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Biomedical subjects

J T Cheng

Publications and source records attributed to J T Cheng.

At least 73 records · Page 4Linked to original sources
PubMed1999

Decrease of nitric oxide synthase in the cerebrocortex of streptozotocin-induced diabetic rats.

In an attempt to know the role of nitric oxide in the disease of insulin-dependent diabetic mellitus (IDDM), the present study examined the change of nitric oxide synthase (NOS) both the activity and gene expression in cerebrocortex of streptozotocin-induced diabetic rats (STZ-diabetic rats). The activity of NOS determined by conversion of [3H] L-arginine to [3H] L-citrulline was markedly decreased in STZ-diabetic rats. Northern blot showed that STZ-diabetic rats expressed a lower mRNA level of neuronal NOS (nNOS). Western blot showed a similar decrease of nNOS in STZ-diabetic rats. However, the NOS activity was increased in rats receiving repeated supply of glucose named glucose-challenged rats. Although the mRNA level of nNOS was not changed in the glucose-challenged rats, the immunoblot of nNOS was also decreased in glucose-challenged rats. These findings suggested that NOS was lowered in the brain of STZ-diabetic rats in a way unrelated to the increase of glucose.

Animals↗
PubMed1999

Effect of trilinolein on the activity and gene expression of superoxide dismutase in cultured rat brain astrocytes.

Cerebrovascular disease is one of the major causes of morbidity and mortality in recent. Oxygen free radicals produced during cerebral infarction increases the damage to neurons. Superoxide dismutase (SOD) is the endogenous antioxidant enzyme that can effectively scavenge superoxide radicals. Trilinolein is a lipophilic antioxidant purified from the herb of Panax pseudoginseng. In the cultured rat brain astrocytes (RBA), the activity of SOD (both Cu,Zn-SOD and Mn-SOD subtypes) was markedly increased by incubation with trilinolein at low concentration (0.1 microM) for 2 days. This stimulatory effect of trilinolein was not related to the incubating concentration. However, long-term (7 days) incubation with trilinolein at same concentration decreased the activity. Similar changes were also observed in the gene expression of SOD in RBA; short-term (2 days) incubation of RBA by 0.1 microM trilinolein increased the mRNA level that was lowered in RBA received a long-term incubation with 0.1 microM trilinolein. This result shows that trilinolein is an effective antioxidant to increase the activity of SOD in RBA which would be beneficial to neurons subjected to oxygen free radical damage. However, long-term medication of antioxidant shall be concerned.

Animals↗
PubMed1999

Nicotine-induced hyperlocomotion is not modified by the estrous cycle, ovariectomy and estradiol replacement at physiological level.

The present study was designed to investigate whether nicotine's effect on locomotion might be modulated by the ovarian hormone at physiological level. Rats at normal cycling of estrus and diestrus were selected for the comparison of nicotine-induced hyperlocomotion based on the document that the release of striatal dopamine was greatest at the estrous phase. Ovariectomized rats primed with or without estrogen at physiological level were also selected for comparison. Increase in spontaneous locomotion by nicotine was statistically significant at the doses of 0.15 and 0.3 mg/kg (p < 0.001). The stimulating effect of nicotine led the locomotor response to almost the same magnitude in all hormonal groups studied. Nicotine-induced hyperlocomotion appeared to be mediated by central nicotinic receptor because it was blocked by mecamylamine (0.5 and 1.0 mg/kg, i.p.). Also it was blocked by haloperidol (0.04 and 0.08 mg/kg, i.p.) indicating the involvement of dopaminergic neurotransmission. These effects were similar in all groups regardless of the estrous cycle or ovariectomy. The observed data provided behavioral evidence to suggest that the effect of nicotine on locomotion-related dopaminergic neurons might not be modified by the physiological action of estrogen.

Animals↗
PubMed1999

Activation of opioid mu-receptor by loperamide to lower plasma glucose in streptozotocin-induced diabetic rats.

