姜素对CD34^+肝癌SMMC-7721细胞增殖及CD34表达的影响

目的:探讨姜素对CD34+肝癌SMMC-7721细胞增殖及其CD34蛋白表达的影响。方法:培养人CD34+肝癌SMMC-7721细胞并用姜素处理,MTT法测定细胞增殖率,流式细胞术测定SMMC-7721细胞中CD34+细胞含量,Western blot法测定CD34蛋白的水平。结果:姜素对人肝癌SMMC-7721细胞的抑制率随姜素浓度和作用时间的增加而升高(P<0.05)。姜素处理组CD34+细胞的含量与正常组中CD34+细胞的含量差异具有统计学意义(P<0.05),且抑制率随浓度升高而升高。Western Blot检测CD34的表达情况,组内及组间条带灰度值比较:CD34的表达量差异均无统计学意义(P>0.05)。结论:姜素能抑制人CD34+肝癌细胞的增殖,但对CD34蛋白的表达无影响。

高良姜素对人肝癌SMMC-7721细胞PI3K/AKT信号通路的影响

目的:观察高良姜素对人肝癌SMMC-7721细胞PI3K/AKT信号通的影响。方法:采用MTT法检测高良姜素对人肝癌SMMC-7721细胞增殖的影响,流式细胞术检测细胞周期和细胞凋亡,Western印迹法检测PI3K/AKT信号通路相关蛋白及Caspase-9蛋白表达情况。结果:高良姜素抑制人肝癌SMMC-7721细胞增殖作用明显,且呈浓度和时间依赖性,顺铂和高良姜素(5.4、10.8、21.6、43.2、86.4μg/ml),72 h抑制率分别为69.4%、34.3%、44.9%、60.8%、73.9%、79.1%。流式细胞术检测结果显示高良姜素(10.8、21.6、43.2μg/ml)可使细胞周期阻滞于G1期。高良姜素(10.8、21.6、43.2μg/ml)处理24h凋亡率分别为9.8%、15.3%、18.6%。Western印迹法检测相关蛋白,药物处理组PI3K、AKT、P-AKT的表达受抑制,PTEN,Caspase-9蛋白的表达率随着药物浓度的增加而增加。结论:高良姜素可能通过抑制PI3K/AKT信号通路诱导人肝癌SMMC-772细胞凋亡。

姜素预防犬运动病的效果观察

目的 观察姜素预防犬运动病的效果和对豚鼠视前庭相互作用的影响。 方法 采用随机双盲和安慰剂对照实验设计 ,观察 7 2mg/kg ,3 6mg/kg和 1 8mg/kg 3种剂量姜素及苯海拉明 (乘晕宁 3 2mg/kg)、盐酸苯环壬酯 (飞塞乐 0 2mg/kg)对犬运动病预防效果和对豚鼠视前庭系统的影响。犬运动病采用三角离心摆动方式 (峰速 2 4 0°/s ,频率 0 0 5Hz)诱发 ,以一定时间内犬的呕吐发生率作为犬运动病的观察指标 ;以正弦摆动 (峰速 6 0°/s,频率 0 0 5Hz)加光条刺激方式诱发豚鼠视前庭相互作用眼震 ,以眼震次数、慢相速度和增益作为视前庭相互作用观察指标。 结果 3种剂量姜素均可显著降低犬呕吐发生率 ,且在 7 2mg/kg和 3 6mg/kg剂量时其效果较苯海拉明、盐酸苯环壬酯显著 ,各种药物对豚鼠VVOR眼震均无显著影响。

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.

Two New Bis—labdanic Diterpenoids from Alpinia calcarata

Two novel bis—labdanic diterpenoids named calcaratarin G and calcaratarin H were isolated from the rhizomes of Alpinia calcarata Rosc．Their structures were elucidated to be a pair of stereoiso-mers on the basis of the spectral evidence．The 2D NMR techniques including’H-1H COSY，HMQC，HMBC，NOESY and HRFABMS were extensively applied to establish the structures．

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.

