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Guo-Qing Liu

Publications and source records attributed to Guo-Qing Liu.

At least 19 recordsLinked to original sources
PubMed2006

The developmental changes and effect on IMF content of H-FABP and PPARgamma mRNA expression in sheep muscle.

Male Kazak sheep and Xinjiang fine wool sheep of different ages were selected to investigate the developmental changes and effect on intramuscular fat (IMF) content of heart fatty acid-binding protein (H-FABP) and peroxisome proliferator-activated receptor gamma (PPARgamma) mRNA expression in muscle. Longissimus dorsal muscle was sampled to measure IMF content; and total RNA was extracted to determine H-FABP and PPARgamma mRNA expression levels by real-time PCR. The results showed that: (1) The IMF content increased continuously with growing and showed significant differences (P<0.05) between ages in male Kazak sheep, but no such differences (P>0.05) existed in Xinjiang fine wool sheep. Furthermore, the IMF content in Kazak sheep was very much higher (P<0.01) than that of the other breed from day 30 to 90; (2) H-FABP mRNA expression level was the highest on day 2 and showed significant differences (P<0.05) between ages in male Kazak sheep as well as in Xinjiang fine wool sheep. In the former breed, the expression reached the lowest point at day 30, and then rose continuously. But in the latter breed, it declined continuously from day 2 to 90, and then increased; (3) Significant differences (P<0.05) of PPARgamma mRNA expression between ages occurred in both breeds. In male Kazak sheep, PPARgamma mRNA expression declined from day 2 to 90, while in the other breed it increased continuously from day 2 to 60, but reached the lowest level at day 90, then increased; (4) In male Kazak sheep, the mRNA expression level of H-FABP was highly positively correlated (r=0.737, P<0.01) with IMF content from day 30 to 90, but that of PPARgamma was highly negatively correlated (r=-0.835, P<0.01) with IMF content from day 2 to 90.

Animals↗
PubMed2006

The tissue distribution and developmental changes of ghrelin mRNA expression in sheep.

Male Kazak sheep and Xinjiang fine wool sheep, six for each different age group (days 2, 30, 60, 90 and 120), were used in the present study to investigate the tissue distribution and developmental changes of ghrelin mRNA expression in abomasum; however, there was no 120-day-old Kazak sheep. After measurement of body weight, the tissues such as hypothalamus, pituitary, heart, liver, rumen, reticulum, omasum, abomasum, duodenum, and longissimus dorsi muscle were sampled. And the total RNA of different tissues was extracted to determine the abundance of ghrelin mRNA by RT-PCR and real-time PCR. The results showed that (1) for both breeds, body weight among different ages was significantly different (P<0.05). And from day 30 to 90, the body weight of Kazak was significantly higher than that of Xinjiang (P<0.01); (2) Ghrelin mRNA existed in all the above tissues and was significantly higher in the abomasum than in other tissues (P<0.05); (3) the temporal patterns of abomasum ghrelin mRNA expression in Kazak and Xinjiang were similar. From day 2 to 60 in Kazak and 2 to 90 in Xinjiang, there was a steady increase in the ghrelin mRNA level. By day 60 in Kazak and day 90 in Xinjiang, the level reached a plateau and remained steady. These results also demonstrated that from birth to day 90, ghrelin mRNA level was significantly higher in Kazak than in Xinjiang (P<0.01).

Animals↗
PubMed2006

Up-regulation of P-glycoprotein expression by glutathione depletion-induced oxidative stress in rat brain microvessel endothelial cells.

