Biomedical subjects

Jing Gao

Publications and source records attributed to Jing Gao.

At least 37 records · Page 2Linked to original sources

PubMed2006

Mechanism underlying mitochondrial protection of asiatic acid against hepatotoxicity in mice.

Asiatic acid (AA) is one of the triterpenoid components of Terminalia catappa L., which has antioxidative, anti-inflammatory and hepatoprotective activity. This research focused on the mitochondrial protection of AA against acute liver injury induced by lipopolysaccharide (LPS) and D-galactosamine (D-GalN) in mice. It was found that pretreatment with 25, 50 or 100 mg kg(-1) AA significantly blocked the LPS + D-GalN-induced increase in both serum aspartate aminotransferase (sAST) and serum alanine aminotransferase (sALT) levels, which was confirmed by ultrastructural observation under an electron microscope, showing improved nuclear condensation, ameliorated mitochondrion proliferation and less lipid deposition. Meanwhile, different doses of AA could decrease both the transcription and the translation level of voltage-dependent anion channels (VDACs), the most important mitochondrial PTP component protein, and block the translocation of cytochrome c from mitochondria to cytosol. On the other hand, pre-incubation with 25, 50 and 100 microg mL(-1) AA inhibited the Ca(2+)-induced mitochondrial permeability transition (MPT), including mitochondrial swelling, membrane potential dissipation and releasing of matrix Ca(2+) in liver mitochondria separated from normal mice, indicating the direct role of AA on mitochondria. Collectively, the above data suggest that AA could protect liver from damage and the mechanism might be related to up-regulating mitochondrial VDACs and inhibiting the process of MPT.

Alanine Transaminase↗

PubMed2006

[Genetic analysis of the UGT1A1 gene mutation sites in a Chinese family suffered from Gilbert's syndrome].

To learn the variation in the gene for UGT1A1 enzyme, the genetic mechanism in a Chinese Han nationality family suffered from Gilbert's syndrome was studied. At first, genomic DNA from peripheral blood of the sufferer in this family was used for amplifying all of the five exons of the UGT1A1 gene by PCR, and then direct sequencing of the PCR product was applied to analyze gene mutation. The results showed that there existed a G-->A homozygous transition at nucleotide 211 leading the substitution of arginine for glycine at position 71 of corresponding protein product (G71R) and a T-->G homozygous transition at nucleotide 1456 leading the substitution of aspartic acid for tyrosine at position 486 of corresponding protein product (Y486D). No mutation was detected in promoter region and the splicing junction sites. The relevant mutation sites of the other family members were sequenced and identified to be heterozygous in the two above-mentioned mutation sites and in the TA repeat mutation in the promoter region. Furthermore, fresh blood samples were collected from all of the members to detect the serum bilirubin levels to determine the sufferer. The result was consistent with the mutation analysis. It could thus be inferred that this family was caused by mutation in the open reading frame of the gene UGT1A1.

Asian People↗

PubMed2006

[Interventional treatment for occlusive lesions in supra-arch vessels with brain ischemic symptoms].

OBJECTIVE: To evaluate the therapeutic effect of percutaneous transluminal angioplasty and stenting for occlusive lesions in supra-arch vessels with brain ischemic symptoms. METHODS: A total of 56 occlusive lesions of the innominate, subclavian, and internal carotid arteries were treated with angioplasty and intravascular stent placement in 52 patients. The degree of stenosis was more than 60% in all patients and the leading symptom was brain ischemia. In 11 patients, the occluded subclavian artery could not be crossed via the femoral route, therefore the brachial route was used and the occlusion was crossed in a retrograde fashion. RESULTS: Technical success was achieved in 54 of 56 procedures (96.4%). Residual stenosis was less than 30% in all cases. The clinical symptoms improved after procedure in all patients. Complications occurred in 3 of 52 (5.8%) procedures, and the 30-day mortality rate was 0. There were no death and severe stroke in the follow-up period (means 24 months). Restenosis was observed in 2 patients after percutaneous transluminal angioplasty treatment. CONCLUSION: Percutaneous transluminal angioplasty with or without stenting is a safe and valid choice for treatment of occlusive lesions of supra-arch vessels in patients with cerebral ischemic symptoms.

Adolescent↗

PubMed2006

[Fluorescence resonance energy transfer quenching method for determination of arsenic with acridine orange-rhodamine B].