Inhibitory Effects of INF-α and Curcumin on the Proliferation of Raji Cells

Objective： To investigate the inhibitory effect of interferon-α （IFN-α） and curcumin on proliferation of Raji cells （B-NHL） and its mechanism. Methods： The morphological, changes of Raji cells were observed in culture medium with IFN-α （500, 1000, 2000, 3000 U/L） and various concentrations of curcumin （6.25, 12.5, 25 μmol/L） for different time in vitro. The inhibitory ratio was measured by MTT assay. Apoptosis was detected by flow cytometry （FCM）. The expression of caspase 6, caspase 8 and caspase 9 in Raji cells treated with IC5025 μmol/L curcumin with IFN-α was examined using Western blot. Results： IFN-α and curcumin could significantly inhibit the growth and induce apoptosis of RAji cells with synergistic effects. They could increase the expression of caspase 6, caspase 8 and caspase 9 in Raji cells in a dose- and time-dependent manner. Conclusion： The combined use of IFN-α and curcumin can inhibit the proliferation of B-NHL Raji cells apparently in vitro. Promotion of the expression of caspase 6, caspase 8, caspase 9 and induction of apoptosis might be one of the important mechanisms.

Prevention of hepatotoxicity due to anti tuberculosis treatment: A novel integrative approach

AIM： To evaluate the ability of Curcuma Ionga （CL） and Tinospora cordifolia （TC） formulation to prevent anti-tuberculosis （TB） treatment （ATT） induced hepatotoxicity. METHODS： Patients with active TB diagnosis were randomized to a drug control group and a trial group on drugs plus an herbal formulation. Isoniazid, rifampicin, pyrazinamide and ethambutol for first 2 mo followed by continuation phase therapy excluding Pyrazinamide for 4 mo comprised the anti-tuberculous treatment. Curcumin enriched （25%） CL and a hydro-ethanolic extract enriched （50%） TC 1 g each divided in two doses comprised the herbal adjuvant. Hemogram, bilirubin and liver enzymes were tested initially and monthly till the end of study to evaluate the result. RESULTS： Incidence and severity of hepatotoxicity was significantly lower in trial group （incidence： 27/192 vs 2/316, P 〈 0.0001）. Mean aspartate transaminase （AST） （195.93 ± 108.74 vs 85 ± 4.24, P 〈 0.0001）, alanine transaminase （ALT） （75.74 ± 26.54 vs 41 ± 1.41, P 〈 0.0001） and serum bilirubin （5.4 ±3.38 vs 1.5 ±0.42, P 〈 0.0001）. A lesser sputum positivity ratio at the end of 4 wk （10/67 vs 4/137, P = 0.0068） and decreased incidence of poorly resolved parenchymal lesion at the end of the treatment （9/152 vs 2/278, P = 0.0037） was observed. Improved patient compliance was indicated by nil drop-out in trial vs 10/192 in control group （P 〈 0.0001）. CONCLUSION： The herbal formulation prevented hepatotoxicity significantly and improved the disease outcome as well as patient compliance without any toxicity or side effects.

NCB-02 (standardized Curcumin preparation) protects dinitrochlorobenzene-induced colitis through down-regulation of NFκ-B and iNOS

AIM： To evaluate the efficacy and mechanism of action of NCB-02, a standardized Curcumin preparation, against 2, 4-dinitrochlorobenzene （DNCB）-induced ulcerative colitis in rats. METHODS： Ulcerative colitis was induced in male rats by sensitizing with topical application of DNCB in acetone for 14 d and intra-colonol challenge with DNCB on day 15. A separate group of animals with vehicle treatment in similar fashion served as control group. Colitis rats were divided into different groups and treated with NCB-02 at doses of 25, 50 and 100 mg/kg b.wt p.o. for 10 d. Sulfasalazine at a dose of 100 mg/kg b.wt for 10 d served as a reference group. On day 10 after respective assigned treatment, all the animals were euthanized and the length of the colon, weight of entire colon and distal 8 cm of the colon were recorded. The distal part of the colon was immediately observed under a stereomicroscope and the degree of damage was scored. Further distal 8 cm of the colon was subject to the determination of colonic myeloperoxidase （MPO）, lipid peroxidation （LPO） and alkaline phosphatase （ALP） activities. A small piece of the sample from distal colon of each animal was fixed in 10% neutral buffered formalin and embedded in paraffin wax and sectioned for immunohistochemical examination of NFK-B and iNOS expression. RESULTS： NCB-02 showed a dose dependent protection against DNCB-induced alteration in colon length and weight. NCB-02 treatment also showed a dose dependent protection against the elevated levels of MPO, LPO and ALP, induced by DNCB. NCB-02 demonstrated a significant effect at a dose of 100 mg/kg b.wt., which was almost equipotent to 100 mg/kg b.wt. of sulfasalazine. Treatment with sulfasalazine and curcuminat a dose of 100 mg/kg b.wt. inhibited the DNCB-induced overexpression of NFK-B and iNOS in the colon. CONCLUSION： Curcumin treatment ameliorates colonic damage in DNCB-induced colitic rats, an effect associated with an improvement in intestinal oxidative stress and downregulation of colonic NFκ-B and iNOS expression.