We investigated the effect of loperamide, a selective agonist of opioid mu-receptor, on the plasma glucose in diabetic rats induced by an intravenous injection of streptozotocin (STZ; 60 mg/kg). Intravenous injection of loperamide induced a dose-dependent decrease of plasma glucose in fasting STZ-diabetic rats at 30 min later, but did not modify the plasma glucose level in Wistar rats. Plasma glucose lowering effect of loperamide was abolished by the pretreatment with naloxone or naloxonazine at the dose sufficient to block opioid mu-receptor. In isolated skeletal muscle, loperamide enhanced the glucose uptake into soleus muscles in a concentration-dependent manner. Blockade of this action by naloxonazine indicated the mediation of opioid mu-receptor. These results suggest that an activation of opioid mu-receptor by loperamide can increase the utilization of glucose in peripheral tissue to lower the plasma glucose in STZ-diabetic rats.

Animals↗
PubMed1999

Effect of serum in medium on the expression of inducible nitric oxide synthase and superoxide dismutases in cultured C6 glioma cells.

It has been documented that C6 glioma cells can be changed into normal glial cells when they were cultured in serum free medium. In the present study, the expressions of inducible nitric oxide synthase (iNOS) and superoxide dismutase (SOD) were investigated. The mRNA level of iNOS was markedly increased by lipopolysaccharide (LPS) in cultured rat brain astrocytes (RBA-1) but not in C6 glioma cells. However, increase of mRNA for iNOS by LPS can be obtained in C6 glioma cells when they were cultured in serum free medium. The mRNA level of magnesium-SOD (Mn-SOD) was increased by LPS in both cells while the expression of constituted SOD (Cu,Zn-SOD) was not stimulated by LPS. Western blotting analysis indicating the amount of protein showed a similar change. After serum deprivation, the protein of iNOS or Mn-SOD was increased by LPS in C6 glioma cells in a way similar as that in RBA-1 cells. These results suggest that serum free conditioned C6 glioma cells were adapted to astroglial cell-like properties which may express more iNOS and Mn-SOD mRNA in the presence of LPS.

Animals↗
PubMed1999

An insulin-dependent hypoglycaemia induced by electroacupuncture at the Zhongwan (CV12) acupoint in diabetic rats.

Acupuncture at the Zhongwan acupoint has been widely used in traditional Chinese medicine to relieve symptoms of diabetes mellitus. Our study investigated the effect on plasma glucose of electroacupuncture applied at the Zhongwan acupoint in rat diabetic models. Plasma concentrations of insulin, glucagon and beta-endorphin- were also determined using radioimmunoassay. A decrease in plasma glucose was observed in rats after electroacupuncture (15 Hz, 10 mA) for 30 min at the Zhongwan acupoint. This was observed in normal rats and rat models with Type II (non-insulin-dependent) diabetes mellitus. No significant effect on plasma glucose was observed in rat models with Type I (insulin-dependent) diabetes mellitus: neither the streptozotocin (STZ)-induced diabetic rats nor the genetic (BB/W) rats. Further, the hypoglycaemic action of electroacupuncture stimulation disappeared in rats with insulin-resistance induced by an injection of human long-acting insulin repeated daily to cause the loss of tolbutamide-induced hypoglycaemia. An insulin-related action can thus be hypothesised. This hypothesis is supported by an increase in plasma insulin-like immunoreactivity after electroacupuncture stimulation in normal rats. Participation of glucagon was ruled out because there was no change in plasma glucagon-like immunoreactivity resulting from electroacupuncture stimulation. In addition to an increase in plasma beta-endorphin-like immunoreactivity, the plasma glucose lowering action of electroacupuncture stimulation at Zhongwan acupoint was abolished by naloxone in a sufficient dose to block opioid receptors. Thus we suggest that electroacupuncture stimulation at the Zhongwan acupoint induces secretion of endogenous beta-endorphin which reduces plasma glucose concentration in an insulin-dependent manner.

