• Textile Coloration and Finishing
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• v.14 no.1
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• pp.11-17
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• 2002

To identify the antimicrobial activity, of tumeric and its active compound tumeric was fractionated into four groups dichloromethane extract, hexane fraction, methanol soluble fraction and residue's extract. They were tested for antibacterial activity against E. coil and S. aureus and the methanol soluble fraction was found lo be the most active fraction. Compound I, II and III were isolated from TLC and silica gel column chromatography in the methanol soluble fraction. These compounds were analyzed by $^1H-NMR\;and\;^{13}C-NMR$ spectra and identified as curcumin I, II and III. They were also tested for antimicrobial activity against E. coli and S. aureus. Curcumin I was the must active curcuminoids due to the phenolic and methoxyl$(OCH_3)$ moiety in the same molecular structure.

• Biomolecules & Therapeutics
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• v.27 no.5
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• pp.484-491
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• 2019

Glioblastoma is the most aggressive common brain tumor in adults. Curcumin, from Curcuma longa, is an effective antitumor agent. Although the same proteins control both autophagy and cell death, the molecular connections between them are complicated and autophagy may promote or inhibit cell death. We investigated whether curcumin affects autophagy, which regulates curcumin-mediated tumor cell death in A172 human glioblastoma cells. When A172 cells were incubated with $10{\mu}M$ curcumin, autophagy increased in a time-dependent manner. Curcumin-induced cell death was reduced by co-incubation with the autophagy inhibitors 3-methyladenine (3-MA), hydroxychloroquine (HCQ), and LY294002. Curcumin-induced cell death was also inhibited by co-incubation with rapamycin, an autophagy inducer. When cells were incubated under serum-deprived medium, LC3-II amount was increased but the basal level of cell viability was reduced, leading to the inhibition of curcumin-induced cell death. Cell death was decreased by inhibiting curcumin-induced autophagy using small interference RNA (siRNA) of Atg5 or Beclin1. Therefore, curcumin-mediated tumor cell death is promoted by curcumin-induced autophagy, but not by an increase in the basal level of autophagy in rapamycin-treated or serum-deprived conditions. This suggests that the antitumor effects of curcumin are influenced differently by curcumin-induced autophagy and the prerequisite basal level of autophagy in cancer cells.

• Nutrition Research and Practice
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• v.17 no.2
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• pp.192-205
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• 2023

BACKGROUND/OBJECTIVES: It is known that the renin-angiotensin system (RAS) in the brain could regulate cognitive functions as well as blood pressure. Inhibition of RAS for the improvement of cognitive function may be a new strategy, but studies so far have mostly reported on the effects of RAS inhibition by drugs, and there is no research on cognitive improvement through RAS inhibition of food ingredients. Therefore, this study investigated the effect of curcumin on blood pressure and cognitive function and its related mechanism in spontaneously hypertensive rat/Izm (SHR/Izm). MATERIALS/METHODS: Six-week-old SHR/Izm rats were divided into 5 groups: control group (CON), scopolamine group (SCO, drug for inducing cognitive deficits), positive control (SCO and tacrine [TAC]), curcumin 100 group (CUR100, SCO + Cur 100 mg/kg), and curcumin 200 group (CUR200, SCO + Cur 200 mg/kg). Changes in blood pressure, RAS, cholinergic system, and cognitive function were compared before and after cognitive impairment. RESULTS: The SCO group showed increased blood pressure and significantly reduced cognitive function based on the y-maze and passive avoidance test. Curcumin treatments significantly improved blood pressure and cognitive function compared with the SCO group. In both the CUR100 and CUR200 groups, the mRNA expressions of angiotensin-converting enzyme (ACE) and angiotensin II receptor type1 (AT1), as well as the concentrations of angiotensin II (Ang II) in brain tissue were significantly decreased. The mRNA expression of the muscarinic acetylcholine receptors (mAChRs) and acetylcholine (ACh) content was significantly increased, compared with the SCO group. CONCLUSIONS: The administration of curcumin improved blood pressure and cognitive function in SCO-induced hypertensive mice, indicating that the cholinergic system was improved by suppressing RAS and AT1 receptor expression and increasing the mAChR expression.

