[Survey on modern researches of traditional Chinese medicine therapy of infantile nephrotic syndrome and its mechanism].
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Animals↗
Biomedical subjects
X M Li
Publications and source records attributed to X M Li.
[Clinical significance of plasma alpha-granule membrane protein-140 in blood stasis of primary glomerular disease].
Plasma alpha-granule membrane protein 140(GMP-140) was determined in 53 patients of primary glomerular disease (PGD) with or without blood stasis. At the same time, the relationships between plasma GMP-140 and hyperlipoidemia and hypertension were investigated. Results showed that plasma GMP-140 in PGD patients was higher than that of normal control subjects, P < 0.01, platelet of patients was in a high activated status. The elevation was more significant in patient with blood stasis than in those without blood stasis, P < 0.01. Among the patients with blood stasis, plasma GMP-140 level in those with Qi-Deficiency was higher than that without Qi-Deficiency (P < 0.05). The above-mentioned results suggested that GMP-140 was an objective indicator for blood stasis of PGD patients. Deficiency of Qi could enhance platelet activation so as to aggravate the tendency of blood stasis. It was in accordance with the traditional Chinese medicine theory of "Qi-Deficiency induces blood stasis". Hyperlipoidemia and hypertension showed close relationship with abnormal increase of GMP-140, suggesting they play important roles in induction of hypercoagulability and blood stasis in PGD patients.
Adult↗
Receptor-receptor interactions and their relevance for receptor diversity. Focus on neuropeptide/dopamine interactions.
Receptor diversity in combination with receptor-receptor subtype specific interactions, which can be antagonistic or synergistic in character, markedly increase plasticity in WT and VT in the nervous system. In this way switching among transmission lines for the various DA receptor subtypes becomes possible. Some of these aspects are supported by our work on selective modulation of D2 receptors by CCK and NT. Selective regulation of D2 receptors via CCK-8 receptor subtypes and NT receptors may underlie CCK/DA interactions and NT/DA interactions in the basal ganglia. These studies underline the importance of receptor-receptor interactions exerted at the membrane level between neuropeptide receptors and D2 receptors, which are determined at least in part by the ongoing activity at D1 receptors. In the case of both CCK/D2 and NT/D2 receptor interactions, it has been possible, by means of intrastriatal and intraaccumbens microdialysis, to obtain a functional correlate to the receptor interactions found in the membrane preparations from the striatum. Schizophrenia may be in part related to reduced release of CCK and/or NT peptides or to alterations in their receptor interactions with the D2 receptor. This view may lead to new therapeutic approaches.
Animals↗
A single (-)-nicotine injection causes change with a time delay in the affinity of striatal D2 receptors for antagonist, but not for agonist, nor in the D2 receptor mRNA levels in the rat substantia nigra.
The in vitro and in vivo effects of (-)-nicotine on dopamine D2 receptors in the rat neostriatum have been studied using biochemical binding, in situ hybridization and immunocytochemistry. A single i.p. injection (1 mg/kg) of (-)-nicotine resulted in a reduction of the KD value of the D2 antagonist [3H]raclopride binding sites in rat neostriatal membrane preparations at 12 h without any significant change in the Bmax value. This action of (-)-nicotine was counteracted by pretreatment 15 min earlier with the nicotine antagonist mecamylamine (1 mg/kg, i.p.). However, the KD and the Bmax values of the D2 agonist [3H]NPA binding sites in the rat neostriatal membrane preparations were not significantly affected 0.5-48 h after a single i.p. injection with 1 mg/kg of (-)-nicotine. No significant change in neostriatal D2 receptor mRNA levels was observed at any time interval after the (-)-nicotine injection. No significant change was observed in tyrosine hydroxylase (TH) immunoreactivity in either the substantia nigra or the neostriatum, nor in nigral TH mRNA levels during the time interval studied (4-24 h posttreatment). Furthermore, addition of low (10 nM) or high (1 microM) concentrations of (-)-nicotine in vitro to rat neostriatal membranes did not alter the characteristics of [3H]raclopride or [3H]NPA binding. These results indicate that a single (-)-nicotine injection can produce a selective and delayed increase in the affinity of D2 receptors for the antagonist, but not for the agonist without modifying the levels of D2 receptor mRNA, probably via the activation of central nicotinic receptors.