Acupuncture Points↗
PubMed1999

Investigations of the mechanism of the reduction of plasma glucose by cold-stress in streptozotocin-induced diabetic rats.

Exposure to a cold environment may increase the activity of the sympathetic nervous system inducing an elevation of plasma norepinephrine and may result in hyperglycemia. In the present study, we found that a hypoglycemic effect was produced in streptozotocin-induced diabetic rats after cold-exposure at 4 degrees C for 1 h. In addition to the blockade of this hypoglycemic effect by guanethidine (a ganglion-blocking agent) and prazosin (an alpha1-adrenoceptor antagonist), an increase of plasma norepinephrine was also observed in streptozotocin-induced diabetic rats receiving this cold-stress. Participation of sympathetic hyperactivity can thus be considered. Furthermore, naloxone, in a dose (0.5 mg/kg, i.p.) sufficient to block opioid receptors, reversed this hypoglycemia. Also, an increase of plasma beta-endorphin-like immunoreactivity was observed in streptozotocin-induced diabetic rats receiving this cold-stress. Intravenous injection of beta-endorphin into streptozotocin-induced diabetic rats produced a lowering of plasma glucose. Administration of methoxamine at a dose sufficient to activate the alpha1-adrenoceptors produced hypoglycemia and a similar increase of plasma beta-endorphin-like immunoreactivity in streptozotocin-induced diabetic rats. However, plasma beta-endorphin-like immunoreactivity level was not modified by similar treatment with methoxamine or cold-stress in normoglycemic rats. Therefore, beta-endorphin appears to be responsible for the induction of hypoglycemic effects in streptozotocin-induced diabetic rats after cold exposure which is different to the response in normal rats.

Animals↗
PubMed1999

Paeoniflorin reverses guanethidine-induced hypotension via activation of central adenosine A1 receptors in Wistar rats.

1. Intravenous injection of paeoniflorin, a glycoside purified from the root of Paeonia lactiflora, reversed guanethidine-induced hypotension in Wistar rats. 2. Pretreatment with the adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine inhibited this effect of paeoniflorin in a dose-dependent manner. 3. The action of paeoniflorin was not modified by 8-(p-sulfophenyl)theophylline, the polar antagonist of the adenosine A1 receptor, which is not able to enter the central nervous system. 4. We conclude that paeoniflorin can reverse guanethidine-induced hypotension via activation of adenosine A1 receptors in the brain of Wistar rats.

Adrenergic Agents↗
PubMed1999

An in vivo evaluation of the therapeutic potential of sympatholytic agents on premature ejaculation.

OBJECTIVE: To evaluate the therapeutic potential of sympatholytic agents on premature ejaculation in an animal model, using monitoring of rat seminal vesicle pressure change in response to electrical stimulation of the lesser splanchnic nerve. MATERIALS AND METHODS: Male Wistar rats (aged 12-14 weeks) were injected intra-arterially with sympatholytic agents (phenoxybenzamine, prazosin, WB-4101, chloroethylclomidine, yohimbine and RX 821002) at various concentrations 10 min before electrical stimulation of the lesser splanchnic nerve. The change in phasic tension (triangle upmmHg) of the seminal vesicle induced by electrical nerve stimulation before and after the addition of sympatholytic agents was used for statistical analysis. The maximum inhibition and the concentration required to induce 50% inhibition of the maximal contractile response (IC50) were obtained from the concentration-response curves, and used to determine the potency of test agents. RESULTS: The seminal vesicle contractile response to electrical nerve stimulation was suppressed in a dose-dependent manner by all test drugs except RX 821002. The mean (sd) maximal inhibition was 78.4 (9. 3)% by 0.03 mg/kg of phenoxybenzamine, 77.1 (10.1)% by 0.03 mg/kg of WB-4101, 73.4 (6.0)% by 0.1 mg/kg of yohimbine, 67.9 (9.7)% by 0.1 mg/kg of prazosin, 75.5 (7.5)% by 3 mg/kg of chloroethylclomidine and 25.3 (4.8)% by 0.01 mg/kg of RX 821002. The potencies of WB-4101 (IC50 3 microgram/kg) and yohimbine (IC50 0.8 microgram/kg) were similar to that of phenoxybenzamine (IC50 0.5 microgram/kg) and much higher than that of prazosin (IC50 0.03 mg/kg) or chloroethylclomidine (IC50 0.3 mg/kg). CONCLUSIONS: Phenoxybenzamine, prazosin, WB-4101, chloroethylclomidine and yohimbine all inhibit the contractile response of the rat seminal vesicle to electrical nerve stimulation. As phenoxybenzamine is effective in treating premature ejaculation, the comparable in vivo potencies of WB-4101 and yohimbine strongly suggest that they have clinical therapeutic potential.

