpes simplex virus-1 (HSV-1) remains a leading cause of viral disease worldwide and is spread by direct contact with infected lesions. There is no vaccine against HSV-1 infections and there remains a need to identify therapeutics that could reduce the spread. In this study various hispolon compounds were analyzed to determine their antiviral potential against HSV-1 infections in cultured Vero cells. To determine the effects on infectivity and possible mechanisms of inhibition, the following assays were conducted. In vitro cytotoxicity assays were conducted to determine the effect of the compounds on cell viability and the maximum non-cytotoxic concentrations. Antiviral assays measured cell viability, percent inhibition of infection following treatment with the compounds, and the effect on the viral infection cycle. These effects were visualized using inverted light and fluorescent microscopy. Of the 24 hispolons tested, only hispolon pyrazole-1 (HISP-1) demonstrated antiviral effects. HISP-1 was demonstrated to effect early stages in HSV-1 infection in cultured Vero cells (attachment, penetration, and post-penetration). In silico modeling analyses were conducted to analyze the interactions between HISP-1 and viral glycoprotein D (gD). HISP-1 is safe at concentrations tested and is effective in inhibiting infection of HSV-1 in cultured cells. HISP-1 has potential for therapeutic use as an antiviral against HSV-1 infection, could work in synergy with other antivirals that work be a different modality, and could be developed as a component of a topical agent to reduce the spread of HSV-1 infections.

Exploring the molecular mechanism of action of curcumin for the treatment of diabetic retinopathy,using network pharmacology,molecular docking,and molecular dynamics simulation

Background:Based on network pharmacology and molecular docking,the present study investigated the mechanism of curcumin(CUR)in diabetic retinopathy treatment.Methods:Based on the DisGeNET,Swiss TargetPrediction,GeneCards,Online Mendelian Inheritance in Man,Gene Expression Omnibus,and Comparative Toxicogenomics Database,the intersection core targets of CUR and diabetic retinopathy were identified.The intersection target was imported into the STRING database to obtain the protein-protein interaction map.According to the Database for Annotation,Visualization and Integrated Discovery database,the intersected targets were enriched in Gene Ontology(GO)and Kyoto Encyclopedia of Genes and Genomes pathways.Then Cytoscape 3.9.1 is used to make the drug-target-disease-pathway network.The mechanism of CUR and diabetic retinopathy was further verified by molecular docking and molecular dynamics simulation.Results:There were 203 intersecting targets of CUR and diabetic retinopathy identified.1320 GO entries were enriched for GO functions,which were primarily involved in the composition of cells such as identical protein binding,protein binding,enzyme binding,etc.It was found that 175 pathways were enriched using Kyoto Encyclopedia of Genes and Genomes pathway enrichment methods,which were mainly included in the lipid and atherosclerosis,AGE-RAGE signaling pathway in diabetic complications,pathways in cancer,etc.In the molecular docking analysis,CUR was found to have a good ability to bind to the core targets of albumin,IL-1B,and IL-6.The binding of albumin to CUR was further verified by molecular dynamics simulation.Conclusion:As a result of this study,CUR may exert a role in the treatment of diabetic retinopathy through multi-target and multi-pathway regulation,which indicates a possible direction of future research.

Dietary Green Tea Extract and Antioxidants Improve Insulin Secretory Functions of Pancreatic β-Cells in Mild and Severe Experimental Rodent Model of Chronic Pancreatitis

Chronic pancreatitis (CP) is a progressive inflammatory disorder of the pancreas. It is predominantly idiopathic (with an unknown cause) in India and mostly due to alcohol in the West. Diabetes that occur secondary to chronic pancreatitis (T3c Diabetes) is often brittle, and is difficult to attain normoglycemia with conventional treatment requiring multiple doses of insulin. Mild and severe model of CP was induced in mice by repeated intraperitoneal injections of cerulein and L-arginine respectively with an intent to study islet dysfunction and develop therapeutic strategy in animal models of CP. Dietary intervention of epigallocatechin-3-gallate (EGCG) was tested in both the models of CP for its beneficial effects on insulin secretory functions. Pancreata collected upon euthanasia were used to study alterations in the morphology of pancreatic parenchyma and inflammation by staining with H&E and fibrotic changes by Masson’s trichrome and picrosirius staining. Insulin secretory functions of islets were evaluated to test the efficacy of the dietary intervention on β-cell functions. Intraperitoneal glucose tolerance test was performed to monitor the glucose homeostasis before and after the dietary intervention. Both the models resulted in CP with dispersed acini, inflammation and fibrosis. The loss of acini and extent of fibrosis was more in L-arginine model. 2-fold improvement in glucose-stimulated insulin secretory functions of islets was observed with 0.5% EGCG dietary intervention in cerulein model of CP and 1.6-fold in L-arginine model of CP. A further improvement in insulin secretion by 3.2-fold was observed with additional dietary supplements like N-acetyl cysteine, curcumin in combination with EGCG. Our results thus demonstrate and highlight the therapeutic potential of dietary green tea (EGCG) supplementation in reversing islet dysfunction and improving glucose homeostasis in experimental chronic pancreatitis in mice.

Preparation and release of curcumin/silk fibroin/sodium alginate film

The aim of this study was to prepare silk fibroin/sodium alginate composite film containing curcumin by casting method.Orthogonal test was used to optimize the formulation according to the values of tensile strength and elongation at break.The release of curcumin in the optimal film was studied in order to explore its application as wound dressing.The results showed that the optimum composition of curcumin/silk fibroin/sodium alginate composite film was as follows:Silk fibroin(70 mg/mL)2.7 g,sodium alginate(24 mg/mL)0.84 g,span 40(5.0 mg/mL)0.4 g,glycerol(3.75%,V/V)3 mL,curcumin(0.2 mg/mL)0.016 g.The optimum film showed the tensile strength and the elongation at break was(0.628±0.032)MPa and(0.794±0.046)%,respectively.

Effect of Curcumin on Influenza Virus HIN1 and H3N2 in Vitro

Objective：To investigate the inhibitory effect of curcumin on influenza virus HIN1 and H3N2 in vitro, Methods：The directly killing role of cureumin extract in vitro to influenza virus type A subtype H1N1 and H3N2 was evaluated by the canine kidney cells （MDCK）, Results：The largest non toxic concentration of curcumin extract was 12, 5g/L and the effective inhibitory concentration to H1N1 and H3N2 was 6, 25G/1 AND 1,56g/L respectively, Conclusion： Curcumin extract have directly killing effect on H1N1 and H3N2 infections.

姜黄素诱导肿瘤细胞凋亡的信号途径研究进展

姜黄素（curcumin）是姜科姜黄属植物根茎中所含的主要有效成分,药理作用广泛,如抗炎、抗氧化、抗肿瘤、抗动脉硬化、清除自由基、降血脂等。姜黄素的抗肿瘤活性于1985年由自印度学者Kuttan等首次提出,至今已由大量文献证实,其具有作用明确、抗瘤谱广、毒性小等优点[1]。姜黄素具有很强的凋亡诱导能力,诱导细胞凋亡是其抗肿瘤作用的重要机制,涉及一系列复杂的生物学过程，并受细胞内外多种途径及信号分子调控，不同的途径所表现的形式不同，它们之间有交叉、有重叠，构成了错综复杂的调控网络，现对其诱导细胞凋亡的主要信号途径综述如下。