Animals↗
Cholecystokinin octapeptide in vitro and ex vivo strongly modulates striatal dopamine D2 receptors in rat forebrain sections.
Receptor autoradiographic experiments together with the filter wipe-off technique were performed to investigate the effects of cholecystokinin octapeptide (CCK-8) on dopamine D2 receptors. In vitro studies showed that 1 nM CCK-8 significantly increased the KD value of binding sites for the D2 agonist [3H]N-propylnorapomorphine (NPA) in the rostral and caudal parts of the nucleus accumbens by 48 and 148% respectively. In contrast, 1 nM CCK-8 significantly decreased the IC50 value of dopamine for binding sites for the D2 antagonist [125I]iodosulpride in the rostral and caudal parts of the caudate-putamen by 46 and 56% respectively, and in the rostral and caudal parts of the nucleus accumbens (areas of CCK-dopamine coexistence) by 57 and 75% respectively. Ex vivo studies demonstrated that 30 min after an intraventricular injection of 1 nmol/rat CCK-8 the KD value of [3H]NPA binding sites in the caudal part of the forebrain and the IC50 value of dopamine for [125I]iodosulpride binding sites in the caudal part of the nucleus accumbens were significantly increased by 160% and decreased by 77% respectively. These results indicate for the first time that in sections CCK-8 in vitro and ex vivo can strongly regulate D2 receptor affinity in the striatum. The present studies also provide evidence for stronger modulation of D2 receptors by CCK-8 in the area of CCK/dopamine coexistence in the nucleus accumbens than in other basal ganglion areas, supporting the existence of CCK/D2 receptor interactions in cotransmission. The stronger interactions found in sections than in membrane preparations may indicate the requirement of intracellular mechanisms and/or a more intact membrane structure for optimal receptor-receptor interactions.
Animals↗
Protein profiles of Streptomyces aureofaciens producing tetracyclines: reappraisal of the effect of benzyl thiocyanate.
Cell protein profiles of submerged cultures of Streptomyces aureofaciens cultivated in the absence or presence of 12 microM benzyl thiocyanate (BT) were analyzed by one-dimensional SDS polyacrylamide gel electrophoresis. Substantial increase in the intensity of the 13, 35, 37, 60, and 100 kDa protein bands was observed in cultures treated with BT. Similar increase in the 35, 37, and 60 kDa bands was found in a mutant blocked in the last chlortetracycline biosynthesis step. Effect of BT on the solid medium-grown cultures was also observed, with a more intensive substrate mycelium pigmentation and alteration in the spore size and shape as the most characteristic features. Earlier studies of BT effect involving those on the stimulation of chlortetracycline biosynthesis are summarized and a possible signal-transducing mechanism is discussed from the point of view of adaptation of S. aureofaciens to the uncoupling of oxidative phosphorylation.
Bacterial Proteins↗
Neurotensin peptides antagonistically regulate postsynaptic dopamine D2 receptors in rat nucleus accumbens: a receptor binding and microdialysis study.
An in vitro receptor binding and in vivo microdialysis study was performed to further investigate the modulation of dopamine (DA) D2 receptors by neurotensin (NT) peptides. Saturation experiments with the D2 agonist [3H]NPA (N-propylnorapomorphine) showed that 10 nM of NT, 10 nM of neuromedin N (NN) and 1 nM of the C-terminal NT-(8-13) fragment significantly increased the KD values by 125%, 181%, and 194%, respectively without significantly affecting the Bmax value of the [3H]NPA binding sites in coronal sections of rat ventral forebrain mainly containing the nucleus accumbens (Acb) and the olfactory tubercle. In line with the previous findings that NT can increase GABA release in the Acb and that NT receptors are not found on DA terminals in this brain region, the present in vivo microdialysis study demonstrated that local perfusion of NT (1 nM) counteracted the D2 agonist pergolide (2 mu M) induced inhibition of GABA, but not of DA release in the rat Acb. This result indicates that NT counteracts the D2 agonist induced inhibition of GABA release in the rat Acb, via an antagonistic postsynaptic NT/D2 receptor interaction as also suggested by the inhibitory regulation of D2 receptor affinity in the Acb by the NT peptides demonstrated in the present receptor binding experiments. Thus, the neuroleptic and potential antipsychotic profile of the NT peptides may involve an antagonistic NT/D2 receptor regulation in the ventral striatum.