• Journal of Korean Medicine Rehabilitation
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• v.18 no.1
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• pp.1-13
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• 2008

목 적 : 동맥경화 유발에 있어서 중요한 역할을 수행하는 부착분자는 혈관내피세포가 염증성 물질에 자극 받아서 생성된다. 본 연구는 항염증성 curcumin이 혈관내피세포 부착분자 발현에 미치는 효과를 조사하였다. 방 법 : 혈관내피세포는 HUVEC을 사용하였고, 염증성 물질 $TNF-\alpha$로 자극하였다. 결 과 : Curcumin은 부착분자 VCAM-1 및 ICAM-1 발현을 억제시켜, 혈관내피세포에 백혈구가 부착되는 것을 억제하였다. Curcumin은 ICAM-1 및 VCAM-1 promoter 활성을 억제하였고, 또한 억제 kB의 인산화를 차단하였다. Curcumin은 NF-kB p65의 핵내 이동을 차단하였고, 세포내 ROS 양을 감소시켰고, JNK 및 p38 인산화를 억제시켰다. 그러나 curcumin은 TNF 수용체 I및 II에 어떠한 영향도 미치지 못했다. 결 론 : Curcumin이 NF-kB 비활성화 및 p38과 JNK의 기능저하를 매개로 VCAM-1 및 ICAM-1의 발현을 억제할 수 있음을 알 수 있었다.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.10
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• pp.5753-5759
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• 2013

Curcumin and curcumin containing polyherbal preparations have demonstrated anti-microbial and antiviral properties in pre-clinical studies. Till date no therapeutic intervention has been proved to be effective and safe in clearing established cervical human papillomavirus (HPV) infection. The present study evaluated the efficacy of Basant polyherbal vaginal cream (containing extracts of curcumin, reetha, amla and aloe vera) and of curcumin vaginal capsules to eliminate HPV infection from cervix. Women were screened by Pap smear and HPV DNA test by PCR. HPV positive women without high grade cervical neoplasias (N=287) were randomized to four intervention arms to be treated with vaginal Basant cream, vaginal placebo cream, curcumin vaginal capsules and placebo vaginal capsules respectively. All subjects were instructed to use one application of the assigned formulation daily for 30 consecutive days except during menstruation and recalled within seven days of the last application for repeat HPV test, cytology and colposcopy. HPV clearance rate in Basant arm (87.7%) was significantly higher than the combined placebo arms (73.3%). Curcumin caused higher rate of clearance (81.3%) than placebo though the difference was not statistically significant. Vaginal irritation and itching, mostly mild to moderate, was significantly higher after Basant application. No serious adverse events were noted.

• The Korean Journal of Physiology and Pharmacology
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• v.15 no.1
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• pp.1-7
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• 2011

Many anticancer agents as well as ionizing radiation have been shown to induce autophagy which is originally described as a protein recycling process and recently reported to play a crucial role in various disorders. In HCT116 human colon cancer cells, we found that curcumin, a polyphenolic phytochemical extracted from the plant Curcuma longa, markedly induced the conversion of microtubule-associated protein 1 light chain 3 (LC3)-I to LC3-II and degradation of sequestome-1 (SQSTM1) which is a marker of autophagosome degradation. Moreover, we found that curcumin caused GFP-LC3 formation puncta, a marker of autophagosome, and decrease of GFP-LC3 and SQSTM1 protein level in GFP-LC3 expressing HCT116 cells. It was further confirmed that treatment of cells with hydrogen peroxide induced increase of LC3 conversion and decrease of GFP-LC3 and SQSTM1 levels, but these changes by curcumin were almost completely blocked in the presence of antioxidant, N-acetylcystein (NAC), indicating that curcumin leads to reactive oxygen species (ROS) production, which results in autophagosome development and autolysosomal degradation. In parallel with NAC, SQSTM1 degradation was also diminished by bafilomycin A, a potent inhibitor of autophagosome-lysosome fusion, and cell viability assay was further confirmed that cucurmin-induced cell death was partially blocked by bafilomycin A as well as NAC. We also observed that NAC abolished curcumin-induced activation of extracelluar signal-regulated kinases (ERK) 112 and p38 mitogen-activated protein kinases (MAPK), but not Jun N-terminal kinase (JNK). However, the activation of ERK1/2 and p38 MAPK seemed to have no effect on the curcumin-induced autophagy, since both the conversion of LC3 protein and SQSTM1 degradation by curcumin was not changed in the presence of NAC. Taken together, our data suggest that curcumin induced ROS production, which resulted in autophagic activation and concomitant cell death in HCT116 human colon cancer cell. However, ROS-dependent activation of ERK1/2 and p38 MAPK, but not JNK, might not be involved in the curcumin-induced autophagy.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.18
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• pp.8271-8279
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• 2016

