Biomedical subjects

Hong-Liang Li

Publications and source records attributed to Hong-Liang Li.

11 recordsLinked to original sources

PubMed2006

Epigallocathechin-3 gallate inhibits cardiac hypertrophy through blocking reactive oxidative species-dependent and -independent signal pathways.

Cardiac hypertrophy is a major cause of morbidity and mortality worldwide. Recent in vitro and in vivo studies have suggested that reactive oxygen species (ROS) may play an important role in cardiac hypertrophy. It was therefore thought to be of particular value to examine the effects of antioxidants on cardiac hypertrophy. Epigallocatechin-3-gallate (EGCG) is a major bioactive polyphenol present in green tea and a potent antioxidant. The current study was designed to test the hypothesis that EGCG inhibits cardiac hypertrophy in vitro and in vivo. In this study, we investigated the effects of EGCG on angiotensin II- (Ang II) and pressure-overload-induced cardiac hypertrophy. Our results showed that EGCG attenuated Ang II- and pressure-overload-mediated cardiac hypertrophy. Both reactive oxygen species generation and NADPH oxidase expressions induced by Ang II and pressure overload were suppressed by EGCG. The increased hypertension by pressure overload was almost completely blocked after EGCG treatment. Further studies showed that EGCG inhibited Ang II-induced NF-kappaB and AP-1 activation. Inhibition of the activity of NF-kappaB was through blocking ROS-dependent p38 and JNK signaling pathways, whereas inhibition of AP-1 activation was via blocking EGFR transactivation and its downstream events ERKs/PI3K/Akt/mTOR/p70(S6K). The combination of these actions resulted in repressing the reactivation of ANP and BNP, and ultimately preventing the progress of cardiac hypertrophy. These findings indicated that EGCG prevents the development of cardiac hypertrophy through ROS-dependent and -independent mechanisms involving inhibition of different intracellular signaling transductional pathways.

Angiotensin II↗

PubMed2006

A20 inhibits oxidized low-density lipoprotein-induced apoptosis through negative Fas/Fas ligand-dependent activation of caspase-8 and mitochondrial pathways in murine RAW264.7 macrophages.

A20 was originally characterized as a TNF-inducible gene in human umbilical vein endothelial cells. As an NF-kappaB target gene, A20 is also induced in many other cell types by a wide range of stimuli. Expression of A20 has been shown to protect from TNF-induced apoptosis and also functions via a negative-feedback loop to block NF-kappaB activation induced by TNF and other stimuli. To date, there are no reports on whether A20 can protect OxLDL-induced apoptosis in macrophages. For the first time we report that A20 expression blocks OxLDL-mediated cell toxicity and apoptosis. OxLDL induced the expression of Fas and FasL, and the subsequent caspase-8 cleavage and treatment with a neutralizing ZB4 anti-Fas antibody blocked apoptosis induced by OxLDL. Expression of dominant negative FADD efficiently prevented OxLDL-induced apoptosis and caspase-8 activation. A20 expression significantly attenuated the increased expression of Fas and FasL, and Fas-mediated apoptosis. These findings suggest that A20-mediated protection from OxLDL may occur at the level of Fas/FADD-caspase-8 and be FasL dependent. Treatment of RAW264.7 cells with OxLDL induces a series of time-dependent events, including the release of cytochrome c, Smac and Omi from the mitochondria to the cytosol, activation of caspase-9, -6, -2, and -3, which are blocked by A20 expression. No cleaved form of Bid was detected, even treatment with OxLDL for 48 h. Expression of dominant negative FADD also efficiently prevented OxLDL-induced the above apoptotic events. The release of cyto c, Smac and Omi from mitochondria to cytosol, activated by OxLDL treatment, and the activation of caspase-9 may not be a downstream event of caspase-8-mediated Bid cleavage. Therefore, the protective effect of A20 on mitochondrial apoptotic pathway activated by OxLDL may be dependent on FADD. A20 expression reversed OxLDL-mediated G(0)/G(1) stage arrest by maintaining the expression of cyclin B1, cyclin D1, and cyclin E, and p21 and p73. Thus, A20 expression blocks OxLDL-mediated apoptosis in murine RAW264.7 macrophages through disrupting Fas/FasL-dependent activation of caspase-8 and the mitochondria pathway.