Animals↗
Increased immunohistochemical expression of neutral metalloendopeptidase (enkephalinase; EC 3.4.24.11) in villi of the human placenta with pre-eclampsia.
The purpose of this study was to identify the presence of placental neutral metalloendopeptidase (NEP; enkephalinase; EC 3.4.24.11) in human normotensive and pre-eclamptic pregnancy. The localization of NEP in placentae from normotensive, chronic hypertensive and pre-eclamptic pregnancies was carried out on fresh frozen tissues by using a monoclonal primary antibody developed against human common acute lymphoblastic leukaemia antigen (CD10) together with the avidin-biotin-peroxidase method. In placentae from normotensive, chronic hypertensive and superimposed pre-eclamptic pregnancies, intense staining was found in the extravillous trophoblast, and also in fibroblasts of the chorionic plate and stem villi. Light to moderate staining was noted in the villous-associated trophoblast and in some cells from the villous core. In cases of pre-eclampsia, very intense staining was detected not only on the surface, but also in the cytoplasm of the villous-associated trophoblast. The increased expression of placental NEP in pre-eclampsia suggests that this enzyme may be involved in the regulation of the local concentration of circulating biologically active peptides at the fetomaternal interface, and thus could be implicated in the pathophysiological changes of this syndrome.
Adult↗
Some new mechanisms underlying the actions of (-)-deprenyl: possible relevance to neurodegeneration.
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Animals↗
Neurochemical, neuroprotective and neurorescue effects of aliphatic N-methylpropargylamines; new MAO-B inhibitors without amphetamine-like properties.
A series of aliphatic N-methylpropargylamine MAO-B inhibitors have been synthesized and their structural and functional relationships have been investigated. 2-Hexyl-N-methylpropargylamine (2-HxMP), for example, has been found to be a highly potent, irreversible, selective, MAO-B inhibitor both in vitro and in vivo. The R-(-)-enantiomers are much more active than the S-(+)-enantiomers at inhibiting MAO-B activity. Some of these compounds protect mouse nigrostriatal dopamine neurons against the neurotoxin MPTP and the mouse hippocampal noradrenergic system against the neurotoxin N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP-4). They rescue hippocampal neurons after damage induced by ischemia and kainic acid treatment, as well as motoneurons in young mice following facial nerve axotomy. Such rescue effects are, interestingly, unrelated to inhibition of MAO-B activity. Some of the aliphatic propargylamines enhance the survival of neuroblastoma cells co-cultured with astrocytes following serum depletion. They stimulate the expression of AADC mRNA and inhibit GFAP mRNA expression. They do not possess amphetamine-like properties and exhibit no effect on noradrenaline or dopamine uptake nor do they increase hypertensive effects in the tyramine pressor test. Unlike R(-)-deprenyl, 2-HxMP does not potentiate dopamine toxicity in vitro. These new MAO-B inhibitors may possess significant chemotherapeutic implications for certain psychiatric and neurodegenerative disorders.
1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
Angiotensin II interferes with steroidogenesis in porcine granulosa cells.
