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Biomedical subjects

Juei-Tang Cheng

Publications and source records attributed to Juei-Tang Cheng.

At least 55 records · Page 3Linked to original sources

Increase of anti-oxidation by exercise in the liver of obese Zucker rats.

1. The effects of endurance training on the anti-oxidant status in diabetes were studied using obese Zucker rats. 2. We used a moderate exercise programme consisting of treadmill running at 20 m/min and 0% incline for 1 h/day, 7 days/week, for 8 weeks. At the end of the experimental period, changes in hepatic anti-oxidant enzymes in terms of protein content and mRNA levels were detected using western blotting analysis and northern blotting analysis, respectively. In addition, anti-oxidant enzyme activity was determined. 2. A significant reduction in mRNA levels and the protein content of hepatic Mn-superoxide dismutase (SOD) and glutathione peroxidase (GPx) were observed in non-exercise obese groups, but the mRNA and protein levels of these enzymes were markedly increased after exercise training. In addition, exercise training reversed the decreased enzyme activities of Mn-SOD and GPx in obese Zucker rats. 3. The diabetes-related lowering of the glutathione (GSH) concentration was elevated in exercised obese Zucker rats, indicating a marked effect of regular moderate exercise on the endogenous anti-oxidant system. 4. There were no marked changes in hepatic Cu/Zn-SOD in terms of mRNA levels, protein content and activity in sedentary obese Zucker rats compared with their lean littermates. Endurance training did not modify the gene expression and activity of hepatic Cu/Zn-SOD. 5. The results of the present study suggest that regular moderate exercise could improve the anti-oxidant defence function of Mn-SOD, GPx and GSH in obese Zucker rats.

Actins↗

The plasma glucose lowering action of tetrandrine in streptozotocin-induced diabetic rats.

The effect of tetrandrine, an active principle of Stephaniae tetrandrae, on the plasma glucose level in streptozotocin-induced diabetic rats (STZ-diabetic rats) was investigated. A single intravenous injection of tetrandrine decreased the plasma glucose in a dose-dependent manner in STZ-diabetic rats. Moreover, tetrandrine (1.0 mg x kg(-1)) significantly attenuated the rise in plasma glucose induced by the intravenous glucose challenge test in normal rats. A stimulatory effect of tetrandrine on glucose uptake was obtained in soleus muscles isolated from STZ-diabetic rats with a concentration-dependent manner from 0.01 to 10.0 micromol L(-1). The increase in glucose utilization by tetrandrine was further characterized using the enhancement of glycogen synthesis in the hepatocytes of STZ-diabetic rats. These results suggest that tetrandrine has the ability to enhance glucose utilization in peripheral tissue, resulting in the lowering of plasma glucose in diabetic rats lacking insulin.

Alkaloids↗

Corni fructus as the major herb of Die-Huang-Wan for lowering plasma glucose in Wistar rats.

Die-Huang-Wan is a mixture of six herbs used to lower plasma glucose by increasing insulin secretion in normal rats. Die-Huang-Wan contains the herbs dioscorea (Dioscoreae rhizoma), cornus (Corni fructus), alisma (Rhizoma alismatis), holelen (Poria), rehmannia (Rehmanniae radix) and tree peony bark (Moutan radicis cortex). The present study was designed to clarify the major herb contributing to the plasma glucose-lowering action of Die-Huang-Wan in rats. A decrease in plasma glucose was not observed in Wistar rats treated with the cornus-deleted formula of Die-Huang-Wan; however, the action was retained in the other herb-deleted formulas containing cornus. In normal rats, the decrease in plasma glucose and increase in plasma insulin concentrations were dependent on the dose of cornus and were similar to those produced by Die-Huang-Wan. Treatment of Wistar rats with each of the other five herbs separately did not result in a decrease in plasma glucose. Moreover, the increase in plasma insulin or reduction in plasma glucose resulting from cornus treatment was blocked by atropine or 4-diphenylacetoxy-N-methylpiperidine methiodide mustard, indicating mediation of muscarinic M(3) receptors similar to that caused by Die-Huang-Wan. These results suggest that cornus is the major contributor to the plasma glucose-lowering action in Die-Huang-Wan in normal rats.

