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Biomedical subjects

H Shi

Publications and source records attributed to H Shi.

At least 199 records · Page 11Linked to original sources

Scavenging effects of baicalin on free radicals and its protection on erythrocyte membrane from free radical injury.

Using electron spin resonance (ESR) spin trapping technique, we found that baicalin (B) could scavenge hydroxyl radicals generated from Fenton reaction. It also could scavenge superoxide radicals generated from the reaction system containing xanthine (X) and xanthine oxidase (XO), as was found by using chemiluminescence (CL) method. Kinetic studies on the competition between baicalin and a spin trap 5,5-dimethyl-1-pyrroline-1-oxide (DMPO) in trapping OH showed that baicalin had a kinetic reactive rate constant of the order of 7.7 x 10(11) M-1 s-1 in its reaction with OH, and the studies on the competition between baicalin and ferricytochrome c (f.c.) in trapping O2- gave a kinetic reactive rate constant of 3.2 x 10(6) M-1 s-1 for baicalin in its reaction with O2-. Furthermore, we have investigated the protective effects of baicalin on erythrocyte membranes from hydroxyl free radical injuries. The results showed that baicalin could reduce hydrogen peroxide-induced hemolysis, protect the conformation of sulfhydryl groups (-SH) on membrane proteins and the membrane fluidity of erythrocytes incubated with hydrogen peroxide. The results indicated that baicalin could protect the membranes of erythrocytes from free radical injuries, and it was even more effective than alpha-tocopherol.

Anions↗

[Influence of SmI lesion on acupuncture-induced analgesia in thalamic Pf neurons and effects of iontophoretic ACh on their nociceptive responses].

This study aimed to investigate the role of ACh in SmI emanating descending modulation of thalamic Pf neurons in acupuncture analgesia. Multi-micropipettes were used for both extracellularly recording responses of thalamic Pf neurons to noxious stimulation of the plantar area and drug application in rats. It was found that (1) lesion of SmI obviously attenuated the inhibitory effect of EA applied at "Zusanli" and "Huantiao" points on nociceptive responses in Pfneurons; (2) after lesion of SmI iontophoretic application of ACh markedly suppressed the nociceptive responses of Pf neurons, which was significantly different from the effect of iontophoretic NaCl (as the control) showing no influence on them; (3) the inhibition induced by iontophoretic ACh applied in the rats with lesion of SmI was similar to that produced by EA applied in those with SmI intact. It is indicated that EA can activate SmI to release ACh to exert descending modulation, in which ACh is involved in SmI originating descending regulation of Pf neruons in acupuncture analgesia.

Acetylcholine↗

[Inhibitory effect of anti-motoneuron serum on the neurite outgrowth of spinal cord explants (in vitro) and the cross-reactivity of serum to human and rat motoneurons].

The effects of rabbit anti-swine motoneuron serum (RAS), normal rabbit serum (NRS), skeletal muscle extracts (MET, 50 and 100 micrograms/ml) and brain extracts (BET, 50 and 100 micrograms/ml) on neurite outgrowth of neonatal rat spinal cord explants (in vitro) were studied after 5 days of treatment. In comparison with NRS (explants possessing neurite outgrowth accounted for 36.7%, n = 30), the neurite outgrowth of spinal cord explants was significantly accelerated by MET (96.7% of explants had neurite outgrowth), but inhibited by RAS (only 13.3% of the explants had neurite outgrowth). The cross-reactivity of RAS to the spinal motoneuron of swine, humans and rats were also demonstrated by immunocytochemical techniques.

Animals↗

[Cost-benefit analysis on Malayan filariasis control in Miaoxi Township, Huzhou City, Zhejiang Province during 1964-1987].

The methods adopted in this paper were as follows: (1) The cost of the filariasis control was estimated to be direct cost and indirect cost; (2) Using the reduction rate of acute inflammatory attack as the measurable indicator of control effectiveness; (3) Estimating the case number of acute inflammatory attack occurred after control year by year basing on the goodness by fitting in the reduction trend of acute inflammatory attack with hyperbola formula; (4) Assuming that the case number of acute inflammatory attack would be relatively stable at the same level of pre-control if filariasis control measures were not implemented; (5) The benefit from the filariasis control was estimated by transforming the increasing man-working day and saving the medicine expenses of patients due to the reduction of acute inflammatory attack. By allowing seven percent discount on cost and benefit, the total cost was 21,182 Yuan, the total benefit was 119,859 Yuan, the ratio of cost-benefit was 1:5.7, implying that putting in one Yuan to filariasis control in this township may gain benefit 5.7 Yuan.

