Biomedical subjects

J T Cheng

Publications and source records attributed to J T Cheng.

At least 55 records · Page 3Linked to original sources

PubMed2000

The change of beta-adrenergic system in lead-induced hypertension.

Lead exposure is considered to be a risk factor of cardiovascular disease. To investigate the relationship between lead and cardiovascular disease/hypertension in lead exposure, beta-adrenergic system is explored in this study. We address three topics in this study: (a) the relationship between beta-adrenergic receptor and lead level in heart, aorta, and kidney of lead-exposed rats; (b) the relationship between beta-adrenergic receptor in heart, aorta, kidney, and blood pressure in lead-exposed rats; and (c) the change of cyclic AMP level in heart, aorta, and kidney of rats with different lead levels. Wistar rats were chronically fed with 2, 1, 0. 5, 0.1, 0.05, and 0.01% lead acetate and water for 2 months. Plasma catecholamine level was measured by high-performance liquid chromatography. Radioligand binding assay was measured by a method that fulfilled strict criteria of beta-adrenoceptor using the ligand [(125)I]iodocyanopindolol. Cyclic AMP (cAMP) level was determined by radioimmunoassay. The levels of lead were determined by electrothermal atomic absorption spectrometry. The results showed that increased plasma norepinephrine level, decreased aorta beta-adrenergic receptor and cAMP, and increased kidney beta-adrenergic receptor and cAMP contributed to the elevation of blood pressure in lead-induced hypertension. The decrement of beta-adrenoceptor and cAMP in heart resulted in decreased contractility in heart.

Administration, Oral↗

PubMed2000

Decrease of adenosine A-1 receptor gene expression in cerebral cortex of aged rats.

Changes of adenosine A-1 receptor (A1-AR) gene expression in aging were investigated in cerebral cortex using the rat aged from 2 months (adult) to 24 months (aged). Quantification of A1-AR protein level by immunoblotting analysis showed an age-related decrease of A1-AR in cerebral cortex of Wistar rats. Compared to the preparations from 2-month-old animals, the levels of A1-AR in the 6-, 12-, and 24-month-old rats were reduced by 14.3+/-5.2, 32.5+/-4.5 and 28.2+/-5.7%, respectively. Similar decrease of mRNA level in A1-AR was also obtained using Northern blotting analysis. Two representative spots of mRNA, a 3.4-kb transcript and a 5.6-kb transcript, were observed in X-ray film from cerebral cortex of rat hybridized with rat A1-AR cDNA probe. Compared to the 2 month-old rats, levels of the 5.6-kb transcript were decreased by 17.9+/-2.5, 27.4+/-3.2 and 23.1+/-2.1% in the 6-, 12- and 24-month-old rats, respectively. These results indicated an age-related decrease of A1-AR in cerebral cortex of the rat that seems responsible for the change of response to adenosine.

Aging↗

PubMed2000

Less of insulin desensitization in sympathetic nerve terminals from wistar rats with insulin resistance.

In an attempt to determine the effect of hyperinsulinemia on sympathetic function, release of norepinephrine (NE) from isolated aorta by insulin was measured in Wistar rats with insulin resistance. Insulin resistance was produced when the hypoglycemic action of glibenclamide at a dose of 10 mg/kg was almost abolished in rats that received daily injections of long-acting insulin for 15 days. Moreover, the stimulatory effect of insulin on glucose uptake was markedly reduced in both skeletal muscle strips and white adipocytes obtained from these rats with insulin resistance. However, the stimulatory effects of insulin at concentrations from 5 to 15 U/l on the release of NE from the aortic strip of insulin-resistant rats were not modified in the same manner but only slightly reduced compared with that of normal rats. These results suggest that insulin desensitization was produced later in sympathetic nerve terminals than in other organs in insulin-resistant rats and this may be helpful to explain the sympathetic hyperactivity associated with diabetes in clinics.

Adipocytes↗

PubMed2000

Differentiation status modulates transcription factor NF-kappaB activity in unstimulated human hepatocellular carcinoma cell lines.