Animals↗

Mediation of beta-endorphin by isoferulic acid to lower plasma glucose in streptozotocin-induced diabetic rats.

We investigated the mechanism(s) by which isoferulic acid lowers plasma glucose levels in streptozotocin-induced diabetic rats (STZ-diabetic rats). In STZ-diabetic rats, isoferulic acid dose dependently lowered plasma glucose concentrations and increased plasma beta-endorphin-like immunoreactivity (BER). Both of these effects of isoferulic acid were abolished by pretreatment of rats with tamsulosin or 2-[2,6-dimethoxyphenoxyethyl]aminomethyl-1,4-benzodioxane hydrochloride (WB 4101) at doses sufficient to block alpha1-adrenoceptors. Also, isoferulic acid enhanced BER release from isolated rat adrenal medulla in a concentration-dependent manner that could be abolished by treatment with alpha1-adrenoceptor antagonists. Moreover, bilateral adrenalectomy in STZ-diabetic rats eliminated the activities of isoferulic acid, including the plasma glucose-lowering effect and the plasma BER-elevating effect. Naloxone and naloxonazine inhibited the plasma glucose-lowering activity of isoferulic acid at doses sufficient to block opioid mu-receptors. In contrast with the effect in wild-type diabetic mice, isoferulic acid failed to lower plasma glucose levels in opioid mu-receptor knockout diabetic mice. Treatment of STZ-diabetic rats with isoferulic acid three times in 1 day resulted in an increase in the expression of the glucose transporter subtype 4 form in soleus muscle. This effect was blocked by alpha1-adrenoceptor or opioid mu-receptor antagonists. The reduction of elevated mRNA or protein level of hepatic phosphoenolpyruvate carboxykinase was also impeded in the same groups of STZ-diabetic rats. In conclusion, our results suggest that isoferulic acid may activate alpha1-adrenoceptors to enhance the secretion of beta-endorphin, which can stimulate the opioid mu-receptors to increase glucose use or/and reduce hepatic gluconeogenesis, resulting in a decrease of plasma glucose in STZ-diabetic rats.

Adrenal Medulla↗

Role of striatal glutamate in heatstroke-induced damage in streptozotocin-induced diabetic rats.

In heatstroke related symptoms in streptozotocin-induced diabetic rats (STZ-diabetic rats) exposed to a high temperature (43 degrees C) for 60 min, like that in normal rats, the high colon temperature and the decreases of mean arterial pressure, heart rate and cerebral blood flow were abolished by MK-801, the NMDA receptor antagonist. Also, striatal glutamate was markedly released in both animals by this exposure while the release was higher and the survival time was shorter in STZ-diabetic rats than in normal rats. After insulin treatment, like that by MK-801 pretreatment, the striatal glutamate and the incidence of heatstroke in STZ-diabetic rats were markedly reduced. Therefore, heatstroke was more easily induced via the elevated striatal glutamate in STZ-diabetic rats by high temperature exposure. Insulin treatment seems helpful in the prevention of heatstroke in STZ-diabetic rats.

Animals↗

Both alpha1-adrenergic and D(1)-dopaminergic neurotransmissions are involved in phenylpropanolamine-mediated feeding suppression in mice.

The anorectic action of phenylpropanolamine (PPA) has been attributed to the activation of alpha1 adrenoceptors. It is unknown whether dopamine (DA) receptor subtype was involved in this action. With a treating dose higher than those used in previous reports and a testing period mainly in the dark phase of a circadian rhythm, we found that DA-ergic transmission was also involved in PPA anorexia. Pretreatment of phentolamine or prazosin could partly block PPA-induced anorexia, confirming the involvement of alpha1 adrenoceptor subtype. In addition, pretreatment of haloperidol or SCH 23390 could also partly block PPA anorexia, revealing the involvement of D(1) receptor subtype. Moreover, co-administration of prazosin and SCH 23390 could completely block PPA anorexia, confirming the co-involvement of alpha1 and D(1) receptor subtypes. These findings suggested that both subtypes of alpha1 adrenoceptor and D(1) receptor were involved in the anorectic action of PPA.

Adrenergic alpha-Agonists↗

Rapid induction of insulin resistance in opioid mu-receptor knock-out mice.