Anti-cancer and anti-angiogenic effects of curcumin and tetrahydrocurcumin on implanted hepatocellular carcinoma in nude mice

AIM: To determine the effect of tetrahydrocurcumin (THC) on tumor angiogenesis compared with curcumin (CUR) by using both in vitro and in vivo models of human hepatocellular carcinoma cell line (HepG2). METHODS: The 3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyl-tetrazolium bromide (MTT) assay was used for testing the anti-proliferating activities of CUR and THC. In male BALB/c nude mice, 2 × 106 human HepG2 cells were inoculated onto a dorsal skin-fold chamber. One day after HepG2 inoculation, the experimental groups were fed oral daily with CUR or THC (300 mg/kg or 3000 mg/kg). On d 7, 14 and 21, the tumor microvasculature was observed using fluorescence videomicroscopy and capillary vascularity (CV) was measured. RESULTS: Pathological angiogenic features including microvascular dilatation, tortuosity, and hyper-permeability were observed. CUR and THC could attenuate these pathologic features. In HepG2-groups, the CV were significantly increased on d 7 (52.43%), 14 (69.17%), and 21 (74.08%), as compared to controls (33.04%,P < 0.001). Treatment with CUR and THC resulted in significant decrease in the CV (P < 0.005 and P < 0.001, respectively). In particular, the anti-angiogenic effects of CUR and THC were dose-dependent manner. However, the beneficial effect of THC treatment than CUR was observed, in particular, from the 21 d CV (44.96% and 52.86%, P < 0.05). CONCLUSION: THC expressed its anti-angiogenesis without any cytotoxic activities to HepG2 cells even at the highest doses. It is suggested that anti-angiogenic properties of CUR and THC represent a common potential mechanism for their anti-cancer actions.

Curcumin-attenuated trinitrobenzene sulphonic acid induces chronic colitis by inhibiting expression of cyclooxygenase-2

AIM： To explore the possible mechanisms of curcumin in rat colitis induced by trinitrobenzene sulfonic （TNBS） acid. METHODS： Rats with TNBS acid-induced colitis were treated with curcumin （30 mg/kg or 60 mg/kg per day ip）. Changes of body weight and histological scores as well as survival rate were evaluated. Leukocyte infiltration was detected by myeloperoxidase （MPO） activity assay. The expression of cyclooxygenase-2 （COX-2） was detected by RT-PCR and Western blot. Inflammation cytokines were determined by RT-PCR. Local concentration of prostaglandin E2 （PGE2） in colon mucosa was determined by ELISA. RESULTS： Curcumin improved survival rate and histological image, decreased the macroscopic scores and MPO activity. Also curcumin reduced the expression of COX-2 and inflammation cytokines. In addition, treatment with curcumin increased the PGE2 level. CONCLUSION： Curcumin has therapeutic effects on TNBS acid-induced colitis, the mechanisms seem to be related to COX-2 inhibition and PGE2 improvement.

Suppression of esophageal cancer cell growth using curcumin,(-)-epigallocatechin-3-gallate and lovastatin