Glutathione (GSH) depletion has been implicated in the pathogenesis of neurological diseases. During GSH depletion, cells of the blood-brain barrier (BBB) are subjected to chronic oxidative stress. In this study, we investigated the effect of such stress, produced with the GSH synthesis inhibitor l-buthionine-(S,R)-sulfoximine (BSO), on expression of P-glycoprotein (Pgp) in primary cultured rat brain microvessel endothelial cells that comprise the blood-brain barrier (BBB). Application of BSO to cell monolayers at concentrations up to 800 microm caused increases in expression of Pgp. Concentrations >or= 400 microm BSO decreased cell viability. Application of 200 microm BSO caused a significant increase in Pgp function activity, as assessed by rhodamine 123 (Rh123) accumulation experiments. At this concentration, BSO produced time-dependent decreases in levels of intracellular GSH and increases in levels of intracellular reactive oxygen species (iROS). The increases were also observed within 48 h following BSO treatment in mdr1a and mdr1b mRNA. Exposure of cells to BSO for 24 h produced maximal effects in the accumulation of iROS, and in expression and function of Pgp. The ROS scavenger N-acetylcysteine prevented ROS generation and attenuated the changes of both expression and activity of Pgp induced by BSO. Therefore, the transport of Pgp substrates may be affected by changing Pgp expression under conditions of chronic oxidative stress induced by GSH depletion.

ATP Binding Cassette Transporter, Subfamily B↗
PubMed2006

CJZ3, a lomerizine derivative, modulates P-glycoprotein function in rat brain microvessel endothelial cells.

AIM: To investigate the modulatory effect of CJZ3, a lomerizine derivative, on P-glycoprotein (P-gp) function in rat brain microvessel endothelial cells (RBMEC). METHODS: RBMEC were isolated and cultured in Dulbecco modified Eagle medium/F12 (1:1) medium, and the amount of intracellular rhodamine 123 (Rh123) was determined using a fluorescence spectrophotometer to evaluate the modulatory effect of CJZ3 on P-gp function. RESULTS: The accumulation of Rh123 was potentiated in a concentration-dependent manner after incubation with CJZ3 for RBMEC, but not for human umbilical vein endothelial cells (HUVEC). CJZ3 caused the accumulation of intracellular Rh123 in a time-dependent manner and significantly decreased the efflux of Rh123 from the cells. The inhibitory effect of CJZ3 on P-gp function was reversible and remained for 120 min after CJZ3 (2.5 micromol/L) was removed from the medium. CONCLUSION: CJZ3 has a potent in vitro effect on the inhibition of P-gp function.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2006

[Relationship between microsatellite DNA polymorphism and hind-quarter development in sheep chromosome 18].

Ten highly polymorphic microsatellite loci possibly linked to or correlated with the Callipyge gene were selected, according to the genetic map and linkage map of sheep chromosome 18. They were ILSTS54, TGLA337, HH47, TGLA122, BP33, OB2, BM3413, MCM38, MCMA26 and CSSM18. Polymorphisms of these microsatellites were detected in 61 Dorset (male) x Xinjiang fine wool sheep (female) samples and 76 Suffolk (male) x Xinjiang fine wool sheep (female) samples. Results showed that the number of alleles for the 10 microsatellite loci, heterozygosity and PIC (polymorphism information content) in the Dorset population were 8-16, 0.8370-0.9252, and 0.8221-0.9167, respectively. The same parameters in the Suffolk population were 5-10, 0.7603-0.8913 and 0.7176-0.8809, respectively. The effect of these loci on hindquarter width was analyzed in a generalized linear model. Results showed that, in the Dorset group, BM3413, MCMA26 and CSSM18 each had a significant effect on hindquarter width (P<0.05), while the other seven loci had no effect on it (P>0.05). In the Suffolk group, TGLA122, BM3413, MCM38 and CSSM18 had a significant effect on hindquarter width (P<0.05), while the other six loci did not (P>0.05). Our results also indicated that the cause of hindquarters hypertrophy in Xinjiang meat sheep may be different from the A-to-G mutation between the region of DLK1 and GTL2 . There may be other genes or QTL (quantitative trait loci) that affect hindquarter muscle development on chromosome 18 in Xinjiang meat sheep.

Animals↗
PubMed2006

[Polymorphism analysis of genes associated with hindquarters muscular development on chromosome 18 in Xinjiang meat sheep].