Animals↗

PubMed2005

Improved controllability of opal film growth using capillaries for the deposition process.

A capillary deposition method for the preparation of opal and inverse opal films has been developed. By this method, one can control the film thickness and the crack arrangement in opal as well as inverse opal structures. This method combines tube capillarity with cell capillarity or with gravity depending on the stability of the suspensions. The combination of tube capillarity with cell capillarity is used to prepare opal films from stable suspensions. The tube capillary transports the suspension, while the cell capillary helps to assemble the spheres. The setup defines the drying fronts, thickness, and crack arrangements of the opal films. The combination of capillarity with gravity is useful for making opal films from unstable suspensions. Opal films of spheres with size up to 1 mum can be easily prepared from this combination. Here, the gravity influences the arrangement of the spheres. The two-capillary setup has also been used to infiltrate the opal films with a titania precursor. After calcination, inverse titania opal films with skeleton structure have been obtained.

Journal Article↗

PubMed2005

Isorhapontigenin, a new resveratrol analog, attenuates cardiac hypertrophy via blocking signaling transduction pathways.

Cardiac hypertrophy is a major cause of morbidity and mortality worldwide. The hypertrophic process is mediated, in part, by oxidative stress-mediated signaling pathways. We hypothesized that isorhapontigenin (ISO), a new resveratrol analog, inhibits cardiac hypertrophy by blocking oxidative stress and oxidative stress-mediated signaling pathways. We treated cardiomyocytes with angiotensin II (Ang II) with or without ISO and found that ISO inhibited Ang II-induced cardiac hypertrophy. These effects were associated with a decrease in the levels of reactive oxygen species and H2O2 and the content of intracellular malonaldehyde and an increase in the activities of superoxide dismutase and glutathione peroxidase. Ang II induced the phosphorylation of PKC, Erk1/2, JNK, and p38 in cardiomyocytes and such phosphorylation was inhibited by ISO. ISO also blocked the PKC-dependent PI3K-Akt-GSK3beta/p70S6K pathway. These effects lead to direct or indirect inhibition of NF-kappaB and AP-1 activation. Our results revealed that pretreatment with ISO significantly inhibited Ang II-mediated NF-kappaB through affecting the degradation and phosphorylation of IkappaBalpha and the activity of IKKbeta and AP-1 activation by influencing the expression of c-Fos and c-Jun proteins. In addition, we also established the molecular link between activation of PKC and MAPKs and activation of NF-kappaB and AP-1 in cardiomyocytes. We also found that ISO treatment significantly attenuated heart weight/body weight ratio by approximately 25%, decreased posterior wall thickness and left ventricle diastolic and systolic diameters, and increased 10% fractional shortening in an aortic-banded rat model. Furthermore, treatment with ISO significantly decreased cardiac myocyte size and systolic blood pressure. These findings suggest that ISO prevents the development of cardiac hypertrophy through an antioxidant mechanism involving inhibition of different intracellular signaling transduction pathways.

Angiotensin II↗

PubMed2003

Paraoxonase gene polymorphisms, oxidative stress, and diseases.

The paraoxonase (PON) gene cluster contains at least three members, including PON1, PON2, and PON3, located on chromosome 7q21.3-22.1. Until now there has been little insight into the role of the respective gene products in human physiology and pathology. However, emerging evidence from biochemical and genetic experiments is providing clues about the role(s) of the products of these genes, which indicates that PON(s) acts as important guardians against cellular damage from toxic agents, such as organophosphates, oxidized lipids in the plasma low-density lipoproteins. In parallel, substantial data have been published on the association between the polymorphisms of PON(s) and coronary heart disease. It has become clear that the polymorphisms significantly affect the prevalence of coronary heart disease. However, the associations between the PON(s) polymorphisms and most of these conditions were found to be inconsistent when additional populations were investigated. This contribution provides an overview of the status of research of each of the three genes and the available association studies and the potential problems in interpreting the data. We also review the current evidence on the association between PON(s) polymorphisms and diseases other than coronary heart disease and some metabolic quantitative phenotypes, such as plasma lipoproteins, plasma glucose, and birthweight. Finally, we suggest directions for the future that might elucidate the role of the PON genetic polymorphisms in this potentially important function of PON(s) and the role in coronary heart disease and other related diseases.