Animals↗

[Simultaneous staining with fluorescein diacetate-propidium iodide to determine isolated cochlear outer hair cell viability of guinea pig].

A simultaneous double-staining procedure using fluorescein diacetate (FDA) and propidium iodide (PI) is discribed for use in the determination of isolated cochlear outer hair cell viability. With exciter light, viable cells fluoresce bright green, while nonviable cells are bright red. In cell culture and cytotoxicity studies, double-staining with FDA-PI is a accurate method to discriminate between live and nonviable cells.

Animals↗

[Low dosage of homoharringtonine for prevention of cicatrization after glaucoma filtering surgery].

To prevent the cicatrization of filtering blebs after glaucoma filtering surgery, subconjunctival injections of low dosage homoharringtonine were administered to 22 glaucomatous eyes (20 patients) postoperatively. The percentage of functional filtering blebs was 90.9% and the mean postoperative IOP was 2.04 +/- 0.68 kPa (1 kPa = 7.5 mmHg). In comparison with the control group, the differences were very significant (P < or = 0.01). The results suggest that the toxicity of low dosage of homoharringtonine be very low, it inhibit fibroblast proliferation and play important roles in the formation of the functional filtering blebs and elevation of the success rate of filtration operation.

Adult↗

[Effects of a platelet-activating factor antagonist ONO-6240 on antigen induced eosinophil infiltration into the airways].

An in vivo mouse model of allergic bronchial asthma was developed to investigate the effects of a platelet activating factor antagonist ONO-6240 on eosinophil (EOS) recruitment into the mouse airway. In the present study, no EOS could be found in bronchoalveolar lavage fluid (BALF) from normal control mice. However, chronic ovalbumin challenge of sensitized mice induced significant bronchoalveolar eosinophilia (9.68 +/- 0.72 x 10(8)/L). In three groups of mice treated intraperitoneally with different doses of ONO-6240 (0.1, 1.0, 10.0 mg/kg), the medication produced 42.1% (5.60 +/- 0.97 x 10(8)/L, P < 0.01), 58.8% (3.99 +/- 0.84 x 10(8)/L, P < 0.01), and 72.6% (2.65 +/- 0.71 x 10(8)/L, P < 0.01) inhibition, respectively, of the antigen-induced influx of EOS into BALF. It was found that the prevention of EOS infiltration into airway with ONO-6240 was accompanied by decrements of both interleukin (IL)-5 and IL-2 levels. These data indicated that ONO-6240 prevented airway eosinophilia by inhibiting production of IL-5 and IL-2. Our results suggested that ONO-6240 may be of value in treating human asthmatic patients.

Animals↗

[Influence of microiontophoretic morphine on nociceptive responses of Pf neurons after lesion of SmI].

Neuronal responses in thalamic nucleus parafasciculus (Pf) to microiontophoretic morphine were examined in 20 wistar rats after lesion of SmI. Extracellular recordings were made with five-barreled glass microelectrodes. The results showed that the spontaneous responses of Pf neurons were not statistically changed (n = 11, P > 0.05), but their nociceptive responses were attenuated at 0-8 minutes after iontophoretic morphine (n = 11, P < 0.05). There were statistically significant differences in nociceptive responses between morphine and saline groups at 0-8 minutes after iontophoresis. The results suggest that morphine may be involved in corticofugal modulation of nociceptive responses in thalamic Pf neurons.

Animals↗

Characterization of a mitogen-response unit in the mouse lactoferrin gene promoter.