Through polymorphism analysis of genes associated with hindquarters development on chromosome 18 in Xinjiang meat sheep, we sought genes that are associated with increased hindquarters musculature in the hope to provide theoretical guidance to molecular marker-assisted selection of meat sheep. The polymorphism of Callipyge (CLPG) gene was analyzed by PCR-SSCP and PCR-RFLP in populations of Dorset and Suffolk breeds and their F1 and F2 crosses with local Xinjiang Fine Wool sheep. Results showed that there was no PCR-RFLP polymorphism at 103849 bp in the region between DLK1 and GTL2 on chromosome 18, which suggested that hindquarters over-development was not controlled by the callipyge gene (CLPG) in Xinjiang meat sheep group. In addition, single nucleotide polymorphisms (SNPs) were detected at the Meg3.9 locus on chromosome 18 by PCR-SSCP. Based on the polymorphism, three genotypes AA, AB and AC could be discerned in this locus, with AA being the major one. The relationship between the genotypes and hindquarters hypertrophy was also investigated in the same group. Results indicated that the AC genotype had a significant impact on the hindquarters hypertrophy while the other two were not related to the muscling trait. In F1 crosses between Dorset and local fine wool sheep breeds, there was a significant difference in carcass weight and slaughter rate between the AC genotype and the other two genotypes (P<0.05), but there was not significant difference in the monthly live weight among the three genotypes (P<0.05). Based on the above, we found the muscling trait did not result from the mutation in at the 9571-268.3 site of the CLPG locus. Thus it may be under the influence of other genes or multiple linked QTL.

Animals↗
PubMed2005

Reversal of p-glycoprotein-mediated multidrug resistance by CJX1, an amlodipine derivative, in doxorubicin-resistant human myelogenous leukemia (K562/DOX) cells.

P-glycoprotein-mediated drug efflux can yield a multidrug resistance (MDR) phenotype that is associated with a poor response to cancer chemotherapy. Development of safe and effective MDR reversing agents is an important approach in the clinic. The aim of this study was to observe the effects of CJX1, an amlodipine derivative, on the inhibition of P-gp function and P-gp-mediated MDR in K562/DOX cells and parental K562 cells. Based on the flow cytometric technology, the uptake, accumulation and efflux of rhodamine123 (Rh123) were detected in these cells by measuring Rh123-associated mean fluorescence intensity (MFI). The effects of CJX1 on the doxorubicin cytotoxicity were evaluated by assaying for MTT (3-(4,5-dimethylthiazol)-2,5-diphenyltetrazolium bromide) reduction and the reversal fold (RF) values. The DNA content, percentage of apoptosis and cell cycle analysis were monitored with flow cytometry. Intracellular accumulation of doxorubicin was also assessed by the determination of doxorubicin-associated MFI. Verapamil was employed as a comparative agent. Incubation of K562/DOX cells with CJX1 caused a marked increase in uptake and a notable decrease in efflux of Rh123, No such results were found in parental K562 cells. The inhibitory effect of the agent of P-gp function was reversible, but it persisted at least for 90 min after removal of 2.5 microM CJX1 from incubation medium. The doxorubicin-induced cytotoxicity, apoptosis and cell cycle perturbations were significantly potentiated by CJX1. The intracellular accumulation of doxorubicin was enhanced in the presence of various concentrations of CJX1. The CJX1 exhibited potent effects in vitro in the reversal of P-gp-mediated MDR, suggesting that the compound may become a candidate of effective MDR reversing agent in cancer chemotherapy.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2005

Modulation of P-glycoprotein function by amlodipine derivatives in brain microvessel endothelial cells of rats.

AIM: To investigate whether the amlodipine derivatives, CJX1 and CJX2, have a modulative effect on P-glycoprotein (P-gp) function in rat brain microvessel endothelial cells (RBMEC). METHODS: Isolated RBMEC were cultured in DMEM/F12 (1:1) medium. The amount of intracellular rhodamine (Rh123) was determined, using a fluorescence spectrophotometer, to evaluate the function of P-gp. RESULTS: The accumulation of Rh123 in RBMEC was potentiated in a concentration-dependent manner after incubation with CJX1 and CJX2 at 1, 2.5, 5, and 10 micromol/L (P<0.01), but no accumulation of Rh123 was observed in human umbilical vein endothelial cells after incubation with CJX1 and CJX2 10 micromol/L (P>0.05). Accumulation of intracellular Rh123 was increased and efflux of intracellular Rh123 was decreased in a time-dependent manner from 0-100 min after CJX1 and CXJ2 at 10 micromol/L treatment. The inhibitory effect of CJX1 and CJX2 on P-gp function was reversible and remained even at 120 min after removal of CJX1 and CJX2 at 2.5 micromol/L from the medium. CONCLUSION: CJX1 and CJX2 exhibited a potent effect in the inhibition of P-gp function in vitro.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2005

Reversal of P-glycoprotein mediated multidrug resistance in K562 cell line by a novel synthetic calmodulin inhibitor, E6.