We report herein a novel finding that under an unstimulated condition, a group of four human hepatocellular carcinoma (HCC) cell lines with varying degrees of differentiation, can spontaneously activate NF-KB. The propensity of activation coincided inversely with the differentiation status, with order being SK-Hep-1 > J5 > Hep3B > HepG2. Further studies indicate that this pattern of activation correlates excellently with the descending order of intracellular GSH/GSSG ratios as well as with the ascending order in the ability of these cells to generate hydrogen peroxide. Taken together, our data suggest that differentiation status may play a pivotal role in modulating intracellular thiol redox status and the extent of catalase expression, which may be crucial in the control of NF-kappaB activity in these HCC cells.

Carcinoma, Hepatocellular↗

PubMed2000

Stimulatory effect of caffeic acid on alpha1A-adrenoceptors to increase glucose uptake into cultured C2C12 cells.

In an attempt to understand the antihyperglycemic action of caffeic acid, the myoblast C2C12 cells were employed to investigate the glucose uptake in the present study. Caffeic acid enhanced the uptake of radioactive glucose into C2C12 cells in a concentration-dependent manner. Similar effect of phenylephrine on the uptake of radioactive glucose was also observed in C2C12 cells. Prazosin attenuated the action of caffeic acid in a way parallel to the blockade of phenylephrine. Effect of caffeic acid on alpha1-adrenoceptors was further supported by the displacement of [3H]prazosin binding in C2C12 cells. Moreover, the glucose uptake-increasing action of phenylephrine in C2C12 cells was inhibited by the antagonists of alpha1A-adrenoceptors, both tamsulosin and WB 4101, but not by the antagonist of alpha1B-adrenoceptors, chlorethylclonidine (CEC). The presence of alpha1A-adrenoceptors in C2C12 cells can thus be considered. Similar inhibition of the action of caffeic acid was also obtained in C2C12 cells co-incubating these antagonists. An activation of alpha1A-adrenoceptors seems responsible for the action of caffeic acid in C2C12 cells. In the presence of U73312, the specific inhibitor of phospholipase C, caffeic acid-stimulated uptake of radioactive glucose into C2C12 cells was reduced in a concentration-dependent manner and it was not affected by U73343, the negative control of U73312. Moreover, chelerythrine and GF 109203X diminished the action of caffeic acid at concentrations sufficient to inhibit protein kinase C. Therefore, the obtained data suggest that an activation of alpha1A-adrenoceptors in C2C12 cells by caffeic acid may increase the glucose uptake via phospholipase C-protein kinase C pathway.

Adrenergic alpha-Agonists↗

PubMed2000

Stimulatory effect of trans-cinnamaldehyde on noradrenaline secretion in guinea-pig ileum myenteric nerve terminals.

The effect of trans-cinnamaldehyde (CNMA) on the release of noradrenaline (NA) from nerve terminal was investigated using isolated ileal synaptosomes of guinea-pig. Release was determined as the amount of NA, quantified by h.p.l.c.-electrochemical detection, from samples incubated with CNMA minus that in parallel blanks treated with same volume of vehicle. CNMA stimulated the secretion of NA in a concentration-dependent manner from 5 microM to 50 microM, while the value of lactate dehydrogenase in the incubated medium was not influenced by CNMA. However, trans-cinnamic acid, cinnamoyl chloride and cinnamamide failed to produce similar effect. Specific action of CNMA can thus be considered. Guanethidine inhibited the release of NA by CNMA in a concentration- dependent manner. Saxitoxin attenuated the action of CNMA at concentrations sufficient to block sodium channels. The depolarizing effect of CNMA on the membrane potential was also illustrated by a concentration-dependent increase in the fluorescence of bisoxonol, a potential sensitive dye. The NA releasing action of CNMA was deleted by removal of calcium chloride from the bathing medium. This action of CNMA was also attenuated by Rp-cAMP at concentrations sufficient to inhibit the action of cyclic AMP. These findings suggest that CNMA can depolarize the membrane to result in a calcium-dependent and cyclic AMP-related release of NA from noradrenergic terminals.