Background: Hepato-carcinogenesis is multifaceted in its molecular aspects. Among the interplaying agents are altered gap junctions, the proteasome/autophagy system, and mitochondria. The present experimental study was designed to outline the roles of these players and to investigate the tumor suppressive effects of curcumin with or without mesenchymal stem cells (MSCs) in hepatocellular carcinoma (HCC). Materials and Methods: Adult female albino rats were divided into normal controls and animals with HCC induced by diethyl-nitrosamine (DENA) and $CCl_4$. Additional groups treated after HCC induction were: Cur/HCC which received curcumin; MSCs/HCC which received MSCs; and Cur+MSCs/HCC which received both curcumin and MSCs. For all groups there were histopathological examination and assessment of gene expression of connexin43 (Cx43), ubiquitin ligase-E3 (UCP-3), the autophagy marker LC3 and coenzyme-Q10 (Mito.Q10) mRNA by real time, reverse transcription-polymerase chain reaction, along with measurement of LC3II/LC3I ratio for estimation of autophagosome formation in the rat liver tissue. In addition, the serum levels of ALT, AST and alpha fetoprotein (AFP), together with the proinflammatory cytokines $TNF{\alpha}$ and IL-6, were determined in all groups. Results: Histopathological examination of liver tissue from animals which received DENA-$CCl_4$ only revealed the presence of anaplastic carcinoma cells and macro-regenerative nodules. Administration of curcumin, MSCs; each alone or combined into rats after induction of HCC improved the histopathological picture. This was accompanied by significant reduction in ${\alpha}$-fetoprotein together with proinflammatory cytokines and significant decrease of various liver enzymes, in addition to upregulation of Cx43, UCP-3, LC3 and Mito.Q10 mRNA. Conclusions: Improvement of Cx43 expression, nonapoptotic cell death and mitochondrial function can repress tumor growth in HCC. Administration of curcumin and/or MSCs have tumor suppressive effects as they can target these mechanisms. However, further research is still needed to verify their effectiveness.

• BMB Reports
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• v.36 no.1
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• pp.35-42
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• 2003

Heterocyclic amines (HCAs) are potent mutagens generated during the cooking of meat and fish, and several of these compounds produce tumors in conventional experimental animals. During the past 5 years or so, HCAs have been tested in a number of novel in vivo murine models, including the following: lacZ, lacI, cII, c-myc/lacZ, rpsL, and $gpt{\Delta}$ transgenics, $XPA^{-/-}$, $XPC^{-/-}$, $Msh2^{+/-}$, $Msh2^{-/-}$ and $p53^{+/-}$ knock-outs, Apc mutant mice ($Apc^{{\Delta}716}$, $Apc^{1638N}$, $Apc^{min}$), and $A33^{{\Delta}N{\beta}-cat}$ knock-in mice. Several of these models have provided insights into the mutation spectra induced in vivo by HCAs in target and non-target organs for tumorigenesis, as well as demonstrating enhanced susceptibility to HCA-induced tumors and preneoplastic lesions. This review describes several of the more recent reports in which novel animal models were used to examine HCA-induced mutagenesis and carcinogenesis in vivo, including a number of studies which assessed the inhibitory activities of chemopreventive agents such as 1,2-dithiole-3-thione, conjugated linoleic acids, tea, curcumin, chlorophyllin-chitosan, and sulindac.

• Food Science and Biotechnology
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• v.17 no.6
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• pp.1151-1155
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• 2008

This study aimed to investigate the alterations in plasma antioxidant activity after the consumption of a single oral dose of curcumin, vitamin C, and E administered individually or in combination to (i) assess possible synergies or antagonism between the antioxidants and (ii) determine the optimal composition of the antioxidant mixture such that the duration of action is prolonged to beyond that of individual antioxidants. Each antioxidant was administered to male Sprague-Dawley rats, and blood samples were drawn at different time points up to 180 min to measure the plasma total antioxidant capacity (TAC). Five antioxidant compositions (M1-M5) were evaluated to assess the possible synergies or antagonisms among them and to determine the optimal composition of the antioxidant mixture. Blood samples were collected up to 360 min post-consumption. A single oral dose of individual antioxidants significantly increased the TAC values; however, the time to reach the peak TAC value varied. Among the 5 antioxidant compositions, M2 exhibited the highest and most prolonged antioxidant effect in plasma; this was greater than the proportional sum of the effects of the individual antioxidants in the composition. This result indicates a synergistic interaction among antioxidants in the optimal composition M2.