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Biomedical subjects

Y M Lee

Publications and source records attributed to Y M Lee.

At least 91 records · Page 5Linked to original sources

Colonic mucosal concentrations of folate are accurately predicted by blood measurements of folate status among individuals ingesting physiologic quantities of folate.

Folate status is inversely related to the risk of colorectal cancer. Whether conventional blood measurements of folate status accurately reflect folate concentrations in the colorectal mucosa has been a controversial topic. This is an important issue because accurate measures of folate status in the colorectal mucosa are important for ascertaining the risk of colorectal cancer in epidemiological studies and for determining the effects of folate supplementation in clinical trials. We examined whether conventional blood measurements of folate and a more sensitive, inverse indicator of systemic folate status, serum homocysteine, accurately reflect folate concentrations in human colonic mucosa obtained by endoscopic biopsy. Study subjects (n = 20) were participants in a randomized trial that investigated the effect of folate supplementation (5 mg daily for 1 year) on provisional molecular markers of colon cancer. Blood samples and biopsies of normal rectosigmoid mucosa were obtained at baseline, at 6 months, and at 1 year. Serum, RBC, and colonic mucosal folate and serum homocysteine concentrations were determined. Colonic mucosal folate concentrations correlated directly with serum folate concentrators at each time point (r = 0.572-0.845; P < 0.015) and with RBC folate concentrations at 6 months and 1 year (r = 0.747-0.771; P < 0.001). Colonic mucosal folate concentrations correlated inversely with serum homocysteine concentrations at each time point (r = -0.622-0.666; P < 0.008). Systemic measures of folate status did not correlate with colonic mucosal folate concentrations among individuals receiving supplemental folate. Our observations indicate that colonic mucosal concentrations of folate may be predicted accurately by blood measurements of folate status only among individuals not ingesting supraphysiological quantities of folate.

Adenoma↗

Human papillomavirus type 18 in colorectal cancer.

Human papillomaviruses (HPVs) have been recognized as the etiological agent of warts, and they may also be associated with many cancers. HPV-18 is very common both in genital papillomas and in large bowel cancer. The relation between HPV-18 infection and natural course of colorectal cancer has not been fully defined. In this study, normal mucosa and colorectal cancer tissue were evaluated for the presence of HPV gene to determine whether or not HPV was involved in the development of colon neoplasm. The DNA extracted from colon tissue was screened for HPV by polymerase chain reaction (PCR) to amplify the viral gene fragment. These PCR products were digested with restriction enzyme, and Southern blotting was then performed to confirm the existence of HPV-18. The nucleotide sequence related to HPV-18 DNA was detected in 53% (10/19) of the normal mucosa specimens and in 84% (16/19) of the colorectal cancer specimens. The correlation between cancer samples and positive rate of HPV-PCR was statistically significant by chi-square test (p < 0.01). These data indicate that HPV-18 can infect the normal mucosa of the colon, and that this infection may be a risk factor for the development of colorectal cancer. The presence of HPV-18 DNA in patients with colorectal cancer suggests that the pathogenesis of colorectal cancer includes viral involvement.

Colorectal Neoplasms↗

Insulin-like growth factor II induces interleukin-6 expression via NFkappaB activation in psoriasis.

IGF-II is known to induce the growth of keratinocytes and the level was significantly elevated in the tissue fluid of psoriatic lesion. However, the role of IGF-II in psoriasis is not well defined. Because an inflammatory cytokine, interleukin-6 (IL-6) is overexpressed in psoriatic lesions, we explored whether IGF-II has some role in psoriasis through induction of IL-6. Therefore, the expression of IL-6 was analyzed after treatment of IGF-II in primary cultured psoriatic cells and human keratinocyte cell line, HaCaT. We found that IGF-II induced the IL-6 mRNA expression significantly. To investigate the inducing mechanism of IL-6 by IGF-II, we examined the promoter activity of IL-6 and the DNA binding activity of NFkappaB, a strong regulator of IL-6. Interestingly, IL-6 promoter activity and the binding activity of NFkappaB were remarkably increased by IGF-II. Western blot data that IkappaB was reduced by IGF-II significantly suggest that NFkappaB activation by IGF-II may be mediated through the downregulation of IkappaB. Therefore, these results suggest a novel role of IGF-II in psoriasis possibly by inducing IL-6 through the activation of NFkappaB mediated by downregulation of IkappaB.