The elements for the synthesis and activity of the vasopressor angiotensin II (AII) are present in the mammalian ovary. In the present investigation, the effects of AII were determined on three parameters of steroidogenic function in porcine granulosa cells in vitro: the accumulation of progesterone, the cellular content of the enzyme 3 beta-hydroxysteroid dehydrogenase delta 5-4 isomerase (3 beta-HSD), and the accumulation of mRNA for 3 beta-HSD. Cells were incubated with LH (200 ng/ml) in the presence or absence of AII (10(-7) M) or phorbol 12-myristate 13-acetate (PMA, 10(-7) M); doses of AII from 10(-10) to 10(-6) M in the presence or absence of LH; the AII reactor antagonist saralasin (10(-6) M) in the presence of AII or in combination of AII and LH; and AII in the presence or absence of (Bu)2 cAMP. The results demonstrate that LH increased progesterone, 3 beta-HSD message, and 3 beta-HSD content. Both PMA and AII interfered with the LH-induced progesterone accumulation, reducing the response by 50% or more. All also abrogated the LH-induced increases in 3 beta-HSD mRNA and 3 beta-HSD enzyme content in porcine granulosa cells. The AII inhibition was dose-dependent. The AII receptor antagonist saralasin blocked the inhibitory effects of AII on LH-induced steroidogenic events. AII interfered with the (Bu)2 cAMP induction of steroidogenesis and 3 beta-HSD mRNA and enzyme accumulation when (Bu)2 cAMP was present at a concentration of 30 microM.(ABSTRACT TRUNCATED AT 250 WORDS)
Angiotensin II↗
[A study on relationship between balance of serum lipoprotein and the phlegm damp-blood stasis syndrome differentiation of coronary heart diseases].
75 patients were divided into A,B and C group. The LDL-C was 2.97 +/- 0.67, 4.05 +/- 0.38 and 5.25 +/- 0.98 mmol/L respectively (P > 0.01); but comparing group A or B with the normal group (D), it had no significant difference (P > 0.05). An abnormal coronary arteriography (CAG) was found in the group A in 62.1% and the group B in 57.6% (P > 0.05), while the group C in 84.6% (P < 0.01). There was unusual serum lipoprotein electrophoretogram (SLPG) in group A 75.9%, group B 84.8% and group C 100%, but it had no change in group D (P < 0.001). Five types of Syndrome Differentiation about the Phlegm damp and blood stasis (PDBS) could be found in the group A,B and C. The incidence (51.5%-55.2%) and abnormality of the SLPG (66.7%-92.5%) and CAG (68.8%-100%) of PDBS type were the highest among them. 82.7% CHD patient's clinical comprehensive diagnosis was in accordance with the SLPG and that of the CAG were 64.0%. As to the abnormal SLPG, the sensitivity and rate of coincidence of CAG was 91.7% and 69.3% (P < 0.05-0.01) respectively. The Syndrome Differentiation of PDBS was valuable in differentiating CHD. The SLPG is a good criterion for the study of CHD in TCM.
Adult↗
Possible mechanisms for the powerful actions of neuropeptides.
In order to understand the mechanisms underlying the powerful actions of neuropeptides, the present article has emphasized the unique ability of neuropeptides to act as VT signals, which via high-affinity G-protein coupled receptors can exert long-lasting actions and control synaptic transmission via receptor-receptor interactions. Also of substantial importance is the ability of neuropeptides to act as a set of signals via the formation of different types of active fragments, which can act as negative-feedback or positive-feedback signals to modulate the response elicited by the parent peptide and to give origin to syndromic responses. Also in the actions of the fragments on the neuronal network, receptor-receptor interactions may play an important role both by modulating the parent peptide receptors and by modulating other types of VT and/or WT receptors. Future work will have to evaluate the role of neuropeptides as transcellular signals and as regulators of neuronal excitabilities after the formation of carbamates, but certainly new important developments are within the horizon of today's research.
Animals↗
Strong effects of NT/NN peptides on DA D2 receptors in rat neostriatal sections.
Quantitative receptor autoradiography was performed to test the effects of neurotensin (NT)/neuromedin N (NN) peptides on dopamine (DA) D2 receptors in rat neostriatal sections. Competition experiments showed that 10 nM of NT, 10 nM of NN, and 1 nM of the C-terminal NT-(8-13) fragment produced a 2-fold increase in the IC50 value and a 20% decrease in the B0 value of DA for the D2 antagonist [125I]iodosulpride binding sites. The results demonstrate a stronger reduction in the affinity of DA for neostriatal D2 receptors by the NT/NN peptides in brain sections compared with membrane preparations indicating the possible involvement of cytoplasmic factors and/or a demand for a more intact membrane structure in these receptor-receptor interactions. Further evidence for the hypotheses that the C-terminal NT fragments may be among the major ligands for the neostriatal NT receptors and that the neostriatal NT receptors may be a new subtype of NT receptor has been obtained.