Acrolein↗

PubMed2000

Antihyperglycemic action of isoferulic acid in streptozotocin-induced diabetic rats.

Wistar rats with streptozotocin-induced diabetes (STZ-diabetic rats), which is similar to human insulin-dependent diabetic mellitus (IDDM), were employed to investigate the antihyperglycemic action of isoferulic acid. A single intravenous injection of isoferulic acid decreased the plasma glucose in a dose-dependent manner in the STZ-diabetic rats. Repeated intravenous administration of STZ-diabetic rats with isoferulic acid (5.0 mg kg(-1)) also resulted in the lowering of plasma glucose after one day. Stimulatory effects of isoferulic acid on the glucose uptake and glycogen synthesis in soleus muscles isolated from STZ-diabetic rats were also obtained indicating an increase of glucose utilization following isoferulic acid treatment which was not dependent on insulin. The mRNA level of glucose transporter subtype 4 form (GLUT4) in soleus muscle was raised by isoferulic acid after repeated treatment for 1 day in STZ-diabetic rats. Similar repeated treatment with isoferulic acid reversed the elevated mRNA level of phosphoenolpyruvate carboxykinase (PEPCK) in liver of STZ-diabetic rats to the normal level. However, expression of GLUT4 and PEPCK genes in nondiabetic rats were not influenced by similar treatment with isoferulic acid. These results suggest that isoferulic acid can inhibit hepatic gluconeogenesis and/or increase the glucose utilization in peripheral tissue to lower plasma glucose in diabetic rats lacking insulin.

Animals↗

PubMed2000

A double-blind placebo-controlled study of the effectiveness and tolerability of oral stevioside in human hypertension.

AIMS: Stevioside is a natural plant glycoside isolated from the plant Stevia rebaudiana which has been commercialized as a sweetener in Japan for more than 20 years. Previous animal studies have shown that stevioside has an antihypertensive effect. This study was to designed to evaluate the effect of stevioside in human hypertension. METHODS: A multicentre, randomized, double-blind, placebo-controlled study was undertaken. This study group consisted of 106 Chinese hypertensive subjects with diastolic blood pressure between 95 and 110 mmHg and ages ranging from 28 to 75 years with 60 subjects (men 34, women 26; mean +/- s.d., 54.1+/-3.8 years) allocated to active treatment and 46 (men 19, women 27; mean +/- s.d., 53.7+/-4.1 years) to placebo treatment. Each subject was given capsules containing stevioside (250 mg) or placebo thrice daily and followed-up at monthly intervals for 1 year. RESULTS: After 3 months, the systolic and diastolic blood pressure of the stevioside group decreased significantly (systolic: 166.0+/-9.4-152.6+/-6.8 mmHg; diastolic: 104.7 +/- 5.2-90.3+/-3.6 mmHg, P<0.05), and the effect persisted during the whole year. Blood biochemistry parameters including lipid and glucose showed no significant changes. No significant adverse effect was observed and quality of life assessment showed no deterioration. CONCLUSIONS: This study shows that oral stevioside is a well tolerated and effective modality that may be considered as an alternative or supplementary therapy for patients with hypertension.

Adult↗

PubMed2000

Effects of trilinolein on superoxide dismutase activity and mrna levels in aortic smooth muscle cells.

1. Atherosclerotic cardiovascular disease is still the leading cause of death in Western countries. Oxygen free radicals are considered to be intimately involved in the development of atherosclerosis. Anti-oxidants may help to protect mammalian cells from the damage induced by these reactive oxygen species. Many reports have indicated that anti-oxidants used in the treatment or prevention of disease could modify the levels of superoxide dismutase (SOD). However, the effects of long-term anti-oxidant treatment on the levels of SOD in smooth muscle cells (SMC) is still unclear. In the present study, the effects of the lipophilic anti-oxidant trilinolein on the activity and gene expression of SOD in SMC were evaluated. 2. After 2 days incubation with 0.1 micromol/L trilinolein, the activity and mRNA levels of SOD were increased in rat aortic SMC (A7r5), but there was no significant change in these parameters with a higher concentration of 1 micromol/L trilinolein. 3. In contrast, after 7 days incubation with trilinolein, both the activity and mRNA levels of SOD were lowered in a dose-dependent manner. 4. These data emphasize the importance of choosing an optimal dosage for supplementation with anti-oxidants in humans for the scavenging of oxygen free radicals.