Base Sequence↗

CDNA cloning of chloroplast omega-3 fatty acid desaturase from Capsicum annuum and its expression upon wounding.

A clone for a plastid omega-3 fatty acid desaturase (FAD) was isolated from a leaf cDNA library of hot pepper (Capsicum annuum L.). The nucleotide sequence of a 1,317 bp open reading frame in the CachFAD showed 80.9% homology with that of tobacco plant. It codes for a polypeptide of 438 amino acids with molecular mass of 50.5 kDa and a pI of 8.14. The CachFAD had a putative transit peptide for targeting the chloroplast. Genomic Southern hybridization indicated that it exists as small gene family. Northern hybridization revealed that its mRNA was present in leaves, but not in roots. Transcript levels in the leaves upon wounding increased rapidly to reach the first peak between 1-3 h, decreased thereafter and slightly increased at 24 h after wounding. The levels of linolenic acid (18:3) in wounded leaves also reached the first peak at 6 h, decreased thereafter and reached the second peak at 18 h. These results indicated that wounding not only enhanced the accumulation of the CachFAD mRNA but also increased the conversion of linoleic acid (18:2) to linolenic acid (18:3) in leaf lipids of hot pepper.

Amino Acid Sequence↗

Affinity purification and characterization of a cutinase from the fungal plant pathogen Monilinia fructicola (Wint.) honey.

Trifluoromethyl ketones (TFK) are potent inhibitors of a variety of serine hydrolases. The TFK inhibitor, 3-(4-mercaptobutylthio)-1,1,1-trifluoro-2-propanone (MBTFP), was found to competitively inhibit cutinase activity (I50 = 9.4 x 10(-3)) from the fungal plant pathogen Monilinia fructicola and to serve as an effective affinity ligand for the purification of cutinases from culture filtrates. The TFK inhibitors, 3-n-octylthio-1,1,1-trifluoro-2-propanone (OTFP) and 3-n-pentylthio-1,1,1-trifluoro-2-propanone (PTFP), also inhibited cutinase activity with I50 values of 1.6 x 10(-6) and 2.3 x 10(-4) M, respectively. Buffer containing OTFP was the strongest eluant for cutinases of M. fructicola and provided the best purification factor and yield, although buffers containing OTFP, detergent, and salt were found to be effective for eluting cutinases bound to MBTFP-Sepharose. Buffer containing 0.5% Triton X-100 also selectively eluted cutinases from the affinity column. Two-dimensional electrophoretic analysis by SDS-PAGE and isoelectric focusing of the affinity-purified cutinase fraction indicated activity associated with proteins of pI 8.2 and molecular masses of approximately 18.6 and 20.8 kDa. These proteins hydrolyzed [3H]cutin and artificial substrates such as p-nitrophenylbutyrate and related esters, typical of other cutinases, but differ from previously characterized cutinases in molecular mass. The two low-molecular-weight proteins resolved by 2-D gel electrophoresis were subjected to in-gel digestion with Lys-C and the resulting peptide fragments were separated by Microbore-HPLC. The amino acid sequences of several internal peptide fragments had high homology with cutinase sequences from other fungi, particularly the plant pathogen Botrytis cinerea. Our study illustrates the potential of TFK ligands for the affinity purification of cutinases and indicates that the cutinases from M. fructicola have novel features warranting further study.

Acetone↗

Identification of the human homologue of mouse KIF4, a kinesin superfamily motor protein.

A combination of RT-PCR with cDNA library screening led to the identification of the human homologue of murine KIF4 (mKIF4), a microtubule-based motor protein. The nucleotide sequence of human KIF4 (hKIF4) comprised part of the 5' untranslated region (UTR), a long open reading frame (ORF) encoding 1232 amino acids, and the entire 3' UTR. Homologies with mKIF4 were 82% and 85% for nucleotides and amino acids, respectively. A single transcript of 5. 0 kb was highly expressed in hematopoietic tissues including fetal liver, spleen, and thymus, and adult thymus and bone marrow. Comparison of the ORF with that of mKIF4 revealed some dissimilarities in the putative cargo binding domain which might affect binding specificities.

Amino Acid Sequence↗

Enhanced guided bone regeneration by controlled tetracycline release from poly(L-lactide) barrier membranes.