The overexpression of P-glycoprotein (P-gp) is associated with multidrug resistance (MDR) of tumor cells to a number of chemotherapeutic drugs. P-gp inhibitors have been shown to effectively reverse P-gp-mediated MDR in both in vitro and in vivo. Our previous studies demonstrated that E6, a novel synthetic calmodulin inhibitor, exhibited potent inhibitory effect on P-gp in rat brain microvessel endothelial cells (RBMECs). In the present study, the effect of E6 on MDR in a K562 MDR cell line (K562/DOX) highly expressing P-gp was studied and compared with that of a conventional P-gp inhibitor, verapamil (VER). E6 at concentrations of 1, 3, 10, 30 microM reduced the IC50 value of doxorubicin in K562/DOX cells from 79.19 microM to 35.18, 21.86, 6.31 and 1.97 microM, respectively. However, the IC50 value of doxorubicin in K562 sensitive subline was not significantly changed by E6. Using a DNA content analysis and an annexin V binding assay, the effects of E6 on doxorubicin-induced apoptosis were also examined. The results indicated that E6 effectively reversed the resistance to doxorubicin-induced apoptosis in K562/DOX cells. In addition, co-treatment of E6 and doxorubicin resulted in a remarkably G2/M blocking effect in K562/DOX cells. Furthermore, the treatment of K562/DOX cells with 10 microM E6 led to increased intracellular accumulation and decreased efflux of doxorubicin. Overall, the pharmacological effects of E6 on P-gp-mediated MDR is much stronger than that of positive control drug VER. These results suggested that E6 is a novel and potent MDR reversal agent and may be a potential adjunctive agent for tumor chemotherapy.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2004

Glutamate up-regulates P-glycoprotein expression in rat brain microvessel endothelial cells by an NMDA receptor-mediated mechanism.

The accumulation of glutamate in the extracellular space in the central nervous system (CNS) plays a major part in ischemic and anoxic damage. In this study, we examined the effect of glutamate on the expression and activity of P-glycoprotein (P-gp) in rat brain microvessel endothelial cells (RBMECs) making up the blood-brain barrier (BBB). The level of P-gp expression significantly increased in RBMECs after the treatment of 100 microM glutamate. At this concentration, glutamate also enhanced rat mdr1a and mdr1b mRNA levels determined by RT-PCR analysis. Flow cytometry was used to study P-gp activity by analysis of intracellular rhodamine123 (Rh123) accumulation. Overexpression of P-gp resulted in a decreased intracellular accumulation of Rh123 in RBMECs. Glutamate-induced increase of intracellular reactive oxygen species (ROS) was observed by using the 2',7'-dichlorofluorescein (2',7'-DCF) assay. MK-801, a non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist, and ROS scavenger N-acetylcysteine obviously blocked ROS generation and attenuated the changes of both expression and activity of P-gp induced by glutamate in RBMECs. These data suggested that glutamate up-regulated P-gp expression in RBMECs by an NMDA receptor-mediated mechanism and that glutamate-induced generation of ROS was linked to the regulation of P-gp expression. Therefore, transport of P-gp substrates in BBB appears to be affected during ischemic and anoxic injury.

ATP Binding Cassette Transporter, Subfamily B↗
PubMed2004

Protection against hydrogen peroxide-induced cytotoxicity in PC12 cells by scutellarin.