Animals↗

PubMed2000

Caffeic acid as active principle from the fruit of Xanthium strumarium to lower plasma glucose in diabetic rats.

The antihyperglycemic effect of caffeic acid, one of the phenolic compounds contained in the fruit of Xanthium strumarium, was investigated. After an intravenous injection of caffeic acid into diabetic rats of both streptozotocin-induced and insulin-resistant models, a dose-dependent decrease of plasma glucose was observed. However, a similar effect was not produced in normal rats. An insulin-independent action of caffeic acid can thus be considered. Otherwise, this compound reduced the elevation of plasma glucose level in insulin-resistant rats receiving a glucose challenge test. Also, glucose uptake into the isolated adipocytes was raised by caffeic acid in a concentration-dependent manner. Increase of glucose utilization by caffeic acid seems to be responsible for the lowering of plasma glucose.

Animals↗

PubMed2000

Effect of N-(biphenylyl-methyl)imidazole, a type 1 angiotensin II receptor inhibitor, on the contractile function of the rat corpus cavernosum.

The effect of N-(biphenylyl-methyl)imidazole, losartan potassium, a newly developed antihypertensive type 1 angiotensin II receptor antagonist on the rat erectile function, was studied. Sexually active 9-week-old male spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats were given losartan 60 mg/kg intraperitoneal injections. Mean blood pressure (MBP) dropped significantly in both SHR and WKY rats (for SHR: from 140 +/- 8 to 114 +/- 5 mm Hg, p < 0.05, n = 8; for WKY: from 113 +/- 7 to 79 +/- 9 mm Hg, p < 0.05, n = 8). On the contrary, the intracavernous pressure (ICP) of SHR and WKY rats did not differ significantly from that of the corresponding controls receiving saline injections (p > 0.05, n = 8 for each group). For the chronic study, the rats were fed with losartan 30 mg/kg/day for 30 days. MBP decreased significantly in SHR but not in WKY rats (for SHR: from 137 +/- 7 to 113 +/- 5 mm Hg, p < 0.05, n = 8; for WKY: from 110 +/- 6 to 107 +/- 5 mm Hg, p > 0.05, n = 8). The ICP of the losartan-treated rats was not significantly different from that of control rats (p > 0.05, n = 8 for each group). In contrast, WKY rats receiving guanethidine 1 mg/kg/day for 30 days showed significantly decreased ICP. Angiotensin II (10(-9)-10(-5) M) and losartan (10(-9)- 10(-5) M) did not induce significant contractile responses of the cavernosal strip when tested in vitro. On the other hand, methoxamine 10(-4) M induced good contractile responses. In conclusion, the present study demonstrated that angiotensin II did not cause significant change in the contractile status of rat corpus cavernosum. Correspondingly, the type 1 angiotensin II inhibitor effectively lowered blood pressure but did not affect cavernosal contractile function, thus is useful clinically in the treatment of hypertensive disorders without significant detrimental effects on male sexual function.

Angiotensin Receptor Antagonists↗

PubMed2000

Review: drug therapy in Chinese traditional medicine.

This article addresses the differences between the basic concepts of drug therapy in Chinese traditional medicine (CTM) and modern Western medicine. In ancient times, throughout the world, humans used plants as food and medicine. In Europe, chemistry developed rapidly after the influence of Paracelsus. Active principles were isolated from plants, and drugs were prepared in the salt form to use as medication. In China, several drugs isolated from plants have been prepared in the salt form in recent years, but herbal medication, developed in the ancient tradition, continued to be widely used in Chinese populations. Some theories such as the yin-yang theory and the five-element theory were commonly employed to explain the rationale for the use of CTM. In this review, hypertension and diabetes mellitus are used as examples to illustrate the applications of CTM. The notions of the "whole" and the use of "relative" rather than absolute are important concepts, which distinguish CTM from modern medicine.