A new method for the determination of trace arsenic was developed by using fluorescence resonance energy transfer from acridine orange (AO) to rhodamine B (RB). It was found that under the condition of lambda(ex)/lambda(em) = 470/580 nm, effective energy transfer could occur between AO and RB in the dodecyl benzene sodium sulfonate solution. The fluorescence intensity of RB was diminished by molybdoarsenide which was formed by the reaction of arsenic (V) with molybdate in sulfuric acid medium. The detection limit of this method was 2. 56 microg x L(-1). This method was used for the determination of trace arsenic in tea. The range of determination for arsenic was 0.01-0.25 mg x L(-1). The relative standard deviation for the determination of arsenic was 0.48%-0.64%. The recoveries for the addition of 0.01-0.03 mg x L(-1) arsenic were 98%-103%. The method has been applied to the determination of arsenic with satisfactory results.

Acridine Orange↗

PubMed2005

Inhibition by [corrected] ursolic acid of [corrected] calcium-induced mitochondrial permeability transition and release of two proapoptotic proteins.

The possible inhibition by [corrected] ursolic acid (UA) of [corrected] mitochondrial permeability transition (MPT) in mouse liver was investigated to identify the mechanisms underlying the hepatoprotective effect of UA. The effect of UA on liver MPT induced by Ca2+ was assessed by measuring changes in mitochondrial volume, mitochondrial membrane potential (MMP), release of matrix Ca2+, and transfer of cytochrome c (Cyt c) and apoptosis-inducing factor (AIF) from the intermembrane space to the cytoplasm. The results showed that obvious mitochondrial swelling, loss of MMP, and release of matrix Ca2+ occurred after the addition of 50 microM Ca2+. However, preincubation with 20, 50 or 100 microg ml(-1) UA significantly blocked the above changes. Addition of 100 microg ml(-1) UA inhibited on mitochondrial swelling by 73.2% after 5 min, while the MMP dissipating and Ca2+ releasing were, respectively, suppressed by 59.3% and 54.1% after 3 min. In addition, Western blot analysis showed Cyt c and AIF transferred from mitochondrial pellet to the supernatant after the addition of 50 microM Ca2+, but the process was significantly inhibited by various concentrations of UA. The results suggest that the mechanisms underlying the hepatoprotection of UA may be related to its direct inhibitory action on MPT.

Animals↗

PubMed2005

Effective protection of Terminalia catappa L. leaves from damage induced by carbon tetrachloride in liver mitochondria.

The protective effects of chloroform extracts of Terminalia catappa L. leaves (TCCE) on carbon tetrachloride (CCl4)-induced liver damage and the possible mechanisms involved in the protection were investigated in mice. We found that increases in the activity of serum aspartate aminotransferase and alanine aminotransferase and the level of liver lipid peroxidation (2.0-fold, 5.7-fold and 2.8-fold) induced by CCl4 were significantly inhibited by oral pretreatment with 20, 50 or 100 mg/kg of TCCE. Morphological observation further confirmed the hepatoprotective effects of TCCE. In addition, the disruption of mitochondrial membrane potential (14.8%), intramitochondrial Ca2+ overload (2.1-fold) and suppression of mitochondrial Ca2+-ATPase activity (42.0%) in the liver of CCl4-insulted mice were effectively prevented by pretreatment with TCCE. It can be concluded that TCCE have protective activities against liver mitochondrial damage induced by CCl4, which suggests a new mechanism of the hepatoprotective effects of TCCE.

Animals↗

PubMed2005

Hepatoprotection of oleanolic acid is related to its inhibition on mitochondrial permeability transition.

The protective effects of oleanolic acid (OA) on carbon tetrachloride (CCl4)-induced liver mitochondrial damage and the possible mechanisms were investigated. Pretreatment with OA prior to the administration of CCl4 significantly suppressed the increases of serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) (4.2- and 19.9-fold, respectively) in a dose-dependent manner in mice. The dissipation of mitochondrial membrane potential (14.8%) and intra-mitochondrial Ca2+ overload (2.1-fold) in livers of CCl4-insulted mice were also dose-dependently prevented by pretreatment with 20, 50 or 100 mg/kg OA. In addition, the effects of OA on liver mitochondria permeability transition (MPT) induced by Ca2+ were assessed by measuring the change in mitochondrial membrane potential, release of matrix Ca2+ and mitochondrial swelling in vitro. The results showed that preincubation with 50 or 100 microg/ml OA obviously inhibited the Ca2+-induced mitochondrial swelling, mitochondrial membrane depolarization and intra-mitochondrial Ca2+ release. It could be concluded that OA has protective effects on liver mitochondria and the mechanisms underlying its protection may be related to its inhibitory action on MPT.

Alanine Transaminase↗

PubMed2005

Antioxidant effects of dehydroepiandrosterone are related to up-regulation of thioredoxin in SH-SY5Y cells.