The present study investigated the protective actions of the antioxidant scutellarin against the cytotoxicity produced by exposure to H2O2 in PC12 cells. This was done by assaying for MTT (3,(4,5-dimethylthiazole-2-yl)2,5-diphenyl-tetrazolium bromide) reduction and lactate dehydrogenase (LDH) release. Reactive oxygen species (ROS) and Ca2+ in cells were evaluated by fluorescent microplate reader using DCFH and Fura 2-AM, respectively, as probes. Lipid peroxidation was quantified using thiobarbituric acid-reactive substances (TBARS). Mitochondrial membrane potential (MMP) was assessed by the retention of rhodamine123 (Rh123), a specific fluorescent cationic dye that is readily sequestered by active mitochondria, depending on their transmembrane potential. The DNA content and percentage of apoptosis were monitored with flow cytometry. Vitamin E, a potent antioxidant, was employed as a comparative agent. Preincubation of PC12 cells with scutellarin prevented cytotoxicity induced by H2O2. Intracellular accumulation of ROS, Ca2+ and products of lipid peroxidation, resulting from H2O2 were significantly reduced by scutellarin. Incubation of cells with H2O2 caused a marked decrease in MMP, which was significantly inhibited by scutellarin. PC12 cells treated with H2O2 underwent apoptotic death as determined by flow cytometric assay. The percentage of this H2O2-induced apoptosis in the cells was decreased in the presence of different concentrations of scutellarin. Scutellarin exhibited significantly higher potency compared to the antioxidant vitamin E. The present findings showed that scutellarin attenuated H2O2-induced cytotoxicity, intracellular accumulation of ROS and Ca2+, lipid peroxidation, and loss of MMP and DNA, which may represent the cellular mechanisms for its neuroprotective action.

Animals↗
PubMed2004

Scutellarin attenuates oxidative glutamate toxicity in PC12 cells.

The present study investigated the protective effects of the antioxidant scutellarin against oxidative toxicity induced by glutamate in PC12 cells. Vitamin E, a classical antioxidant was employed as a comparative agent. Incubation of PC12 cells with 10 mM glutamate resulted in significant cytotoxity as evaluated by the MTT and lactate dehydrogenase (LDH) assays, decreases of GSSG reductase activity, disturbance of the cell redox state as indicated by the GSH/GSSG ratio, and accumulation of intracellular reactive oxygen species (ROS) and lipid peroxidation products. Scutellarin at 0.1, 1 and 10 microM significantly protected against the cytoxicity and production of ROS and lipid peroxidation induced by glutamate. Scutellarin did not prevent the reduction of cellular GSH levels, but it up-regulated GSSG reductase activity, thus preventing an increase in cellular GSSG levels, and concomitantly improved the cell redox status. Our data also show that the protective effects of scutellarin against glutamate-induced oxidative toxicity are more potent than that of vitamin E. These results demonstrate that scutellarin can protect PC12 cells from oxidative glutamate toxicity by scavenging ROS, inhibiting lipid peroxidation and improving the cell redox status, and may reduce the cellular damage in pathological conditions associated with excessive glutamate release.

Animals↗
PubMed2004

Patensin-induced apoptosis is accompanied by decreased bcl-2 expression and telomerase activity in HL-60 cells.

The present study aimed to investigate the effect of telomerase activity in patensin-induced apoptosis and the regulation of B cell leukemia/lymphoma 2 (bcl-2) gene expression in human leukemia HL-60 cells. Apoptosis of HL-60 cells was induced by patensin (100 micromol L(-1)) for 3, 6, 12 and 24 h. Apoptosis and bcl-2 were determined by flow cytometry analysis. A polymerase-chain-reaction-based telomeric repeat amplification protocol assay was used to detect the telomerase activity. Patensin induced growth arrest and apoptotic cell death in HL-60 cells. The telomerase activity was inhibited in a time-dependent manner during the patensin-induced apoptosis of HL-60 cells, and the expression of bcl-2 was progressively down-regulated by patensin. Inhibition of the telomerase activity of HL-60 cells was closely related to the patensin-induced apoptosis. The present results indicate that inhibition in telomerase and reduced bcl-2 gene expression may play a role in the patensin-induced apoptosis of HL-60 cells.