Drugs, Chinese Herbal↗

PubMed2000

Structure-activity relationships of anthraquinones in the decrease of intestinal motility.

The effects of substituted anthraquinones on intestinal motility were evaluated in-vitro using rabbit small intestinal strips. This structure-activity relationship study revealed the critical requirement of a hydroxy group at R2 position. The intestinal motility was inhibited 50% (IC50) by emodine (8 microM), 2-hydroxy anthraquinone (20 microM), 2,6-dihydroxy anthraquinone (25 microM), 2,7-dihydroxy anthraquinone (10 microM), 1,2,4-trihydroxy anthraquinone (80 microM) and 1,2,5,8-tetra-hydroxyanthraquinone (9 microM). The presence of other polar groups at R2 position such as an amino, aldehyde and carboxylic acid group significantly reduced the activity (IC50 360-400 microM). The presence of a methyl group and esterification of the carboxylic acid at R2 position was found to abolish the activity. These data are useful for the future development of anthraquinones as laxative agents.

Animals↗

PubMed2000

Role of adenosine in insulin-stimulated release of leptin from isolated white adipocytes of Wistar rats.

Leptin, the ob gene product that can decrease caloric intake and increase energy expenditure, is functionally released by insulin from adipose tissue. Adenosine is thought to be an important regulator of the action of insulin in adipose tissue. The present study investigated the role of adenosine in the release of leptin by insulin in isolated rat white adipocytes. Release of leptin, measured by radioimmunoassay, from insulin-stimulated samples was seen after 30 min. Adenosine deaminase, at concentrations sufficient to metabolize endogenous adenosine, decreased insulin-stimulated leptin release. Also, the insulin-stimulated leptin release was completely blocked by the adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX). Mediation of endogenous adenosine in this action of insulin was further supported by the assay of adenosine released into the medium from adipocytes stimulated with insulin. In addition, activation of adenosine A1 receptors by N6-cyclopentyladenosine (CPA) induced an increase in leptin release in a concentration-dependent manner that could be blocked by antagonists, either DPCPX or 8-(p-sulfophenyl)theophylline (8-SPT). In the presence of U73312, a specific inhibitor of phospholipase C (PLC), CPA-stimulated leptin secretion from adipocytes was reduced in a concentration-dependent manner, but it was not affected by U73343, the negative control for U73312. Moreover, chelerythrine and GF 109203X diminished the CPA-stimulated leptin secretion at concentrations sufficient to inhibit protein kinase C (PKC). These results suggest that, in isolated white adipocytes, the released adenosine acts as a helper and/or a positive regulator for insulin in the release of leptin via an activation of adenosine A1 receptors that involves the PLC-PKC pathway.

Adenosine↗

PubMed2000

Changes in superoxide dismutase activity and mRNA in vivo after short-term supplementation with trilinolein in rats.

BACKGROUND: Oxidative damage plays a central role in atherogenesis and antioxidation defense mechanisms may prevent atherosclerosis. This study evaluated the effect of short-term supplementation of the natural lipophilic antioxidant trilinolein on superoxide dismutase (SOD) activity and SOD-mRNA gene expression in vivo in rat vital organs. METHODS: Male Wistar rats (n = 8) were injected intraperitoneally with trilinolein (1 mM/ml/kg/day in 0.5% ethanol) daily for three consecutive days. Two control groups (n = 8) were administered saline or 0.5% ethanol in saline, respectively, for three days. RESULTS: Assay of SOD activity and SOD-mRNA by Northern blotting in rat liver, spleen and brain showed significant increases in SOD activity and increased SOD-mRNA gene expression. CONCLUSIONS: The natural lipophilic antioxidant trilinolein potentiates the SOD antioxidation defense mechanism and increases gene expression of SOD-mRNA after short-term supplementation in rats.

Animals↗

PubMed2000

Stimulatory effect of trans-cinnamaldehyde on norepinephrine secretion in cultured pheochromocytoma (PC-12) cells.