With the aim of providing effective periodontal therapeutic modality, drug-releasing membranes for guided tissue regeneration (GTR) were developed. As GTR membranes, biodegradable barrier membranes composed of porous poly(L-lactide) (PLLA) films cast on poly(glycolide) (PGA) meshes were fabricated using an in-air drying phase inversion technique. PLLA was dissolved in methylene chloride-ethylacetate mixtures, cast on knitted PGA mesh, and then air-dried. Tetracycline, which is used in periodontal therapy because of its antibacterial activity and tissue regenerating effects, including osteoblast chemotactic effect and anti-collagenolytic activity, was incorporated into the membranes by adding it to PLLA solutions. The guided bone regenerating potential of tetracycline-loaded membranes was evaluated using release kinetics both in vitro and in vivo, biodegradation tests, and cell attachment tests. Homogeneous pores were generated both at the surface and in a sublayer of the membranes. The release kinetics of tetracycline depended mainly upon the hydrophilicity of tetracycline and the porosity of the membrane. The release rate further could be controlled by loaded drug contents. The release of tetracycline was appropriate for maintaining anti-microbial activity and for its tissue-regenerating potential. The membranes retained a proper degradation property, maintaining their mechanical integrity for the barrier function for 4 weeks. Tetracycline-loaded membranes induced increased cell attachment levels compared with those of unloaded membranes. Tetracycline-loaded membranes markedly increased new bone formation in rat calvarial defects and induced bony reunion after 2 weeks of implantation. These results suggest that tetracycline-loaded PLLA membranes potentially enhance guided tissue regenerative efficacy.

Animals↗

Anti-angiogenic activity of torilin, a sesquiterpene compound isolated from Torilis japonica.

Torilin is a sesquiterpene compound purified from fruits of Torilis japonica (Umbelliferae). In this study, we demonstrated the anti-angiogenic activity of torilin using in vivo and in vitro assay systems. Torilin decreased both neovascularization of chick embryos in the chorioallantoic membrane assay and basic fibroblast growth factor-induced vessel formation in the mouse Matrigel plug assay. Torilin also reduced the proliferation and tube formation of human umbilical vein endothelial cells. In addition, the concentrated conditioned media obtained from torilin-treated HepG2 human hepatoblastoma cells blocked the angiogenic activation of torilin-untreated concentrated conditioned media, indicating that torilin may have an inhibitory effect on tumor-induced angiogenesis. To determine what molecules were involved in the anti-angiogenic activity, we examined the expression of hypoxia-inducible angiogenic factors in torilin-treated HepG2 cells. Torilin significantly down-regulated the expression of hypoxia-inducible vascular endothelial growth factor and insulin-like growth factor-II. Taken together, our data suggest that torilin may be a strong angiogenic inhibitor with the ability to decrease tube formation of vascular endothelial cells and to reduce expression of angiogenic factors of tumor cells.

Angiogenesis Inhibitors↗

Controlled release of platelet-derived growth factor-BB from chondroitin sulfate-chitosan sponge for guided bone regeneration.

Platelet-derived growth factor-BB (PDGF-BB) releasing porous chondroitin-4-sulfate (CS)-chitosan sponge was designed with an aim of controlling growth factor delivery in order to improve bone formation. Porous CS-chitosan sponge was fabricated by freeze drying and crosslinking aqueous CS-chitosan solution. PDGF-BB was incorporated into the CS-chitosan sponge by soaking CS-chitosan sponge into the PDGF-BB solution. CS-chitosan sponge retained a porous structure with a 150-200-microm pore diameter that was suitable for cellular migration and osteoid ingrowth. Release rate of PDGF-BB could be controlled by varying the composition of CS in the sponge or initial loading content of PDGF-BB. CS-chitosan sponge induced increased osteoblast migration and proliferation as compared with chitosan sponge alone. Furthermore, the release of PDGF-BB from CS-chitosan sponge significantly enhanced osteoblast proliferation. These results suggest that PDGF-BB-releasing CS-chitosan sponge may be beneficial to enhance bone cell adaptation and regenerative potential when applied in wound sites.

Animals↗

The antihypertensive and cardioprotective effects of (-)-MJ-451, an ATP-sensitive K(+) channel opener.