Neuroprotective effects of dehydroepiandrosterone (DHEA) have been shown to be associated with its antioxidant properties, but the mechanisms remain unknown. Considering that the thioredoxin (Trx) system, an important cellular redox modulation system, changes under oxidative stress and could exert protective effects, the relationship between the antioxidant effects of DHEA and the Trx system regulation was explored. Using MTT assay and morphological observation, the effects of DHEA in the model of H2O2-induced oxidative stress in SH-SY5Y cells were analyzed, then RT-PCR and Western blot assay were used to detect the alteration in mRNA and protein level of Trx. The results showed that a pre-treatment of DHEA (10-100 nM) protected cells against the toxicity induced by H2O2 in a dose-dependent manner, which could be confirmed in morphological observation by phase-contract microscope. In addition, Trx mRNA transcription was inhibited by H2O2 (300 microM), which could be reversed by the pre-administration of DHEA in various concentrations (0.1100 nM). Western blot assay confirmed that protein level of Trx could be elevated by the pre-treatment of DHEA (10100 nM) with the exposure of H2O2. Taken together, these data suggest that DHEA may be useful in treating age-related neurodegenerative diseases based on its up-regulating effects on an antioxidant and neuroprotective protein thioredoxin, a substrate in the Trx redox system.

Antioxidants↗

PubMed2005

[A study on the risk factors of cardiovascular between hypertensive patients and normal subjects in the same family].

OBJECTIVE: Through studying the difference between the hypertensive patients and those with normal blood pressure who all from the same hypertensive pedigree, we tried to find the factors which would decrease the risk of hypertension. METHODS: Hypertensive patients, when coming to the cardiovascular clinic of Xuan Wu Hospital from 2003 to 2004, were defined as the members of the hypertensive pedigrees through inquiry. 84 families including 368 persons, with 192 syblings were involved. Metabolic syndrome could be defined by the criterion of adult treatment panel III. RESULTS: When compared with normal blood pressure persons, clinical examinations of the hypertensive patients had an higher levels of triglyceride, total cholesterol, glucose and body mass index (BMI). The hypertensive group showed higher ratios among male patients, smokers, alcohol drinkers, having irritable personality and high-salt-intake. Through logistic regression, overweight, smoking and irritable temperament showed positive relations with hypertension. The rate of metabolic syndrome was higher in hypertension group. CONCLUSION: It is important that either persons with normal blood pressure or hypertension should control their body weights (BMI) since the rate of metabolic syndrome in hypertension group was high.

Adult↗

PubMed2005

[Green tea consumption and the risk of endometrial cancer: a population-based case-control study in urban Shanghai].

OBJECTIVE: To assess the effect of tea consumption on the risk of endometrial cancer. METHODS: In a population based case-control study conducted in urban Shanghai, face-to-face interviews were completed for 995 incidence cases aged 30 - 69 from January 1997 to December 2002 and 1087 controls that frequency-matched to cases on age. Unconditional logistic model was used for analysis. RESULTS: An inverse association was observed in tea drinking and endometrial cancer risk. Compared to non-tea drinkers, regular tea drinkers had reduced risk of endometrial cancer (OR = 0.74; 95% CI: 0.54 - 1.01) in premenopausal women. Green tea had a protective effect on endometrial cancer among non-smoking or non-alcohol drinking women (OR = 0.77, P = 0.0199) and the ORs reduced with the increasing concentration of tea being served (P for trend = 0.0493). The multivariate ORs for drinking green tea < 7 times/week and >or= 7 times/week were 0.90 (95% CI: 0.53 - 1.54) and 0.76 (95% CI: 0.60 - 0.95) with the trend test of P = 0.0163. CONCLUSION: Tea drinking, with green tea in particurlar, seemed to have weak but inverse association with endometrial cancer risk, but this effect of protection might only limit to premenopausal women.

Adult↗

PubMed2005

[Determination of vitamin B12 concentration by fluorescence quenching with acridine orange-rhodamine 6G energy transfer system].

An energy transfer technique between acridine orange (AO) and rhodamine 6G (R6G) was studied, and the optimum experimental conditions of energy transfer were defined. It was found that the effective energy transfer could occur between AO and R6G in the dodecylbenzene sodium sulfonate solution with Na2 HPO4-citric acid buffer solution at pH 5.0. The fluorescence intensity of AO-R6G system was diminished by vitamin B12 in an alkalescence medium. Based on the AO-R6G energy transfer system anovel fluorescence quenching method for the determination of vitamin B12 has been developed. Under optimal conditious, the linear range of calibration curves for the determination of vitamin B12 was 0-3.0 x 10(-5) mol x L(-1). The detection limits were 4.8 x 10(-7) mol x L(-1) for Vitamin B12. Among six times of determination, the relative standard deviation was 0.51%-0.64%, and the recovery was 98.40% -103.62%. The method features good recurrence, rapidity of reaction, good stability, and few interfering substances. It can be satisfactorily used in the determination of the injection content of vitamin B12.