AIM: The effect of trans-cinnamaldehyde (CNMA) on the release of norepinephrine (NE) from nerve terminal was investigated using rat pheochromocytoma 12 (PC-12) cells. METHODS: The amount of NA released from PC-12 cells incubated with CNMA or related substances was quantified by high performance liquid chromatography (HPLC)-electrochemical detection. The lipophilic anion bisoxonol was used to monitor the effect of CNMA on the membrane potential. RESULTS: CNMA stimulated the secretion of NE in a concentration-dependent manner from 5 mumol/L to 50 mumol/L, while the value of lactate dehydrogenase in the incubated medium was not influenced by CNMA. However, acetaldehyde, cinnamic acid, cinnamoyl chloride and cinnamamide failed to produce similar effect. The action of CNMA can thus be considered specific. The depolarizing effect of CNMA on the membrane potential was also illustrated by a concentration-dependent increase in the fluorescence of bisoxonol, a potential-sensitive dye. Saxitoxin attenuated the depolarizing action of CNMA at concentrations sufficient to block sodium channels. Besides, the effect of CNMA to depolarize the membrane potential in PC-12 cells is greater than that of 4-aminopyridine (4-AP). The action of CNMA on NE releasing depends on extracellular Ca2+ and is attenuated by 8-bromo-cAMP at concentrations sufficient to inhibit the action of cyclic AMP. CONCLUSION: These findings suggest that CNMA can depolarize the membrane to result in a Ca(2+)-dependent and cyclic AMP-related release of NE from PC-12 cells.

8-Bromo Cyclic Adenosine Monophosphate↗

PubMed1999

Alterations in urinary bladder M2-muscarinic receptor protein and mRNA in 2-week streptozotocin-induced diabetic rats.

The M2 receptor (M2-mAChR) is quantitatively the dominant muscarinic subtype in animal bladders. The alterations in its protein quantity and biosynthesis during diabetic cystopathy were investigated. Three-month-old male Wistar rats were divided into two groups: (1) 2-week-old diabetics; and (2) normoglycemic control rats. Diabetes was induced by single intravenous injection of 60 mg/kg streptozotocin. The amount of M2 receptor protein in the rat bladder body tissue was measured by Western immunoblotting using monoclonal antibodies. For determination of M2 muscarinic receptor mRNA in the bladder tissue, the method of Northern blotting was employed. The results of the Western immunoblotting showed that the amount of M2-mAChR protein in the diabetic bladder was significantly increased by 40.0 +/- 6.2% when compared with the control bladder (P < 0.05, n = 8). The Northern blotting demonstrated a 69.3 +/- 8.5% increase of the M2-mAChR mRNA in the diabetic bladder (P < 0.05, n = 8). The findings of the present study demonstrated an up-regulation of M2-mAChR biosynthesis in the diabetic urinary bladder. This phenomenon could lead to increased reactivity to acetylcholine and thus results in detrusor instability.

Animals↗

PubMed1999

Changes of superoxide dismutase gene expression and activity in the brain of streptozotocin-induced diabetic rats.

In an attempt to discover the changes of superoxide dismutase (SOD) in the brain of diabetic state, we investigated the level of SOD in streptozotocin-induced diabetic rats (STZ-diabetic rats) using enzyme activity assay, Northern blotting analysis of mRNA levels and Western blotting of enzyme amount. Five discrete brain regions, cerebrocortex, hypothalamus, hippocampus, the remaining non-cortex cerebrum (NCC area) and cerebellum, were examined in STZ-diabetic rats to compare with age-matched normal rats. Higher levels of Mn-SOD including the activity, mRNA expression and immunoblot of enzyme were found in all areas of the brain from STZ-diabetic rats as compared with that in Wistar rats. Except in the cerebellum, similar changes of Cu,Zn-SOD were found in the brain of STZ-diabetic rats. These results indicate an increase of SOD both gene expression and activity in the brain of STZ-diabetic rats. This alteration of SOD may be one of the important factors for the vulnerability of the brain to oxygen free radicals or may be related to the pathophysiology of diabetes.

Animals↗