Apoptosis↗
PubMed2004

[Application of RNAi technology to knockdown gene expression in vivo in mammalians].

Post-transcriptional gene silencing (PTGS) initiated by dsRNA, which result in specific degradation of homologous mRNA, is called RNAi. The discovery of RNAi greatly intrigued researchers, and was followed by a flood of papers that described the phenomenon and mechanism of RNAi. More excitingly, RNAi has recently been developed into a new tool, showing promising role in reverse genetics, gene therapy and anti-viral infection. This review provides the progress of the application of RNAi technology in mammalian animals.

Animals↗
PubMed2003

Current status and perspectives on the development of neuroprotectants for ischemic cerebrovascular disease.

The concept of neuroprotection is based on the understanding that delayed neuronal damage occurs after ischemia. Each step along the ischemic cascade provides an opportunity for therapeutic intervention. Based on the excellent results obtained in experimental models of ischemia, many clinical trials have been conducted with different neuroprotective drugs. The results obtained in most studies were negative and in some cases the studies were terminated due to safety problems. However, the mechanisms that underlie the development of ischemic damage are still being discovered, creating new therapeutic possibilities for neuroprotection that might be clinically applicable in the future. This article reviews the mechanisms of ischemic neuronal injury, the mechanism of action of neuroprotective agents, current neuroprotective clinical trials, and probable reasons for the failure of clinical neuroprotection. (c) 2003 Prous Science. All rights reserved.

Adult↗
PubMed2003

EDT, a tetrahydroacridine derivative inhibits cerebral ischemia and protects rat cortical neurons against glutamate-induced cytotoxicity.

AIM: To study the effects of 9-(4-ethoxycarbonylyphenoxy)-6,7-dimethoxy-1,2,3,4-tetrahydroacridine (EDT) on cerebral ischemia and glutamic acid (Glu) and sodium nitroprusside (SNP)-induced neurocytotoxicity in primary cortical culture. METHODS: Focal cerebral ischemia was produced by permanent occlusion of left middle cerebral artery (MCA) in mice. The infarct tissue was measured by 2,3,5-triphenyltetrazolium chloride (TTC) staining technique. The extent of neurological deficits was evaluated. In primary cortical culture, colorimetric MTT assay was used to determine cell survival rate, and leakage of LDH and NO release assay were measured. RESULTS: In focal cerebral ischemia, pretreatment with EDT 2.5, 5, and 10 mg/kg and nimodipine 2 mg/kg for 5 d effectively improved the abnormal neurological symptoms and reduced the infarct rate. In primary cortical culture, EDT 0.01-3 micromol/L concentration-dependently attenuated NO release induced by Glu 500 micromol/L and increased the cell survival. It also remarkably reduced the LDH excessive efflux. CONCLUSION: EDT possessed protective effects against cerebral ischemia, which may be related to blocking Glu receptor and inhibiting NO formation.

Acridines↗
PubMed2003

Effect of E6, a novel calmodulin inhibitor, on activity of P-glycoprotein in purified primary cultured rat brain microvessel endothelial cells.

AIM: To study the effect of E6, a novel calmodulin inhibitor, on the activity of P-glycorprotein (P-gp) in purified primary cultured rat brain microvessel endothelial cells (RBMEC). METHODS: Flow cytometry was used to purify RBMEC from other cell types. Fluorescence of P-gp substrate rhodamine123 (Rh123) in RBMEC was measured to evaluate the effect of E6 on the function of P-gp. RESULTS: Purified RBMEC was obtained after being sorted from other cell types by flow cytometry. Intracellular fluorescence of Rh123 in RBMEC increased after incubation with E6 3, 10 micromol/L or verapamil (VER) 50 micromol/L (P<0.01), respectively. After the treatment of E6 10 micromol/L, intracellular Rh123 accumulation was increased nearly to 3-fold. E6 and VER have no effect on accumulation of Rh123 in human umbilical vein endothelial cells (HUVEC), which do not express P-gp. CONCLUSION: E6 exhibited a strong inhibitory effect on the activity of P-gp in RBMEC.

ATP Binding Cassette Transporter, Subfamily B, Mem↗