Adrenergic alpha-Antagonists↗
PubMed1999

Calcium influx inhibition: possible mechanism of the negative effect of tetrahydropalmatine on left ventricular pressure in isolated rat heart.

The active ingredient dl-tetrahydropalmatine (THP) isolated from the traditional Chinese herb Corydalis racemosa has been found to have antihypertensive effects. However, severe cardiac and neurological toxic effects were reported from using this herb for the treatment of pain. In an isolated perfused rat heart model, THP at the concentration of 100 microM was found to have a negative effect (-45%) on left ventricular pressure and this effect was produced concentration-dependently from concentrations lower than 50 microM. In isolated cardiomyocytes, radioactive calcium influx was also inhibited significantly by THP at the concentration of 100 microM and this effect was also in a concentration-dependent manner (-39%). In a patient with latent heart disease, the use of Corydalis should probably be detrimental, the toxic effect was probably due to calcium influx inhibition.

Animals↗
PubMed1999

Effects of a nitric oxide scavenger, carboxy-PTIO, on isoflurane MAC and cerebellar nitric oxide synthase activity in rats.

Recent studies have indicated that nitric oxide may play a role in inhalation anaesthesia. Inhibition of nitric oxide synthase reduces the minimum alveolar concentration (MAC) for inhalation anaesthetics and decreases cerebellar nitric oxide synthase (NOS) activity in rats. In this study, we have explored further the role of nitric oxide in isoflurane anaesthesia by examining the effects of a nitric oxide scavenger, 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (carboxy-PTIO 0.075-0.6 mg kg-1) on MAC values and cerebellar NOS activity in rats. Bolus injection of carboxy-PTIO at doses greater than 0.15 mg kg-1 reduced the MAC value of isoflurane (mean 1.36 (SEM 0.07)% at 0.15 mg kg-1, 1.39 (0.14)% at 0.3 mg kg-1 and 1.31 (0.06)% at 0.6 mg kg-1 vs control value of 1.61 (0.19)%. Administration of carboxy-PTIO 0.125 and 0.15 mg kg-1 resulted in increased cerebellar NOS activity during isoflurane anaesthesia (P < 0.05). These findings suggest that the level of nitric oxide may set a baseline from which isoflurane then acts.

Anesthetics, Inhalation↗
PubMed1999

Effects of losartan on the sexual behavior of male rats.