Animals↗

PubMed2003

[The relationship between insulin resistance and endothelium-dependent vasodilatation in obese subjects].

OBJECTIVE: To study the relationship between insulin resistance and endothelium-dependent vasodilatation function in obese subjects with normal blood glucose, serum cholesterol and blood pressure and to explore the non-traditional risk factors associated with atherosclerosis. METHODS: 24 euglycemic obese males (OB) and 12 age and sex matched lean controls (Lean) underwent oral glucose tolerance test (OGTT), euglycemic hyperinsulinemia clamp study with an insulin infusion rate of 120 mU/m(2)/min to evaluate the peripheral glucose disposal rate (GDR) in steady-state, brachial artery ultrasound study to assess the endothelium-dependent vasodilation (EDV) and independent vasodilation (EIV), the combined intima-media thickness (IMT) of common carotid arteries examined by high resolution ultrasound, and fasting lipids profile and free fatty acids (FFAs) concentration. RESULTS: The blood glucose and serum cholesterol levels were all normal in the OB group but the serum FFA and triglyceride concentrations were elevated compared with those of the controls (FFA: 888 microM/l +/- 158 microM/l vs 508 microM/l +/- 137 microM/l, P < 0.05; TG: 1.8 mM/l +/- 0.6 mM/l vs 1.1 mM/l +/- 0.5 mM/l, P < 0.05) The GDR in steady-state was 6.7 mg x min(-1) x kg(-1) +/- 1.4 mg x min(-1) x kg(-1) in the OB group, significantly lower than that of the controls (12.2 mg x min(-1) x kg(-1) +/- 3.1 mg x min(-1) x kg(-1), P < 0.05). In the OB group the flow-mediated dilation of the brachial artery caused by reactive hyperemia (EDV) were impaired and the relaxation time was shorter than that of the controls (P < 0.05) but the EIV was not significantly different between these two groups. There was a significantly positive correlation between GDR and EDV (r = 0.438, P < 0.05). The IMT of common carotid arteries was thicker in the OB group than in the control group (0.50 mm +/- 0.02 mm vs 0.34 mm +/- 0.19 mm). CONCLUSION: The endothelium-dependent vasodilation was impaired in obese subjects even though without hyperglycemia, hypercholesterolemia, and hypertension. Traditional cardiovascular risk factors cannot fully account for the increased risk of cardiovascular disease in metabolic syndrome. Elevated circulating FFA concentration, is characteristic of metabolic syndrome, may play a role in endothelial dysfunction.

Adult↗

PubMed2002

Sonochemical preparation of GaSb nanoparticles.

A room temperature sonochemical method for the preparation of GaSb nanoparticles using less hazardous Ga and antimony chloride (SbCl(3)) as the precursors has been described. The formation of GaSb has been confirmed by means of XRD, EDAX, and XPS characterization. TEM and SAED results show that the as-prepared solid consists of nanosized GaSb crystals with sizes in the range 20-30 nm. The photoacoustic spectrum result reveals that the GaSb nanoparticles have a direct band gap of about 1.21 eV. On the basis of the control experiments and the extreme conditions produced by ultrasound, an ultrasound-assisted in-situ reduction/combination mechanism has been proposed to explain the reaction.

Journal Article↗

PubMed2002

JTE-522-induced apoptosis in human gastric adenocarcinoma [correction of adenocarcinoma] cell line AGS cells by caspase activation accompanying cytochrome C release, membrane translocation of Bax and loss of mitochondrial membrane potential.