AIM:To determine the effects of curcumin,(-)-epigallocatechin-3-gallate (EGCG),lovastatin,and their combinations on inhibition of esophageal cancer.METHODS:Esophageal cancer TE-8 and SKGT-4 cell lines were subjected to cell viability methyl thiazolyl tetrazolium and tumor cell invasion assays in vitro and tumor formation and growth in nude mouse xenografts with or without curcumin,EGCG and lovastatin treatment.Gene expression was detected using immunohistochemistry and Western blotting in tumor cell lines,tumor xenografts and human esophageal cancer tissues,respectively.RESULTS:These drugs individually or in combinations significantly reduced the viability and invasion capacity of esophageal cancer cells in vitro.Molecularly,these three agents reduced the expression of phosphorylated extracellular-signal-regulated kinases (Erk1/2),c-Jun and cyclooxygenase-2 (COX-2),but activated caspase 3 in esophageal cancer cells.The nude mouse xenograft assay showed that EGCG and the combinations of curcumin,EGCG and lovastatin suppressed esophageal cancer cell growth and reduced the expression of Ki67,phosphorylated Erk1/2 and COX-2.The expression of phosphorylated Erk1/2 and COX-2 in esophageal cancer tissue specimens was also analyzed using immunohistochemistry.The data demonstrated that 77 of 156 (49.4%) tumors expressed phosphorylated Erk1/2 and that 121 of 156 (77.6%) esophageal cancers expressed COX-2 protein.In particular,phosphorylated Erk1/2 was expressed in 23 of 50 (46%) cases of esophageal squamous cell carcinoma (SCC) and in 54 of 106 (50.9%) cases of adenocarcinoma,while COX-2 was expressed in 39 of 50 (78%) esophageal SCC and in 82 of 106 (77.4%) esophageal adenocarcinoma.CONCLUSION:The combinations of curcumin,EGCG and lovastatin were able to suppress esophageal cancer cell growth in vitro and in nude mouse xenografts,these drugs also inhibited phosphorylated Erk1/2,c-Jun and COX-2 expression.

Protective effect of curcumin against liver warm ischemia/reperfusion injury in rat model is associated with regulation of heat shock protein and antioxidant enzymes

AIM： To investigate the hypothesis that the protective effects of curcumin in hepatic warm ischemia/reperfusion （I/R） injury are associated with increasing heat shock protein 70 （Hsp70） expression and antioxidant enzyme activity. METHODS： Sixty Sprague-Dawley male rats were randomly divided into sham, I/R, C ＋ I/R groups. The model of reduced-size liver warm ischemia and reperfusion was used. Curcumin （50 mg/kg） was administered by injection through a branch of superior mesenteric vein at 30 min before ischemia in C ＋ I/R group. Five rats were used to investigate the survival during 1 wk after operation in each group. Blood samples and liver tissues were obtained in the remaining animals after 3, 12, and 24 h of reperfusion to assess serum alanine aminotransferase （ALT）, aspartate aminotransferase （AST）, liver tissue NO2- ＋ NO3-, malondialdehyde （MDA） content, superoxide dismutase （SOD）, catalase （CAT）, nitricoxide synthase （NOS） and myeloperoxidase （MPO） activity, HspT0 expression and apoptosis ratio. RESULTS： Compared with I/R group, curcumin pretreatment group showed less ischemia/reperfusioninduced injury. CAT and SOD activity and Hsp70 expression increased significantly. A higher rate of apoptosis was observed in I/R group than in C ＋ I/R group, and a significant increase of MDA, NO2^- ＋ NO3^- and MPO level in liver tissues and serum transaminase concentration was also observed in I/R group compared to C ＋ I/R group. Curcumin also decreased the activity of inducible NO synthase （iNOS） in liver after reperfusion,but had no effect on the level of endothelial NO synthase （eNOS） after reperfusion in liver. The 7 d survival rate was significantly higher in C ＋ I/R group than in I/R group. CONCLUSION： Curcumin has protective effects against hepatic I/R injury. Its mechanism might be related to the overexpression of Hsp70 and antioxidant enzymes.