Many commonly used antihypertensive drugs such as diuretics and beta-blockers can interfere with sexual function in both sexes, causing loss of libido, impairment of erectile function and ejaculation in men, and delay or prevent orgasm in women. Newly developed antihypertensive drugs should ideally not interfere with the patients' quality of life including sexual function. This study examined the effects of losartan, a nonpeptide, specific antagonist for type I angiotensin II receptors, on the male sexual behavior of rats. Spontaneously hypertensive rats (SHRs) and normotensive Wistar-Kyoto (WKY) rats were treated with losartan 30 mg/ kg/day or saline control for 7, 30 and 90 days. Dark-cycle video recording was used to analyze the male sexual activities of the rats. No significant alteration in male sexual performance was observed after 7 and 30 days of treatment with losartan. In contrast, SHRs treated with propranolol 5 mg/kg/day showed increases in intromission latency, ejaculation latency and postejaculatory period indicating decreased libido and erectile and ejaculatory function. Upon completion of 90 days of losartan administration, the mount latency of the SHR was significantly increased, suggesting a decrease in libido although other parameters were unchanged and there was no effect in WKY rats. It is therefore concluded that losartan may have an advantage in preservation of sexual function when used clinically for the treatment of hypertensive disorders.

Animals↗
PubMed1999

The antihypertensive effect of the berberine derivative 6-protoberberine in spontaneously hypertensive rats.

Berberine is a natural isoquinoline alkaloid found in plants of the Ranunculaceae and Berberidaceae families. Extracts from berberine-containing plants have been used as traditional Chinese folk remedies for centuries. The antihypertensive effects of the berberine derivative 6-protoberberine (PTB-6) were studied in spontaneously hypertensive rats (SHRs). In conscious SHRs, PTB-6 lowered the systolic blood pressure in a dose-dependent manner (6-PTB: 5 mg/kg, -31.1 +/- 1.6 mm Hg; 10 mg/kg, -42.4 +/- 3.1 mm Hg). Cardiac output using the thermodilution method was reduced in PTB-6-treated anesthetized SHRs with a tendency to decrease in heart rate. Injection of PTB-6 into the intracerebral ventricles of SHRs lowered the systolic arterial blood pressure and heart rate. The berberine derivative PTB-6 is an effective antihypertensive agent. The mechanism of the antihypertensive effect of PTB-6 is probably through a central sympatholytic effect.

Animals↗
PubMed1999

Hepatitis C virus-associated glomerular disease in patients with human immunodeficiency virus coinfection.

Chronic infection with hepatitis C virus (HCV) has been linked to the development of glomerular disease. HCV infection is highly prevalent among intravenous drug users, a population that is also at risk for HIV coinfection. This study reports the clinical-pathologic features and outcome of HCV-associated glomerular disease (HCV-GD) in 14 patients with HIV coinfection. All were intravenous drug users and all but one were African-Americans. Renal presentations included renal insufficiency, microscopic hematuria with active urine sediment, hypertension, and nephrotic syndrome or nephrotic-range proteinuria without hypercholesterolemia. Hypocomplementemia and cryoglobulinemia were present in 46 and 33% of patients, respectively. The predominant renal biopsy findings were membranoproliferative glomerulonephritis type 1 or type 3 (Burkholder subtype) in 79% of patients and membranous glomerulopathy with atypical features in 21% (including overlap with collapsing glomerulopathy in one patient). The clinical course was characterized by rapid progression to renal failure requiring dialysis. The overall morbidity and mortality were high with median time of 5.8 mo to dialysis or death. Although most patients died in renal failure, cause of death was primarily attributable to long-term immunosuppression and advanced AIDS. Patients with AIDS had shorter survival than those without (median survival time of 6.1 mo versus 45.9 mo, log-rank test P = 0.02). Only two patients were alive with stable renal function at follow-up of 28.5 mo. In patients with HCV-GD, coinfection with HIV leads to an aggressive form of renal disease that can be easily confused with HIV-associated nephropathy. Although hypocomplementemia, cryoglobulinemia, and more prominent hypertension and microscopic hematuria may provide clues to the presence of HCV-GD, renal biopsy is essential to differentiate HCV-GD from HIV-associated nephropathy.

AIDS-Associated Nephropathy↗
PubMed1999

Superoxide dismutase gene expression and activity in the brain of spontaneously hypertensive rats and normotensive rats.