Acridine Orange↗

PubMed2005

[The effect of sodium phenylbutyrate to agents used in induction chemotherapy on laryngeal carcinoma cells Hep-2 in vitro].

OBJECTIVE: To study the effect of sodium phenylbutyrate when it combined with agents used in induction chemotherapy on laryngeal carcinoma cells Hep-2 in vitro. METHOD: MTT were used to examine the growth inhibition of Hep-2 cells treated by the combination of PB with 5-FU or CDDP in vitro. RESULT: When 5-FU or CDDP combined with PB respectively, there was significantly difference between every two dose groups of the two agents or every dose group and control group ( P < 0.05). When the dosage of 5-FU or CDDP was definition,there was significantly difference between every two dose groups of PB ( P < 0.05). CONCLUSION: PB could enhance the cytotoxic effects of agents used in induction chemotherapy on laryngeal carcinoma cells Hep-2 in vitro, which showed the possibility in reinforcement the treatment effect and reduction the occurrence of the complication and toxic reaction of induction chemotherapy on laryngeal carcinoma.

Antineoplastic Agents↗

PubMed2005

[Changes of masticatory muscles after occlusal recovery in rats with unilateral chew].

PURPOSE: To study the effect of occlusal recovery on masticatory muscles in rats with unilateral chew. METHODS: 40 white rats were divided into two experimental groups and two control groups. The right upper and lower posterior teeth of all the rats were ground to the gingival level without occlusal contact. The rats of the first experimental and control group were killed 10 weeks late,those of the second groups were killed 16 weeks late. The pathological changes of masticatory muscles were studied. SPSS 10.0 software package was used for statistical analysis. RESULTS: There was significant correlation between the first experimental group and control group in the damage of masticatory muscles (Chi(2)=40, P<0.01). However,there was no significant correlation between the second experimental group and control group in the damage of masticatory muscles (Chi(2)=3.66, P>0.05). CONCLUSION: Early occlusal recovery can rehabilitate the damage of masticatory muscles in rats with unilateral chew.

Animals↗

PubMed2005

Needling Neiguan (P 6) for treatment of low pulse pressure syndrome--a report of 31 cases.

OBJECTIVE: To observe the impact of needling Neiguan (P 6) on the cardiovascular functional status in low pulse pressure syndrome. METHOD: 49 eligible patients were randomly assigned to a acupuncture group with bilateral Neiguan (P 6) needled for successive 3 days, and a medication group given a daily 20 mL of Shenmai Injectio intravenously dripped for successive 6 days. The blood pressure, pulse pressure, stroke volume (SV), cardiac output(CO)/min, left ventricle work index (LVWI), mean arterial pressure (MAP), total peripheral resistance (TPR), coronary perfusion pressure (CPP), pulmonary arterial wedge pressure (PAWP), effective blood volume (BV), blood viscosity (N), microcirculation half renewal rate (MHR), and cardiac muscle blood volume (CMBV) were determined before and after the treatment, which were compared with the parameters obtained in 23 healthy subjects. RESULTS: The decreased pulse pressure of all patients before treatment (P<0.01) increased significantly after treatment (P<0.001). The levels of SV, CO, LVWI, PAWP, BV, MHR and CMBV were lowed when compared with the healthy subjects before treatment (P<0.01), but all of them significantly increased after treatment (P<0.01). The increased CPP, TPR and N before treatment (P<0.01) were decreased after treatment (P<0.01). CONCLUSION: The therapeutic effect of acupuncture at point Neiguan (P 6) was better than medication though some of the indexes showed no significant difference (P<0.05).

Acupuncture Points↗

PubMed2004

A thermostable manganese-containing superoxide dismutase from the thermophilic fungus Thermomyces lanuginosus.

A thermostable superoxide dismutase (SOD) from a Thermomyces lanuginosus strain (P134) was purified to homogeneity by fractional ammonium sulfate precipitation, ion-exchange chromatography on DEAE-Sepharose, Phenyl-Sepharose hydrophobic interaction chromatography, and gel filtration on Sephacryl S-100. The molecular mass of a single band of the enzyme was estimated to be 22.4 kDa, using sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Using gel filtration on Sephacryl S-100, the molecular mass was estimated to be 89.1 kDa, indicating that this enzyme was composed of four identical subunits of 22.4 kDa each. The SOD was found to be inhibited by NaN3, but not by KCN or H2O2, suggesting that the SOD in T. lanuginosus was of the manganese superoxide dismutase type. The SOD exhibited maximal activity at pH 7.5. The optimum temperature for the activity was 55 degrees C. It was thermostable at 50 and 60 degrees C and retained 55% activity after 60 min at 70 degrees C. The half-life of the SOD at 80 degrees C was approximately 28 min and even retained 20% activity after 20 min at 90 degrees C.