Curcumin prevents indomethacin-induced gastropathy in rats

AIM： To investigate the effects of curcumin on gastric microcirculation and inflammation in rats with indo- methacin-induced gastric damage. METHODS： Male Sprague-Dawley rats were randomly divided into three groups. Group 1 （control group, n = 5） was fed with olive oil and 5% NaHCOf （vehicle）. Group 2 [indomethacin （IMN） group, n = 5] was fed with olive oil 30 min prior to indomethacin 150 mg/kg body weight （BW） dissolved in 5% NaHCO3- at time 0th and 4th h. Group 3 （INN ± Cur group, n = 4） was fed with curcumin 200 mg/kg BW dissolved in olive oil 0.5 mL, 30 min prior to indomethacin at 0th and 4th h. Leukocyte-endothelium interactions at postcapillary venules were recorded after acridine orange injection. Blood samples were determined for intercellular ad- hesion molecule （ICAM）-1 and tumor necrosis factor （TNF）-a levels using enzyme linked immunosorbent assay method. Finally, the stomach was removed for histopathological examination for gastric lesions and grading for neutrophil infiltration. RESULTS： In group 2, the leukocyte adherence in postcapillary venules was significantly increased com- pared to the control group （6.40±2.30 cells/frame vs 1.20 ± 0.83 cells/frame, P = 0.001）. Pretreatment with curcumin caused leukocyte adherence to postcapil- lary venule to decline （3.00±0.81 cells/frame vs 6.40 ± 2.30 cells/frame, P = 0.027）. The levels of ICAM-1 and TNF-aincreased significantly in the indomethacin- treated group compared with the control group （1106.50 ± 504.22 pg/mL vs 336.93 a= 224.82 pg/mL, P = 0.011 and 230.92±114.47 pg/mL vs 47.13±65.59 pg/mL, P = 0.009 respectively）. Pretreatment with curcumin sig- nificantly decreased the elevation of ICAM-1 and TNF-a levels compared to treatment with indomethacin alone （413.66 ± 147.74 pg/mL vs 1106.50 ± 504.22 pg/mL, P = 0.019 and 58.27 ± 67.74 pg/mL vs 230.92 ± 114.47 pg/mL, P = 0.013 respectively）. The histological appear- ance of the stomach in the control group was normal. In the indomethacin-treated group, the stomachs showed a mild to moderate neutrophil infiltration score. Gastric lesions were erosive and ulcerative. In rats treated with indomethacin and curcumin, stomach histopathology improved and showed only a mild neutrophil infiltration score and fewer erosive lesions in the gastric mucosa. CONCLUSION： The results indicate that curcumin pre- vents indomethacin-induced gastropathy through the improvement of gastric microcirculation by attenuating the level of ICAM-1 and TNF-a,

Study on the mechanism of apoptosis of myelocytic leukemia cell lines induced by curcumin

Objective: To investigate the mechanism of apoptosis of myelocytic leukemia lines NB4, K562 and THP-1 cells induced by curcumin. Methods: After the cells were treated with curcumin at different concentration (25, 12.5, 6.25, 3.125, 0 μmol/L) for various times (0, 12, 24, 48 h), flow cytometry (FCM) was used to determine the rate of apoptosis of cells. After the cells were treated with curcumin at 25 μmol/L for 24 h, flow cytometry was used to determine the expression level of Fas, and Western blot was performed to determine the expression of Caspase-8 and Caspase-9. Results: (1) Curcumin could induced the apoptosis of NB4, K562 and THP-1 cells in a time- and dose-dependent manner. After the cells were treated with curcumin at 25 μmol/L for 48 h, the rate of apoptosis of cells was over fifty percent. (2) Fas level showed remarkable increase (P < 0.01) after above cells were treated with 25 μmol/L curcumin for 24 h. (3) The apoptosis proteins of Caspase-8 and Cas- pase-9 were also increased obviously (P < 0.01) after the cells were treated with 25 μmol/L curcumin for 24 h. Conclusion: The molecular pathway of apoptosis of myelocytic leukemia lines induced by curcumin are concerned with death receptor and mitochondria.

Antifungal susceptibility analysis of berberine,baicalin,eugenol and curcumin on Candida albicans

Objective:To analyze the antifungal effects of Chinese herb monomers,i.e.berberine,baicalin,eugenol and curcumin,on Candida albicans.Methods:After Candida albicans strain Y01-09 was incubated for 48 h in YEPD broth which contained different concentrations of Chinese herb components,the cell cycle,fluorescent intensity and the size of cell volume were detected by flow cytometry.Results:The 4 Chinese herb monomers could affect the cell cycle of Candida albicans in different ranges.The ratio of cells in S-G2-M period decreased as the agents concentration increased,indicating that the cell division was inhibited.The fluorescent intensity of Candida albicans cells became weaker after being incubated,which reflected the loss of DNA fragments.The higher the concentration was,the weaker the fluorescent intensity became.The cell size,cell diopter and particle size changed much as the agents concentration increased.Conclusion:Chinese herb monomers play the antifungal role in inhibiting cell division.FCM could be used to determine the susceptibility of antifungal agents.