OBJECTIVE: To determine if changes in superoxide dismutase (SOD) in the brain occur in the hypertensive state. METHODS: We compared the levels of the two main subtypes of this enzyme in spontaneously hypertensive rats (SHR) with age-matched normotensive Wistar Kyoto (WKY) rats using enzyme activity estimation, Western blotting for enzyme contents, and Northern blotting of mRNA level. Five discrete brain regions, cerebrocortex, hypothalamus, hippocampus, the remaining non-cortex cerebrum (NCC area), and cerebellum, were employed for comparison in 30-31 weeks old rats. RESULTS: A lower level of both Mn-SOD activity and Mn-SOD mRNA expression was found in all areas of the brain of SHR as compared with WKY rats. Also, the mRNA levels of Cu, Zn-SOD in the brain of SHR differed from WKY rats in parallel to the enzyme activities. The activity and mRNA expression of Cu, Zn-SOD were lower in the hypothalamus and cerebellum of SHR but the mRNA level and the activity in hippocampus were significantly higher in the SHR compared to WKY rats. No differences for Cu, Zn-SOD were observed in cerebrocortex or NCC area in the two species. However, the amount of SOD enzyme subtypes, determined by Western blotting analysis, was not different between SHR and WKY rats. CONCLUSIONS: The results indicate a lower gene expression and less activity of Mn-SOD in SHR brain. This alternation of SOD may be one of the important factors for the vulnerability of the brain from oxygen free radicals or may be related to the pathogenesis of hypertension in this species.

Animals↗
PubMed1998

Activation of beta3-adrenoceptors by exogenous dopamine to lower glucose uptake into rat adipocytes.

The effect of dopamine hydrochloride on beta3-adrenoceptors was studied in isolated adipocytes of Wistar rats using uptake of [14C]-deoxy-D-glucose (2-DG) as the indicator. Dopamine induced a concentration-dependent decrease of 2-DG uptake into adipocytes in a manner which was not modified by haloperidol at concentrations sufficient to block dopaminergic receptors. Failure of blockade was also observed in samples receiving the pretreatment with a mixture of SCH23390 and domperidone, the dopaminergic antagonists. Absence of dopaminergic receptors in rat white adipocytes was further supported by the findings that dopaminergic agonists did not modify the glucose uptake and the negative response to receptor antibodies in immunoblotting analysis. Pindolol and propranolol reversed this inhibition of dopamine in a concentration-dependent manner. However, this action of dopamine was not affected by prazosin at concentrations sufficient to block alpha-adrenoceptors. Effect of dopamine was reduced in the presence of Rp-cyclic AMPS triethylamine, the membrane-permeable antagonist of cyclic AMP (cAMP), indicating the mediation of cAMP in this inhibition. Direct effect of exogenous dopamine on beta3-adrenoceptors was identified using the antibody for beta3-adrenoceptors that reversed the inhibition of dopamine. These results suggest that dopamine can activate beta3-adrenoceptors to lower glucose uptake into rat white adipocytes which lack dopaminergic receptors.

Adipocytes↗
PubMed1998

Sympathetic hyperactivity in Wistar rats with insulin-resistance.

In an attempt to know the effect of sustained hyperinsulinemia on sympathetic function, plasma norepinephrine (NE) and glucose levels were measured in Wistar rats with insulin resistance. Both the basal plasma glucose and the plasma NE levels in insulin-resistant rats were markedly higher than that obtained in normal or streptozotocin (STZ)-induced diabetic rats. Treatment with guanethidine and prazosin reversed these sympathetic hyperactive responses in insulin-resistant rats. Moreover, increase of plasma insulin in rats receiving an intraperitoneal glucose challenge test confirmed the mediation of endogenous insulin in this sympathetic hyperactivity. These results suggest an increase of sympathetic activity in insulin-resistant state that may be related to the hypertension-prone associated with diabetes mellitus in clinics.

Adrenergic alpha-Antagonists↗