Role of opioid mu-receptor that has been showed to involve in the insulin-dependent diabetic rats in the induction of insulin resistance remains unclear. The present study is performed to clarify this point. The wild-type mice or opioid mu-receptor knockout mice were employed to induce insulin resistance by feeding with fructose-rich chow or by the repeated intraperitoneal injections of long-acting form of human insulin at 0.5 IU/kg three times daily. The basal plasma glucose concentration was not markedly changed in fructose-fed mice regardless the presence of opioid mu-receptor or not. However, the plasma glucose lowering activity of tolbutamide (10.0 mg/kg) disappeared rapidly in opioid mu-receptor knockout mice receiving fructose-rich chow as compared to that in wild type group. In opioid mu-receptor knockout mice, the elevation of plasma glucose concentration and the loss of plasma glucose lowering activity of tolbutamide were observed at 15 days after insulin injection. However, similar change was obtained at 21 days later of insulin injection in wild-type mice, showing that decrease of insulin action was more markedly in opioid mu-receptor knockout mice. Our results indicated that opioid mu-receptor is related to the delay of insulin resistance induced by fructose-fed method or insulin repeated injection.

Animals↗

Antihyperglycemic effect of puerarin in streptozotocin-induced diabetic rats.

The antihyperglycemic action of puerarin, purified from the roots of Pueraria lobata, was investigated in streptozotocin-induced diabetic rats (STZ-diabetic rats). Bolus intravenous injection of puerarin decreased the plasma glucose concentrations in a dose-dependent manner in STZ-diabetic rats. Similar treatment with puerarin also decreased the plasma glucose in normal rats, although the effect was not as great as that in STZ-diabetic rats. Puerarin at the effective dose (15.0 mg/kg) significantly attenuated the increase of plasma glucose induced by an intravenous glucose challenge test in normal rats. In the isolated soleus muscle of STZ-diabetic rats, puerarin enhanced the uptake of radioactive glucose in a concentration-dependent manner. Moreover, the mRNA and protein levels of the subtype 4 form of glucose transporter (GLUT4) in soleus muscle were increased after repeated intravenous administration of puerarin in STZ-diabetic rats for 3 days. These results suggest that puerarin can increase the glucose utilization to lower plasma glucose in diabetic rats lacking insulin.

Animals↗

Antidiabetic dimeric guianolides and a lignan glycoside from Lactuca indica.

Three novel sesquiterpene lactones, lactucain A (1), B (2), and C (3), and a new furofuran lignan, lactucaside (4), were isolated from Lactuca indica along with nine known compounds, 11beta,13-dihydrolactucin, cichoriosides B, quercetin, quercetin 3-O-glucoside, rutin, apigenin, luteolin, luteolin 7-O-glucuronide, and chlorogenic acid. Among these compounds, latucain C (3) and lactucaside (4) showed significant antidiabetic activity.

Animals↗

Effect of tetramethylpyrazine on potassium channels to lower calcium concentration in cultured aortic smooth muscle cells.

1. Tetramethylpyrazine (TMP) is one of the active principles contained in Ligusticum chuanxiong Hort. (Umbelliferae), a herb that has been used widely in China to treat vascular disorders. 2. In an attempt to elucidate the possible mechanisms of action of TMP, the effect of TMP on intracellular calcium concentrations ([Ca2+]i) was investigated in cultured vascular smooth muscle (A7r5) cells using the Ca(2+)-sensitive dye Fura-2 as an indicator. 3. The increase in [Ca2+]i in A7r5 cells produced by vasopressin (1 micromol/L) or phenylephrine (1 micromol/L) was attenuated by TMP in a concentration-dependent manner. Only inhibitors specific to ATP-sensitive potassium (KATP) channels or small conductance calcium-activated potassium (SKCa) channels attenuated the action of TMP (10 micromol/L) on [Ca2+]i. However, blockers of other K+ channels failed to modify the inhibitory action of TMP (10 micromol/L) on [Ca2+]i. 4. The action of TMP on membrane potential in A7r5 cells was monitored by the fluorescence of bisoxonol. Tetramethylpyrazine caused a concentration-dependent inhibition of changes in membrane potential elicited by KCl (20 mmol/L) or phenylephrine (1 micro mol/L), an effect that was totally reversed by glibenclamide (100 micromol/L) and apamin (100 nmol/L) in combination. 5. The results obtained indicate that the decrease in [Ca2+]i in A7r5 cells produced by TMP is mediated mainly by opening of KATP and/or SKCa channels.

