Biomedical subjects

X N Zhu

Publications and source records attributed to X N Zhu.

10 recordsLinked to original sources

PubMed2001

Activation of p42/44 mitogen-activated protein kinase pathway in long-term potentiation induced by nicotine in hippocampal CA1 region in rats.

AIM: To investigate the relationship between activation of p42/44 mitogen-activated protein kinase (MAPK) pathway and hippocampal long term potentiation (LTP) induced by nicotine in area CA 1. METHODS: Extracellular recording of population spike (PS) was performed within the pyramidal cell layer of hippocampal area CA1 in vitro; Western blot analysis was employed to detect the active phosphorylated state and the total protein expression of p42/44 MAPK. RESULTS: PD98059 concentration-dependently (25 micromol/L, 50 micromol/L) attenuated the induction of LTP induced by nicotine 10 micromol/L; both p42 and p44 MAPK were activated with their total protein expression increasing in CA1 subregion in response to LTP induced by nicotine. CONCLUSION: Activation of p42/44 MAPK pathway is required for hippocampal LTP induced by nicotine.

Animals↗

PubMed2000

Long-term potentiation induced by nicotine in CA1 region of hippocampal slice is Ca(2+)-dependent.

AIM: To observe the effects of Ca2+ on hippocampal long-term potentiation (LTP) induced by nicotine in CA1 region of rat hippocampal slice. METHODS: Extracellularly recorded population spikes (PS) of the pyramidal cell layer in the hippocampal CA1 region in vitro. RESULTS: Nicotine 1 mumol.L-1 induced LTP in the hippocampal CA1 region. It did not induce LTP in CA1 region when CA2+ was removed from artificial cerebrospinal fluid (ACSF). Nifedipine 1 and 10 mumol.L-1 partly inhibited LTP induced by nicotine, and thapsigargin 1 and 10 mumol.L-1 completely inhibited LTP induced by nicotine. CONCLUSION: LTP induced by nicotine in hippocampal CA1 region is Ca(2+)-dependent. Both Ca2+ influx and Ca2+ release participate in the induction of LTP.

Animals↗

PubMed2000

[Nitric oxide changes aortic function in rats with renal hypertension].

This work was undertaken to investigate the effect of nitric oxide (NO) on aortic function of two-kidney and one-clip (2K1C) rats with renal hypertension. Animals were divided into 5 groups: the sham operation, 2K1C, captopril, L-arginine and L-NAME groups. The results are as follows. At the 4th week after constriction of the left renal artery, the mean arterial pressure was significantly elevated. In isolated aortic rings, acetylcholine-induced dilation was attenuated, and phenylephrine induced contractile response was markedly enhanced. The level of aorta cGMP content was significantly lowered. These changes were abolished in 2K1C rats treated with captopril. L-arginine partially reversed the aortic vascular reactivity of 2K1C rats, and elevated aortic cGMP content. In 2K1C rats treated with nitric oxide synthase inhibitor, L-NAME, blood pressure was increased further, acetylcholine-induced aorta diastolic response was attenuated further and cGMP content reduced, while phenylephrine-induced contractile response was unaffected. These results suggest that deficiency of nitric oxide production and increase in renin-angiotensin system activity may contribute to vascular endothelial dysfunction of 2K1C rats, and these factors may be involved in development and maintenance of 2K1C renal hypertension.

Animals↗

PubMed1999

[Effect of angiotensin II on c-fos expression and protein synthesis in cultured rat myocardial cells].

The present study was to investigate the effects of angiotensin II on c-fos mRNA expression and protein synthesis in cultured neonatal rat myocardial cells. The results showed that angiotensin II induced c-fos mRNA expression, increased protein content in a dose-dependent manner and stimulated 3H-leucine incorporation rate. All these effects were blocked by angiotensin II receptor antagonist saralasin. The angiotensin II-induced expression of c-fos gene was also blocked by Ca2+ channel antagonist nicardipine.

Angiotensin II↗

PubMed1999

[Effect of ET-1 on intracellular free calcium in cultured neonatal myocardial cells].

In this present study, the effects of ET-1 on intracellular free calcium concentration ([Ca2+]i) and the underlying mechanisms were investigated in cultured neonatal rat myocardial cells loaded with fura-2/AM. The results are as follows. ET-1 induced an increase of [Ca2+]i in a dose-dependent manner, which consisted of a transient and sustained phase. BQ123, a selective ETA receptor antagonist, blocked the ET-1 induced [Ca2+]i responses, suggesting that these responses were mediated by ETA receptors. After removal of extracellular Ca2+, ET-1 induced the transient increase of [Ca2+]i without the sustained change. Protein kinase C (PKC) agonist PMA attenuated the ET-1 induced transient [Ca2+]i increase. Amiloride and nifedipine did not block the [Ca2+]i change induced by ET-1. After pretreatment of myocardial cells with pertussis toxin, ET-1 also induced the transient increase of [Ca2+]i but did not affect the sustained increase. These results suggest that the transient [Ca2+]i increase may involve pertussis toxin-insensitive G protein and the sustained one may be caused by extracellular calcium influx, in which pertussis toxin sensitive G protein is involved. Furthermore, PKC, but not Na+/H+ exchange, plays an important role in these effects.