ATP-sensitive K(+) (K(ATP)) channel openers have been shown to be a potential class of therapeutic agents for the control of cardiovascular diseases, including angina, arrhythmias, and hypertension. In this study, the pharmacological activity of 6-cyano-3S,4R-dihydro-2, 2-dimethyl-2H-3-hydroxy-4-[5S-(1-hydroxymethyl)-2-oxo-1-pyrrolidinyl] -1-benzopyran ((-)-MJ-451), a synthetic K(ATP) opener, was evaluated in anesthetized rat models and in isolated rat thoracic rings. Results demonstrated that intravascular injection of (-)-MJ-451 (0. 02, 0.05 and 0.1 mg/kg) produced an immediate, dose-related reduction in mean arterial blood pressure in anesthetized spontaneously hypertensive rats (SHR), which persisted for more than 3 h and was not accompanied by reflex tachycardia. The hemodynamic changes were completely abolished by pretreatment with glibenclamide (4 mg/kg, i.v. bolus), a selective K(ATP) channel blocker. In isolated thoracic aorta, (-)-MJ-451 (10 nM-3 microM) produced a concentration-dependent vasodilator effect on the phenylephrine (0.3 microM)-induced vasoconstriction. Moreover, (-)-MJ-451 relaxed the thoracic aorta contracted by low (5, 20 and 30 mM), but not high (40 and 60 mM) concentrations of extracellular potassium. In addition, (-)-MJ-451 showed cardioprotective effects in the rat model of 45-min left coronary artery occlusion followed by 1-h reperfusion. In myocardial ischemia, pretreatment with (-)-MJ-451 (2, 5 and 10 microg/kg, i.v. bolus) significantly reduced the incidence of ventricular fibrillation and the mortality, also reducing the total number of ventricular premature contractions, total duration of ventricular tachycardia and ventricular fibrillation. A significant reduction in infarct size was noted in three (-)-MJ-451 (2, 5 and 10 microg/kg)-treated groups. Also, the cardioprotective effects of (-)-MJ-451 were virtually abolished by pretreating the rats with glibenclamide (4 mg/kg, i.v. bolus). In conclusion, (-)-MJ-451, through opening the K(ATP) channel, exerted antihypertensive and cardioprotective effects. Therefore, it is suggested that (-)-MJ-451 has potential in the treatment of hypertension or acute myocardial infarction.

Adenosine Triphosphate↗

Poly(ethylene oxide)-poly(propylene oxide)-poly(ethylene oxide)/poly(epsilon-caprolactone) (PCL) amphiphilic block copolymeric nanospheres. II. Thermo-responsive drug release behaviors.

Amphiphilic block copolymers composed of relatively hydrophilic PEO-PPO-PEO block copolymer (Pluronic) and poly (epsilon-caprolactone) with hydrophobic character were synthesized by ring-opening polymerization of epsilon-caprolactone in the presence of PEO-PPO-PEO block copolymer using stannous octoate as a catalyst. Pluronic/PCL block copolymeric nanospheres with core-shell structure were prepared by dialysis method. They showed the average diameter of 116-196 nm depending on the type of copolymer. All the nanosphere samples exhibited a narrow size distribution. The critical micelle concentrations of Pluronic/PCL amphiphilic block copolymers determined by fluorescence spectroscopy were lower than that of the common low molecular weight surfactant. Their core-shell structure was confirmed by 1H NMR spectroscopy. Pluronic/PCL block copolymeric nanospheres exhibited the reversible change of size depending on the temperature. Release behaviors of indomethacin from Pluronic/PCL block copolymeric nanospheres also showed temperature dependence and a sustained release pattern. In addition, cytotoxicity test using an MTT assay method revealed that these indomethacin-loaded Pluronic/PCL nanospheres could remarkably reduce the cell damage compared with the unloaded free indomethacin.

Algorithms↗

Human hepatitis B virus X protein is a possible mediator of hypoxia-induced angiogenesis in hepatocarcinogenesis.