Lactoferrin is present in a variety of tissues and biological fluids; however, the amount differs significantly due to differential expressions. We have previously demonstrated that the mouse lactoferrin gene is regulated by estrogen through an estrogen-response DNA element located at -349, upstream from the transcription start site (+1). In this report, we characterized by deletion and mutation analyses a cluster of mitogen-response elements located between -80 and -40 of the mouse lactoferrin promoter. We demonstrated that the chimeric chloramphenicol acetyltransferase reporter constructs (the -103 to +1 sequence of the mouse lactoferrin gene) containing the mitogen-response unit of the lactoferrin gene were stimulated by cAMP, forskolin, 12-O-tetradecanoylphorbol-13-acetate, and epidermal growth factor/recombinant transforming growth factor-alpha (EGF/TGF-alpha) in a time- and dose-dependent manner. The sequence at position -52 to -40 (mLF-CRE) of the gene conferred transcriptional activation in the presence of forskolin, cyclic AMP, and 12-O-tetradecanoylphorbol-13-acetate in transiently transfected human endometrium carcinoma RL95-2 cells, whereas the region at -80 to -60 responded to EGF/TGF-alpha stimulation. Overexpression of the catalytic unit of protein kinase C or protein kinase A in the RL95-2 cells elevated the chloramphenicol acetyl-transferase activity of the reporter construct 5-6-fold. The mobility shift assay suggested that AP1 and CREB or related proteins participated in complex formation with the mLF-CRE, whereas different proteins bound to the EGF/TGF-alpha-response element.

Animals↗

Impairment of GABAA receptor function by N-methyl-D-aspartate-mediated calcium influx in isolated CA1 pyramidal cells.

Mechanisms of regulation of GABAA receptor function by intracellular calcium ([Ca2+]i) were examined in cell somata and apical dendrites of pyramidal cells, acutely dissociated from the CA1 hippocampal subfield of adult guinea-pigs. GABAA receptor-mediated currents were measured by whole-cell clamp recordings. N-methyl-D-aspartate receptor-mediated currents were used as conditioning source of calcium influx. Peak amplitudes of somatic GABAA whole-cell currents were reduced to about 15% of control values when net inward charge accumulation by N-methyl-D-aspartate currents reached 1.85 nC. A similar decline of GABAA currents was observed in dendritic recordings. The N-methyl-D-aspartate-mediated reduction of somatic and dendritic GABAA currents was accompanied by a well correlated decrease in peak and chord conductances. Pharmacological blockade of N-methyl-D-aspartate currents by 2-amino-5-phosphonopentanoic acid prevented the N-methyl-D-aspartate-mediated suppression of GABAA responses. The N-methyl-D-aspartate effect was mediated by the calcium component of N-methyl-D-aspartate receptor-mediated currents as demonstrated by a lack of effect in the absence of extracellular calcium and faster N-methyl-D-aspartate-mediated suppression of GABAA responses in lower intracellular 1,2-bis(2-aminophenoxy)ethane-N,N,N',N"-tetra-acetate. N-methyl-D-aspartate-mediated suppression of GABAA currents was significantly less expressed when intracellular ATP was replaced by its analog adenosine 5'-O-(3-thiotriphosphate) and when the specific phosphatase 2B inhibitor cypermethrin was added intracellularly. The reduction of GABAA responses persisted after cessation of N-methyl-D-aspartate-mediated calcium influx, indicating a long-term action of N-methyl-D-aspartate on GABAA responses. Voltage-activated calcium currents did not affect GABAA responses under the experimental conditions applied. In conclusion, the data presented show that calcium influxes through N-methyl-D-aspartate receptor channels result in long-term suppression of GABAA receptor function in CA1 pyramidal cells. Intracellular mechanisms of N-methyl-D-aspartate-mediated reduction of GABAA conductances involve activation of phosphatase 2B and consecutive dephosphorylation of the GABAA receptor or a closely associated GABAA receptor-regulating enzyme. Possible mechanisms of such a distinct N-methyl-D-aspartate-dependent calcium signalling pathway in the dephosphorylation-dependent suppression or GABAA receptor function are discussed.

Adenosine Triphosphate↗

Interactions of both melittin and its site-specific mutants with bacteriorhodopsin of Halobacterium halobium: sites of electrostatic interaction on melittin.