AIM: To investigate the role of the mitochondrial pathway in JTE-522-induced apoptosis and to investigate the relationship between cytochrome C release, caspase activity and loss of mitochondrial membrane potential (Deltapsim). METHODS: Cell culture, cell counting, ELISA assay, TUNEL, flow cytometry, Western blot and fluorometric assay were employed to investigate the effect of JTE-522 on cell proliferation and apoptosis in AGS cells and related molecular mechanism. RESULTS: JTE-522 inhibited the growth of AGS cells and induced the apoptosis. Caspases 8 and 9 were activated during apoptosis as judged by the appearance of cleavage products from procaspase and the caspase activities to cleave specific fluorogenic substrates. To elucidate whether the activation of caspases 8 and 9 was required for the apoptosis induction, we examined the effect of caspase-specific inhibitors on apoptosis. The results showed that caspase inhibitors significantly inhibited the apoptosis induced by JTE-522. In addition, the membrane translocation of Bax and cytosolic release of cytochrome C accompanying with the decrease of the uptake of Rhodamin 123, were detected at an early stage of apoptosis. Furthermore, Bax translocation, cytochrome C release, and caspase 9 activation were blocked by Z-VAD.fmk and Z-IETD-CHO. CONCLUSION: The present data indicate a crucial association between activation of caspases 8, 9, cytochrome C release, membrane translocation of Bax, loss of Deltapsim and JTE-522-induced apoptosis in AGS cells.

Adenocarcinoma↗

PubMed2002

Changes of NF-kB, p53, Bcl-2 and caspase in apoptosis induced by JTE-522 in human gastric adenocarcinoma cell line AGS cells: role of reactive oxygen species.

AIM: To identify whether JTE-522 can induce apoptosis in AGS cells and ROS also involved in the process, and to investigate the changes in NF-kB, p53, bcl-2 and caspase in the apoptosis process. METHODS: Cell culture, MTT, Electromicroscopy, agarose gel electrophoresis, lucigenin, Western blot and electrophoretic mobility shift assay (EMSA) analysis were employed to investigate the effect of JTE-522 on cell proliferation and apoptosis in AGS cells and related molecular mechanisms. RESULTS: JTE-522 inhibited the growth of AGS cells and induced the apoptosis. Lucigenin assay showed the generation of ROS in cells under incubation with JTE-522. The increased ROS generation might contribute to the induction of AGS cells to apoptosis. EMSA and Western blot revealed that NF-kB activity was almost completely inhibited by preventing the degradation of IkBalpha. Additionally, by using Western blot we confirmed that the level of bcl-2 was decreased, whereas p53 showed a great increase following JTE-522 treatment. Their changes were in a dose-dependent manner. CONCLUSION: These findings suggest that reactive oxygen species, NF-kB, p53, bcl-2 and caspase-3 may play an important role in the induction of apoptosis in AGS cells after treatment with JTE-522.

Adenocarcinoma↗

PubMed2002

JTE-522, a selective COX-2 inhibitor, inhibits cell proliferation and induces apoptosis in RL95-2 cells.

AIM: To investigate whether JTE-522 [4-(4-cyclohexyl-2-methyloxazol-5-yl)-2-fluorobenzenesulfonamide], a selective COX-2 inhibitor, can induce apoptosis and inhibit cell proliferation in human endometrial cancer cell line RL95-2 cells and to explore the molecular mechanisms. METHODS: [3-(4,5)-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide (MTT), DNA ladder, enzyme-linked immunosorbent assay (ELISA), flow cytometry, RT-PCR, and Western blot analysis were employed to investigate effect of JTE-522 on human endometrial cancer cell line RL95-2 cells and the related molecular mechanisms. RESULTS: JTE-522 inhibited the growth of RL95-2 cells and induced the apoptosis. Furthermore, it arrested G0/G1 phase and inhibited S phase in RL95-2 cells. JTE-522 inhibited the expressions of COX-2 mRNA, phosphorylated Rb, and CDK4 proteins, while increased the levels of p53, p21, cyclin D1 proteins, and the activity of caspase-3 in RL95-2 cells. CONCLUSION: JTE-522 inhibits cell proliferation and induces apoptosis in RL95-2 cells, which may be associated with the activation of caspase-3-like proteases, down-regulation of the expression of COX-2 mRNA, phosphorylated Rb, and CDK4 proteins, and up-regulation of the expressions of p53, p21, and cyclin D1 proteins.

Apoptosis↗

PubMedDate not supplied

Predictive functional control (PFC) and its application in chlorinated polyethylene process.

The main principle and the characteristic of Predictive Functional Control (PFC) strategy are presented in this paper and the corresponding control system aid design software APC-PFC is also introduced. For a chlorinated polyethylene (CPE) process, a design scheme of cascade predictive functional control system is described and the control performance is improved obviously.

Algorithms↗