Ammonium Sulfate↗

PubMed2004

p53 deficiency provokes urothelial proliferation and synergizes with activated Ha-ras in promoting urothelial tumorigenesis.

Mutation and deletion of the p53 tumor suppressor gene are arguably the most prevalent among the multiple genetic alterations found in human bladder cancer, but these p53 defects are primarily associated with the advanced diseases, and their roles in bladder tumor initiation and in synergizing with oncogenes in tumor progression have yet to be defined. Using the mouse uroplakin II gene promoter, we have targeted into urothelium of transgenic mice a dominant-negative mutant of p53 that lacks the DNA-binding domain but retains the tetramerization domain. Urothelium-expressed p53 mutant binds to and stabilizes the endogenous wild-type p53, induces nuclear abnormality, hyperplasia and occasionally dysplasia, without eliciting frank carcinomas. Concurrent expression of the p53 mutant with an activated Ha-ras, the latter of which alone induces urothelial hyperplasia, fails to accelerate tumor formation. In contrast, the expression of the activated Ha-ras in the absence of p53, as accomplished by crossing the activated Ha-ras transgenic mice with the p53 knockout mice, results in early-onset bladder tumors that are either low-grade superficial papillary or high grade in nature. These results provide the first in vivo experimental evidence that p53 deficiency predisposes the urothelium to hyperproliferation, but is insufficient for bladder tumorigenesis; that the mere reduction of p53 dosage, as produced in transgenic mice expressing the dominant-negative p53 or in heterozygous p53 knockouts, is incapable of synergizing with Ha-ras to induce bladder tumors; and that the complete loss of p53 is a prerequisite for collaborating with activated Ha-ras to promote bladder tumorigenesis.

Animals↗

PubMed2004

Influence of expressed TRAIL on biophysical properties of the human leukemic cell line Jurkat.

The cDNA fragment of human TRAIL (TNF-related apoptosis inducing ligand) was cloned into RevTet-On, a Tet-regulated and high-level gene expression system. The gene expression system was constructed in a human leukemic cell line: Jurkat. By using RevTet-On TRAIL gene expression system in Jurkat as a cell model, we studied the influence of TRAIL gene on the changes of cellular apoptosis before and after the TRAIL gene expression, which was induced by adding tetracycline derivative doxycycline (Dox). The results indicated that the cellular apoptosis ratio was largely dependent on the trail gene expression level. Moreover, it was found that the apoptosis-inducing TRAIL could cause significant changes in the biophysical properties of Jurkat cells. The cell surface charge density decreased, the membrane fluidity declined, the elastic coefficients K1 increased, and the proportion of a-helix in membrane protein secondary structure decreased. Thus, the apoptosis-inducing TRAIL gene caused significant changes on the biomechanic properties of Jurkat cells.

Anti-Bacterial Agents↗

PubMed2004

Inhibitory effect of TCCE on CCl4-induced overexpression of IL-6 in acute liver injury.

Terminalia catappa L. leaves have been shown to protect against acute liver injury produced by some hepatotoxicants, but the active components and mechanisms are not clear. This study was designed to characterize the protective effects of the chloroform fraction of the ethanol extract of T. catappa leaves (TCCE) against carbon tetrachloride (CCl4)-induced hepatotoxicity in mice, and analyze the changes in expression level of interleukin-6 (IL-6) in the process. It was found that TCCE pretreatment (10 or 30 mg/kg, ig) protected mice from CCl4 toxicity, as evidenced by the reversed alterations in serum alanine aminotransferase (sALT) and serum aspartate aminotransferase (sAST) activities. Additionally liver tissues were subjected to RT-PCR, Western blot and immunohistochemistry to analyze changes in IL-6 expression. It was found that TCCE markedly suppressed the CCl4-induced over-transcription of IL-6 gene. Consistent with the result, the expression of IL-6 protein was also blocked by TCCE in CCl4-stimulated mice, especially in the area around central vein on liver tissue section. In conclusion, TCCE is effective in protecting mice from the hepatotoxicity produced by CCl4, and the mechanisms underlying its protective effects may be related to the inhibition on the overexpression of IL-6 mainly around terminal hepatic vein.

Animals↗