Animals↗

PubMed1999

[ET-1 induces the expression of prooncogene c-fos in cultured neonatal rat myocardial cells].

In the present study, the effect of endothelin-1 (ET-1) on the expression of proto-oncogene c-fos in cultured neonatal rat myocardial cells was investigated. The results are as follows: ET-1 induced c-fos expression in a dose-dependent manner. Selective ET(A) receptor antagonist blocked ET-1-induced responses. Protein kinase C(PKC) agonist PMA induced c-fos expression.PKC inhibitor staurosporine blocked ET-1 induced c-fos expression. Calcium channel blocker, nifedipine did not significantly affect the expression of c-fos induced by ET-1. These results suggest that in cultured neonatal cardiomyocytes, ET-1 induced c-fos gene expression is mediated by ET(A) receptor with the participation of protein kinase C, while the voltage-dependent L-type Ca(2+) channel is not involved.

Animals↗

PubMed1998

[The role of G protein, protein kinase C and Na(+)-H+ exchanger in endothelin-1-induced cardiomyocyte hypertrophic responses].

Endothelin-1 (ET-1) has been shown to be a potent growth factor and to induce cardiac hypertrophy. In the present study, we examined the role of G protein, protein kinase C (PKC) and Na(+)-H+ exchanger in ET-1-induced cardiac hypertrophy in cultured neonatal rat cardiac myocytes. ET-1 (10(-10)-10(-7) mol/L) induced promotion of 3H-leucine incorporation, increase in cell protein content and cell surface area in a dose-dependent manner with EC50 value of 5.2 x 10(-10), 5.2 x 10(-10) and 7.3 x 10(-10) mol/L respectively. All of these ET-1-induced cardiomyocyte hypertrophic responses were completely blocked by pretreatment with staurosporine (2 nmol/L), a protein kinase C inhibitor, and stimulated by 4-phorbol, 12-myristate, 13-acetate (PMA) (10(-8)-10(-6) mol/L), a protein kinase C activator, in a dose-dependent manner. Pretreatment of amiloride (10(-4) mol/L), a Na(+)-H+ exchange inhibitor completely inhibited the ET-1-induced, but not PMA-induced cardiomyocyte hypertrophic responses. The ET-1-induced increase in cardiomyocyte protein synthesis and cell surface area was significantly inhibited by pretreatment with pertussis toxin (150 ng/ml). These results suggest that ET-1-induced cardiomyocyte hypertrophy was linked with pertussis toxin sensitive G protein, and PKC and Na(+)-H+ exchange may be an important intracellular signaling transduction pathway during ET-1-induced cardiac hypertrophy in cultured neonatal rat cardiac myocytes.

Animals↗

PubMed1995

[Reduction of incidence of ischemia-reperfusion induced ventricular fibrillation by captopril].

To investigate the role of catecholamine and prostacyclin in ischemia reperfusion-induced ventricular fibrillation, experiments were performed in rat hearts using methods of radioimmunoassay and fluorohistochemistry. Regional myocardial ischemia was induced by ligation of the left coronary artery followed by reperfusion. In the ischemia reperfusion group, ventricular fibrillation during reperfusion took place in 78% of the hearts. In the group pretreated with captopril, the incidence of ventricular fibrillation decreased significantly (65.5%). In comparison with the ischemia reperfusion group, myocardial catecholamine content and 6-keto-PGF1 alpha of the captopril group were significantly increased (P < 0.01) while thromboxane B2 (TxB2) and TxB2/6-keto-PGF1 alpha were decreased (P < 0.01). In Ang II group, infusion of angiotensin II reversed the protective effect of captopril and restored the incidence of ventricular fibrillation (85%), while myocardial catecholamine content was not different from the ischemia reperfusion group (P > 0.05). Above results suggest that reduction of the incidence of ischemia reperfusion-induced ventricular fibrillation by captopril may be due to its inhibition on angiotensin II production with consequent reduction of the release of myocardial catecholamine, suppression of TxB2 and promotion of PGI2 synthesis.

6-Ketoprostaglandin F1 alpha↗

PubMed1990

Human leukocyte antigens -A, -B, -C, and -DR and nasopharyngeal carcinoma in northern China.

We observed HLA associations in patients with nasopharyngeal carcinoma from northern China. There was an increased risk of nasopharyngeal carcinoma associated with HLA-B35 and a difference in the HLA association between patients with early- and late-onset disease. The frequency of B35 was significantly higher in patients than in control subjects, especially in early-onset patients (less than 30 years old). Late-onset patients had a higher frequency of DR2 as compared with normal subjects.

Adult↗

PubMed1990

Immunoglobulin E and circulating immune complexes in endolymphatic hydrops.

Levels of circulating immune complexes (CICs) in 59 patients with Meniere's disease and total serum immunoglobulin E (IgE) levels in a subgroup of 42 of the 59 were determined quantitatively for possible abnormalities of humoral immunity. Significant differences in average IgE levels between the 42 patients with Meniere's disease and 18 normal control subjects were not determined; however, five (11.9%) of the 42 patients were found to have obviously raised IgE levels. Elevated CIC levels were found in 19 (32.2%) of the 59 patients with Meniere's disease and in one (2.3%) of the 43 control subjects. This difference was statistically significant. The possible mechanisms of immune-mediated endolymphatic hydrops are discussed.

Adult↗