Animals↗
Dopamine D1 receptors are involved in the modulation of D2 receptors induced by cholecystokinin receptor subtypes in rat neostriatal membranes.
The action of cholecystokinin octapeptide (CCK-8) on rat neostriatal dopamine (DA) D2 receptors was evaluated in membrane binding experiments. 0.1 nM of CCK-8 increased the Kd value of the D2 agonist [3H]N-propylnorapomorphine (NPA) binding sites by 42%. The CCKB antagonist PD134308 blocked this action. Kinetic analysis demonstrated that this effect of CCK-8 was related to a reduction by 45% of the association rate constant of [3H]NPA. In contrast, 1 nM of CCK-8 decreased the KH and the KL values of DA for the D2 antagonist [3H]raclopride binding sites by 56% and 50%, respectively. Both the CCKA antagonist L364718 and the CCKB antagonist PD134308 blocked this effect. The D1 antagonist SCH23390 counteracted the CCK-8 induced decrease in the KH and the KL values of DA, and allowed 1 nM of CCK-8 to produce a significant increase in the IC50 value of NPA for the [3H]raclopride binding sites. These results indicate that CCK-8 can reduce the affinity of the neostriatal D2 agonist binding sites, but increase the affinity of D2 receptors for DA. D1 receptors may exert a switching role in the modulation of the neostriatal D2 receptors by the CCK receptors.
Animals↗
Cholecystokinin receptor subtypes regulate dopamine D2 receptors in rat neostriatal membranes. Involvement of D1 receptors.
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Animals↗
Effect of lanthanide ions on the phase behavior of dipalmitoylphosphatidylcholine multilamellar liposomes.
The effect of lanthanide ions (Ln3+) and their coordination compounds of diethylenetriamine pentaacetic acid (DTPA) on the phase behavior of dipalmitoylphosphatidylcholine (DPPC) multi-lamellar liposomes has been studied by differential scanning calorimetry (DSC), Raman spectroscopy, and freeze-fracture electron microscopic techniques. The displacement of Ca2+ binding on DPPC liposomes by lanthanide ions was also studied. The results show that the binding degree of four kinds of chloride salts with DPPC liposomes is: YbCl3 > GdCl3 > LaCl3 > CaCl2. Lanthanide ions increase the phase transition temperature of DPPC liposomes and decrease the membrane fluidity. Freeze-fracture electron microscopic results show that La3+ enhances the order of DPPC membrane. The effect of coordination compounds of lanthanides with DTPA on the phase behavior of DPPC liposomes is smaller than that of their chlorides. La3+, Gd3+, and Yb3+, can displace Ca2+ binding on DPPC liposomes, but there coordination compounds of DTPA can hardly displace Ca2+. Raman spectroscopic results show that a very slight effect in lateral packing order of DPPC liposomes was observed at various concentrations of lanthanides.
1,2-Dipalmitoylphosphatidylcholine↗
Induction of aromatic L-amino acid decarboxylase mRNA by interleukin-1 beta and prostaglandin E2 in PC12 cells.
Aromatic 1-amino acid decarboxylase (AADC) is involved in the synthesis of the putative neurotransmitters dopamine (DA), norepinephrine (NA) and 5-hydroxytryptamine (5-HT). We report here that the gene expression of AADC can be regulated by interleukin (IL) 1-beta and prostaglandin (PG) E2 in PC12 cells. The cells were treated with different doses of IL 1-beta and PGE2 for 3 days. Slot blot hybridization was performed to detect AADC mRNA and Western immunoblot to detect AADC protein. The cDNA probe for rat AADC was generated by the PCR method. IL 1-beta and PGE2 produced a dose- and time-dependent up-regulation in AADC mRNA levels (up to 200% of the control values) which was followed by a stable increase in AADC protein. The data further support the suggestion that AADC is a regulated enzyme and that the regulation occurs at the level of gene expression. Because IL-1 is synthesized, and acts locally, within the brain to influence neuronal and glial functions, it has been proposed to be a mediator with both beneficial and detrimental responses to inflammation and injury. The regulation of AADC by IL-1 may indicate a possible involvement for AADC in neuronal injury and recovery. Since IL-1 promotes PGE2 formation, its effects may be occurring by increasing level of PGE2.
Animals↗