Melittin and its site-specific mutants differentially delay the slow-decaying component of the photocycle intermediate M412 of bacteriorhodopsin in the purple membrane and the acetylated purple membrane whose several lysine residues are modified. This effect is attributed to the interaction of the total positive charges of melittin or its mutants with the total negative charges of bacteriorhodopsin. The effects of melittin and its mutants on the Triton X-100-solubilized bacteriorhodopsin monomers are somewhat complicated but are associated with their charges. These results show that there is electrostatic interaction between bacteriorhodopsin and melittin and that both N- and C-termini of melittin function as sites of the interaction, with Arg 22 and Arg 24 making a prominent contribution to the effective surface charge of melittin. Melittin, at certain concentrations, partially restores the decreased photoactivity of the bacteriorhodopsin monomers trapped in the Triton-lipid-protein mixed micelles, which suggests that melittin may compete with Triton X-100 for the binding sites on the bacteriorhodopsin monomers. Other kinds of interactions between bacteriorhodopsin and melittin are also indicated. The possible states of melittin in membranes are discussed.

Amino Acid Sequence↗

Spatial distribution of 3-hydroxy-3-methylglutaryl coenzyme A reductase messenger RNA in the ocular lens: relationship to cholesterologenesis.

This study probes the regulation of cholesterol biosynthesis in the ocular lens by estimating the concentration and distribution of the messenger RNA for the rate-controlling enzyme for sterol synthesis, 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGR). Because the lens is dependent on biosynthesis for cholesterol, HMGR activity is crucial for the life-long growth of this organ. Young rat lenses were serially divided into several fractions by dissolution in an SDS-containing buffer and each fraction was equated to a percent of the lens radius based upon its protein content. HMGR enzyme activity and cholesterol synthesis has been shown to disappear from the lens cortex over a narrow arc of radius due to loss of enzyme protein. Using a published competitive reverse transcriptase-polymerase chain reaction method for amplifying HMGR mRNA (Powell, E. E., and P. A. Kroon. 1992. J. Lipid Res. 33: 609-614), an average of about 46,000 copies of this mRNA was estimated per lens at all rat ages examined (5-day-old to adult). However, copies/microgram total RNA decreased with aging. The distribution of HMGR mRNA across 95-60% of the lens radius was essentially uniform at 2000-3000 copies/mm3 tissue. But the very superficial cortex contained 5- to 7-times this concentration and accounted for about 35% of the total copies/lens. We estimated that cells in this region each contained 1 to 2 copies of message, a value similar to the estimated copy number of HMGR message in human lymphocytes (Powell and Kroon, ibid). This suggests that the translational efficiency and stability of lens HMGR mRNA must be very high.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗

[Influence of cooling motor cortex on the inhibitory effect of stimulation of SII on nociceptive responses in ILN neurons].

Fibers from the cortical somatosensory area II (SII) or motor cortex (MCtx) to intralaminar nuclei (ILN) have been proven to exist, and SII was found to be connected with MCtx by cortico-cortical fibers. The present work was undertaken to study whether MCtx participated in SII producing descending modulation of ILN. All experiments were performed on sodium pentobarbitone anaesthetised cats. Single unit activities of ILN neurons were extracellularly recorded by glass microelectrodes. The effects of stimulating SII on nociceptive responses of ILN neurons were observed before and after cooling MCtx. The nociceptive responses of ILN neurons were attenuated by stimulating SII. There was a statistically significant difference at 0'-2' after the stimulation (n = 14, P < 0.05). The inhibitory effect of stimulating SII was reduced after cooling MCtx (19 degrees C-20 degrees C) in 8 neurons, and abolished in other neurons when the temperature was below 18 degrees C. MCtx was involved in SII producing descending modulation of ILN.

Animals↗

[Molecular cytogenetic study of Turner's syndrome with the 45, X/46,X,r(?) karyotype].

Two small marker chromosomes were identified as X-derived ring chromosomes by using the high-resolution banding technique and in situ hybridization with a radioactively labelled human X-chromosome-specific satellite DNA probe. This procedure clearly determined the origin of the marker chromosome, which had been impossible using conventional cytogenetic techniques. The clinical significance of this work is briefly discussed.

Adolescent↗