Animals↗

Stimulatory effect of paeoniflorin on adenosine release to increase the glucose uptake into white adipocytes of Wistar rat.

The present study investigated the role of adenosine in the stimulatory action of paeoniflorin on in vitro glucose transport. Paeoniflorin increased the uptake of a radiolabeled, non-metabolizable glucose derivative into isolated white adipocytes of Wistar rat in a concentration-dependent manner and this action was abolished by the antagonist, 8-cyclopentyltheophylline, at concentrations sufficient to block the adenosine A 1 receptor. However, paeoniflorin failed to displace the binding of [3H]-8-cyclopentyl-1,3-dipropylxanthine in the isolated cerebrocortex of Wistar rat. Direct activation of the adenosine A 1 receptor does not seem to be responsible for the action of paeoniflorin. The stimulatory effect of paeoniflorin on radioactive glucose uptake was abolished in isolated rat white adipocytes pre-incubated with the adenosine deaminase at concentrations sufficient to metabolize endogenous adenosine. Mediation of endogenous adenosine in the action of paeoniflorin was further supported by the assay of adenosine released into the medium from rat white adipocytes incubated with paeoniflorin. These findings suggest that paeoniflorin could induce the release of adenosine from isolated rat white adipocytes and the released adenosine may activate the adenosine A 1 receptor to enhance glucose uptake.

Adenosine↗

Tetramethylpyrazine as potassium channel opener to lower calcium influx into cultured aortic smooth muscle cells.

In the present study, the effect of tetramethylpyrazine (TMP) on calcium (Ca 2+) influx was investigated in cultured vascular smooth muscle (A7r5) cells using Fura-2 as an indicator. The increase of Ca 2+ concentration in A7r5 cells produced by vasopressin or phenylephrine was attenuated by TMP from 0.01 micromol/L to 1 mmol/L. The decrease in the intracellular potassium concentration in A7r5 cells by TMP from 0.01 micromol/L to 10 micromol/L was characterized using PBFI/AM. Inhibitors specific to the small conductance calcium-activated potassium (SKCa ) channel or the ATP-sensitive potassium (K ATP ) channel abolished the actions of TMP. The obtained results indicate that the decrease of Ca 2+ influx into A7r5 cells by TMP is mainly mediated by the opening of potassium channels.

Animals↗

Antihyperglycemic effect of andrographolide in streptozotocin-induced diabetic rats.

The antihyperglycemic action of andrographolide, an active principle in the leaves of Andrographis paniculata (Burm. f.) Nees, was investigated in streptozotocin-induced diabetic rats (STZ-diabetic rats). Oral treatment of andrographolide decreased the plasma glucose concentrations of STZ-diabetic rats in a dose-dependent manner. Similar treatment with andrographolide also decreased the plasma glucose in normal rats and the maximal effect was more marked than that in STZ-diabetic rats. Andrographolide at the effective dose (1.5 mg/kg) significantly attenuated the increase of plasma glucose induced by an intravenous glucose challenge test in normal rats. In the isolated soleus muscle of STZ-diabetic rats, andrographolide enhanced the uptake of radioactive glucose in a concentration-dependent manner. Moreover, the mRNA and protein levels of the subtype 4 form of the glucose transporter (GLUT4) in soleus muscle were increased after repeated intravenous administration of andrographolide in STZ-diabetic rats for 3 days. These results suggest that andrographolide can increase the glucose utilization to lower plasma glucose in diabetic rats lacking insulin.

Administration, Oral↗

Antihyperglycemic action of angiotensin II receptor antagonist, valsartan, in streptozotocin-induced diabetic rats.