The hepatitis B virus (HBV)-encoded transcriptional activator HBV-X protein (HBx) was known to be involved in hepatocarcinogenesis. Hepatocarcinogenesis generally included an active angiogenesis that was mainly considered to be due to a local hypoxia in liver tissues. However, the exact mechanisms of HBx-induced hepatocarcinogenesis were poorly understood. In this study, we examined the role of HBx in the increased angiogenesis and the possible regulating mechanisms of HBx by hypoxia. We demonstrated that HBx stimulated the transcription of vascular endothelial growth factor (VEGF), a potent angiogenic factor, in HBx-stable transfectants. HBx-induced angiogenesis was confirmed by in vivo tumor angiogenesis assay, resulting in that the HBx transfectants increased the formation of new blood vessels compared to the control transfectants. Then, we demonstrated that the expression of HBx was enhanced after incubating HBV-infected hepatoma cells under hypoxia. Moreover, the activity of HBV enhancer 1 (Enh1) was increased when hepatoma cells transfected with the reporter plasmid containing HBV Enh1 were exposed to hypoxic conditions. These results strongly suggest that HBx may play a critical role in the hypoxia-induced angiogenesis through transcriptional activation of VEGF during hepatocarcinogenesis.

Cell Hypoxia↗

Involvement of mi-transcription factor in expression of alpha-melanocyte-stimulating hormone receptor in cultured mast cells of mice.

The microphthalmia (mi) locus encodes a member of the basic-helix-loop-helix-leucine zipper (bHLH-Zip) protein family of transcription factors (MITF). We have reported that expression of several genes was impaired in cultured mast cells (CMCs) of mi/mi mice due to a defective transactivation ability of mutant MITF (mi-MITF). We also found that mi/mi CMCs did not express a receptor (MC1R) for alpha-melanocyte-stimulating hormone. The overexpression of the wild-type (+/+) MITF but not mi-MITF normalized the expression of the MC1R in mi/mi CMCs, indicating the involvement of +-MITF in the MC1R gene expression. Next, we analyzed the promoter region of the MC1R gene by the transient cotransfection assay. The luciferase construct under the control of the MC1R promoter and the cDNA-encoding +-MITF or mi-MITF were cotransfected into NIH/3T3 fibroblasts. The cotransfection of +-MITF but not mi-MITF increased the luciferase activity. There were five CANNTG motifs recognized by bHLH-Zip-type transcription factors in the cloned promoter region. We found +-MITF bound two of five CANNTG motifs, and both motifs were essential for the transactivation of the MC1R gene by +-MITF. These results indicated that +-MITF directly transactivated the MC1R gene through these two motifs.

Animals↗

Glucose-6-phosphatase gene mutations in Taiwan Chinese patients with glycogen storage disease type Ia.

Glycogen storage disease type Ia (GSD Ia) is caused by a deficiency of glucose-6-phosphatase (G6Pase) activity. Eighteen GSD Ia families were studied for G6Pase gene mutations. Thirty-two mutations were found in 36 GSD Ia chromosomes: 16 were 727 G-->T (44.44%); 13 were R83H (327 G-->T; 36.11%); 1 was 341delG; 1 was 933insAA; and 1 was 793 G-->T. The 727 G-->T and R83H mutations together accounted for 80.56% (29/36) of the GSD Ia chromosomes. These two mutations were easily examined by polymerase chain reaction-based methods, and the prenatal diagnosis of a non-affected fetus was successfully made. The 727 G-->T mutation is the predominant mutation in Japanese GSD Ia patients, but is rarely seen in Western counties. The 727 G-->T mutation is also the most prevalent mutation in Taiwan Chinese, although the incidence is not as high as in Japan.

Asian People↗

Platelet derived growth factor releasing chitosan sponge for periodontal bone regeneration.

With an aim of improving bone regeneration, chitosan sponge containing platelet-derived growth factor-BB (PDGF-BB) were developed. For fabrication of chitosan sponge, chitosan solution was freeze-dried, crosslinked and freeze-dried again. PDGF-BB was incorporated into the chitosan sponge by soaking chitosan sponge into the PDGF-BB solution. Release kinetics of PDGF-BB, cell attachment, proliferation capacity and bony regenerative potentials of PDGF-BB-loaded chitosan sponge were investigated. Prepared chitosan sponge retained porous structure with 100 microm pore diameter that was suitable for cellular migration and growth. Release rate of PDGF-BB could be controlled by varying initial loading content of PDGF-BB to obtain optimal therapeutic efficacy. PDGF-BB-loaded chitosan sponge induced significantly high cell attachment and proliferation level, which indicated good cellular adaptability. PDGF-BB-loaded chitosan sponge demonstrated marked increase in new bone formation and rapid calcification. Degradation of the chitosan sponge was proceeded at defect site and subsequently replaced with new bone. Histomorphometric analysis confirmed that PDGF-BB-loaded chitosan sponge significantly induced new bone formation. These results suggested that chitosan sponge and PDGF-BB-loaded chitosan sponge may be beneficial to enhance periodontal bone regeneration.