The Effect of Curcumin on Proliferation and Apoptosis in LNCaP Prostate Cancer Cells

OBJECTIVE To observe the effect of curcumin on proliferation and apop-tosis in the prostate cancer LNCaP cell line. METHODS The AXSYMTM system luciferase method was used to examine the effect of various concentratious of curcumin on the content of prostate specific antigen (PSA) in prostate cancer LNCaP cells. A pGL3-PSA luciferase expression vector, containing 640 bp DNA of the PSA gene 5' -promoter region was constructed and transfected into the LNCaP cells with lipofectin. By measuring luciferase activity, the effect of 10 μmol/L, 20 μmol/L, 30 and 40 μmol/L curcumin on the promoter was studied. Effects on cell growth and apoptosis were analyzed by microscopy, the MTT colorimetric assay and flow cytometry. Western-blotting was used to measure expression of the androgen receptor (AR) in the LNCaP cells treated with different concentrations of curcumin. RESULTS The results showed that the expression of PSA was inhibited as curcumin reduced the activity of luciferase. Curcumin also caused a sigificant concentration-dependent decrease in AR expession measured by Western -blotting. Cell growth was inhibited and apoptosis was induced. CONCLUSION By inhibiting AR expression, curcumin reduced the function of the PSA promoter and inhibited PSA protein expression. Curcumin decreased the cellular proliferation and induced apoptosis in LNCaP cells in a concention-dependent manner.

Curcumin suppresses PPARδ expression and related genes in HT-29 cells

AIM:To investigate the effects of curcumin on the expression of peroxisome proliferator-activated receptorδ(PPARδ)and related genes in HT-29 cells. METHODS:HT-29 cells were treated with curcumin (0-80μmol/L)for 24 h.The effects of curcumin on the morphology of HT-29 cells were studied by Hoechst 33342 staining.The activity of caspase-3 was determined using DEVD-p NA as substrate.The levels of peroxisome PPARδ,14-3-3εand vascular endothelial growth factor(VEGF)in HT-29 cells were determined by Western blotting analysis and their mRNA expression was determined by real-time quantitative RT-PCR. RESULTS:Treatment with 10-80μmol/L curcumin induced typical features of apoptosis and activated the caspase-3 in HT-29 cells.The expression of PPARδ, 14-3-3εand VEGF was reduced and the activity of β-catenin/Tcf-4 signaling was inhibited by curcumin treatment. CONCLUSION:Curcumin can induce apoptosis of HT-29 cells and down-regulate the expression of PPARδ,14-3-3εand VEGF in HT-29.

Facile Synthetic Design and Characterization of Curcumin-Metformin Adduct： Potential Insights into the Role of This Conjugate in Diseases of Aging

Recently, the anti-glycation and anticancer properties of curcumin longa and okra seed extract were studied alone and also in combination with the well-established drug metformin. The combined effect of curcumin with metformin and metformin with okra seed extract was found to be highly efficacious in inhibiting Advanced Glycation End-products （AGEs）. In order to understand the mechanistic implications of curcumin combined with metformin and its enhanced anti-glycation activity, a Curcumin-Metformin Adduct was chemically synthesized. This adduct was fully characterized by thin-layer chromatography, Nano Drop spectrophotometry and electrospray-ionization mass spectrometry. The adduct may be helpful not only in elucidating the mechanism of anti-glycation and anti-cancer activities but also in studying the role of curcumin in binding of AI3-oligomers and disaggregating fibrillar formation in Alzheimer＇s disease.

Curcumin： A putative chemopreventive agent

Curcumin （diferuloylmethane）, the main yellow bioactive component of turmeric has been shown to have a wide spectrum of biological actions. It is anti-inflammatory, antioxidant, anticarcinogenic, antimutagenic, anticoagulant, antidiabetic, antibacterial, antifungal, antiprotozoal, antiviral, antifibrotic, antivenom, anti-ulcer and hypocholesteremic. Its anticancer effect is mainly mediated through induction of apoptosis. Its anti-inflammatory, anticancer and antioxidant roles may be clinically exploited to control rheumatism, carcinogenesis and oxidative stress-related pathogenesis. Clinically, curcumin has already been used to reduce post-operative inflammation, Thus, curcumin has the potential of chemopreventive action and has been used in the development of modern medicine to treat various diseases.