OBJECTIVES: In the present study, we use valsartan, a highly selective antagonist for angiotensin(1) (AT(1)) receptor subtype, to investigate the effect of AT(1) receptor on the plasma glucose metabolism in streptozotocin-induced diabetic rats (STZ-diabetic rats). METHODS: The plasma glucose concentration was assessed by glucose oxidase method and plasma insulin was measured using enzyme-linked immunosorbent assay. Systolic blood pressure (SBP) was determined by the tail-cuff method. The intravenous glucose challenge test (IVGCT) was carried out to evaluate the effect of valsartan on the glucose utilization in vivo. The mRNA levels of the subtype 4 form of glucose transporter (GLUT4) in soleus muscle and phosphoenolpyruvate carboxykinase (PEPCK) in the liver were detected by Northern blotting analysis. Moreover, the protein levels of GLUT4 in isolated soleus muscle and hepatic PEPCK were investigated using Western blotting analysis. RESULTS: A single intravenous injection of valsartan decreased the plasma glucose concentrations in a dose-dependent manner in STZ-diabetic rats. Plasma glucose-lowering action of valsartan also observed in normal rats although in a way not so effective as that in STZ-diabetic rats. Valsartan at the dose of 0.2 mg/kg that produced the maximal plasma glucose-lowering activity in STZ-diabetic rats is also effective to lower the SBP. However, oral treatment with nifedipine or nicorandil in STZ-diabetic rats at the dose sufficient to decrease SBP showed no change of plasma glucose. Otherwise, infusion of saralasin (10 microg/kg per min) into STZ-diabetic rats produced a plasma glucose-lowering activity similar to that by valsartan at 0.2 mg/kg. Moreover, valsartan (0.2 mg/kg) significantly attenuated the raise of plasma glucose induced by IVGCT in normal rats. Repeated intravenous administration of valsartan (0.2 mg/kg) in STZ-diabetic rats resulted in the lowering of plasma glucose after 3 days. The mRNA and protein levels of GLUT4 in the soleus muscle were increased after repeated intravenous administration of valsartan in STZ-diabetic rats for 3 days. Moreover, similar repeated treatment with valsartan reversed the elevated mRNA and protein levels of PEPCK in the liver of STZ-diabetic rats. CONCLUSIONS: These results suggest that the plasma glucose-lowering activity of AT(1) receptor antagonism was associated with an increase in the glucose utilization in peripheral tissue and/or a reduction in hepatic gluconeogenesis in the absence of insulin.

Angiotensin II Type 1 Receptor Blockers↗

Mechanism of the antihypertensive effect of stevioside in anesthetized dogs.

Stevioside is a sweet-tasting glycoside isolated from the leaves of Stevia rebaudiana. It has been used as a noncaloric sugar substitute in Japan and Brazil for decades. Previous studies have shown that it lowered blood pressure in spontaneously hypertensive rats by intravenous injection. This study was designed to evaluate the hypotensive effect of stevioside in dogs and to define the underlying mechanism. After nasogastric administration of stevioside powder (200 mg/kg), the blood pressure of healthy mongrel dogs began to significantly decrease at 60 min and returned to baseline level at 180 min. The reduction of blood pressure was more rapid (at 5-10 min) and effective after intravenous injection. However, no significant change of blood pressure was noted after injection through left vertebral artery, implicating that the hypotensive effect is not related to the central nervous system. Stevioside also showed significant hypotensive effects in renal hypertensive dogs, in a dose-dependent manner. In cultured rat aortic smooth muscle cells (A7r5 cell line), stevioside can dose-dependently inhibit the stimulatory effects of vasopressin and phenylephrine on intracellular Ca(2+) in a calcium-containing medium. However, no intracellular Ca(2+) inhibitory effect was observed in calcium-free medium, implicating that stevioside may inhibit the Ca(2+) influx from extracellular fluid. Our present data show that stevioside did not influence the calcium ionophore (A23187) induced Ca(2+) influx, indicating that the antagonistic effect was through Ca(2+) channels. This study confirmed that stevioside is an effective antihypertensive natural product, and its hypotensive mechanism may be probably due to inhibition of the Ca(2+) influx.

Administration, Intranasal↗

Alteration of alpha(1A)-adrenoceptor gene expression in the prostate of streptozotocin-induced diabetic rats.