Animals↗

Nitric oxide production by high molecular weight water-soluble chitosan via nuclear factor-kappaB activation.

High molecular weight water-soluble chitosan (WSC), having an average molecular weight of 300000 Da and a degree of deacethylation over 90%, can be produced using a simple multi-step membrane separation process. In this study, the effect of WSC on the production of nitric oxide (NO) in RAW 264.7 macrophages was evaluated. Water-insoluble chitosan alone has been previously shown to exhibit in vitro stimulatory effect on macrophages NO production. However, WSC had no effect on NO production by itself. When WSC was used in combination with recombinant interferon-gamma (rIFN-gamma), there was a marked cooperative induction of NO synthesis in a dose-dependent manner. The optimal effect of WSC on NO synthesis was shown 24 h after treatment with rIFN-gamma. The increased production of NO from rIFN-gamma plus WSC-stimulated RAW 264.7 macrophages was decreased by the treatment with N(G)-monomethyl-L-arginine (N(G)MMA). The increase in NO synthesis was reflected, as an increased amounts of inducible NO synthase protein. In addition, synergy between rIFN-gamma and WSC was mainly dependent on WSC-induced tumor necrosis factor-alpha (TNF-alpha) and nuclear factor-kappaB (NF-kappaB) activation. The present results indicate that the capacity of WSC to increase NO production from rIFN-gamma-primed RAW 264.7 macrophages is the result of WSC-induced TNF-alpha secretion via the signal transduction pathway of NF-kappaB activation.

Animals↗

Effects of butylated hydroxyanisole and butylated hydroxytoluene on DNA adduct formation and arylamines N-acetyltransferase activity in PC-3 cells (human prostate tumor) in vitro.

The effects of butylated hydroxyanisole (BHA) and butylated hydroxytoluene (BHT) on the N-acetyltransferase (NAT) activity and DNA adduct formation in PC-3 cells (human prostate tumor) was studied. PC-3 cells were placed into tissue culture flasks and grown in an incubator as cytosols and intact cells. The BHA or BHT were added to the cytosols and intact cells. The NAT activity in cytosol and intact PC-3 cells were measured by HPLC assaying exhibited for the amounts of N-acetyl-2-aminofluorene and N-acetyl-p-aminobenzoic acid, 2-aminofluorene and p-aminobenzoic acid. The NAT activity in PC-3 cells and cytosols were inhibited by BHA or BHT in a dose-dependent manner; that is, the higher the concentrations of BHA or BHT the higher inhibition of NAT activity. The NAT values of K(m) and V(max) from PC-3 cells were also decreased by BHA or BHT in both cytosols and intact cells. The data also demonstrated concomitant exposure to BHA or BHT decreased AF-DNA adduct formation which was seen in the PC-3 cells. In addition, the formation of DNA adduct was decreased after BHA or BHT exposure. These findings suggested the usefulness of using human cultured PC-3 cells for assessing arylamine-induced DNA adduct formation. Furthermore, the findings illustrate how effectively BHA or BHT reduce the adduct formation.

Arylamine N-Acetyltransferase↗

Inhibition of tumor necrosis factor-alpha-induced apoptosis by Asparagus cochinchinensis in Hep G2 cells.

A human hepatoma cell line, Hep G2 cells, is a reliable system for the study of alcohol-induced hepatotoxicity. In this study, we investigated the effect of an aqueous extract of Asparagus cochinchinensis(MERRIL) (Liliaceae) roots (ACAE) on ethanol (EtOH)-induced cytotoxicity in Hep G2 cells. ACAE (1-100 microg/ml) dose-dependently inhibited the EtOH-induced tumor necrosis factor-alpha (TNF-alpha) secretion. ACAE (1-100 microg/ml) also inhibited the EtOH and TNF-alpha-induced cytotoxicity. Furthermore, we found that ACAE inhibited the TNF-alpha-induced apoptosis of Hep G2 cells. These results suggest that ACAE may prevent the EtOH-induced cytotoxicity through inhibition of the apoptosis of Hep G2 cells.

Apoptosis↗