Diabetes-associated alterations in prostate alpha(1A)-adrenoceptor (alpha(1A)-AR) gene expression were studied using a streptozotocin (STZ) induced diabetic rat model. Male Wistar rats were divided into four groups: group I animals were vehicle-treated normal rats; group II consisted of vehicle-treated, STZ-diabetic rats; group III represented insulin-treated, STZ-diabetic rats (0.5 IU/kg three times daily for 4 days), and group IV animals were phlorizin-treated, STZ-diabetic rats (1 mg/kg three times daily for 4 days). The expression of mRNA that encoded protein of alpha(1A)-AR in the rat prostate was studied using reverse transcription combined with polymerase chain reaction. The alpha(1A)-AR protein expression in the prostate was studied by Western blotting analysis with a polyclonal antiserum. A 2.51 +/- 0.21-fold increase in the mRNA level of alpha(1A)-AR was observed in the prostate of diabetic rats (n = 8, p < 0.05). Similarly, there was a 2.23 +/- 0.10-fold increase in the alpha(1A)-AR protein level (n = 8, p < 0.05). Both insulin and phlorizin treatments restored the normal levels of mRNA and protein expression. In conclusion, the gene expression of alpha(1A)-AR is increased in the prostate of diabetic rats. Hyperglycemia plays a major role in this alteration.

Animals↗

Stimulatory effect of cinnamic acid analogues on alpha1A-adrenoceptors in-vitro.

We have characterized the effects of cinnamic acid and its derivatives on alpha(1)-adrenoceptor subtypes. The cinnamic acid with a methoxyl group and/or a hydroxyl group showed the ability to stimulate radioactive glucose uptake into C(2)C(12) cells, a cell line that specifically expresses the alpha(1A)-adrenoceptor subtype of alpha(1)-adrenoceptors. However, cinnamic acid without chemical modification diminished the glucose uptake into C(2)C(12) cells. It was shown that methoxylation and/or hydroxylation of cinnamic acid had higher affinities for alpha(1A)-adrenoceptors investigated using [(3)H]prazosin binding experiments in C(2)C(12) cells. The effect of these derivatives on alpha(1A)-adrenoceptors was further characterized using the displacement of [(3)H]prazosin binding in rat prostate. We found that 3,5-dimethoxy-4- hydroxycinnamic acid, the cinnamic acid derivative with two methoxyl groups and hydroxylation at the fourth carbon on the benzene ring, had a higher affinity for the alpha(1A)-adrenoceptor subtype, showing a smaller IC50 value (the concentration for production of 50% inhibition) to displace [(3)H]prazosin binding in rat prostate. Affinity of these compounds for alpha(1B)-adrenoceptors was identified using [(3)H]prazosin-binding experiments in rat spleen. However, we found no marked differences in the IC50 values between these cinnamic acid analogues to displace the [(3)H]prazosin binding in rat spleen. In conclusion, our data indicated that methoxylation and/or hydroxylation of cinnamic acid might raise the affinity for alpha(1A)-adrenoceptors.

Animals↗

Effects of Ba-Wei-Die-Huang-Wan on the cholinergic function and protein expression of M2 muscarinic receptor of the urinary bladder in diabetic rats.

The study investigated the effect of a traditional Chinese herbal preparation 'Ba-Wei-Die-Huang-Wan' on the cholinergic function of the urinary bladder in diabetic rats, as well as its influence on the protein expression of muscarinic M(2) receptors. Wistar rats were divided into three groups: (1) control rats; (2) 2-week streptozotocin-induced diabetic rats; and (3) diabetic rats treated with Ba-Wei-Die-Huang-Wan 26 mg/kg thrice daily for 3 days. A dose-response study was performed for bladder muscle strip contractile response to a muscarinic agonist, arecaidine propargyl ester (APE). The amount of M(2) receptor protein in the bladder was measured by Western immunoblotting using monoclonal antibodies. The bladder contractile response to APE was significantly increased in the diabetic rats compared to the control. The M(2) receptor protein density was also significantly higher by 106% (P < 0.01, n = 8) in diabetes. Ba-Wei-Die-Huang-Wan treatment significantly lowered the plasma glucose level of the diabetic rats. The increases in contractile response to APE as well as the M(2) receptor protein density were partially reversed by the treatment. In conclusion, there was an over-expression of M(2) receptor resulting in hyper-contractility in the bladder of diabetic rats. Ba-Wei-Die-Huang-Wan significantly alleviated the alterations.

Animals↗