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Electrophysiological effects of phytoestrogen genistein on guinea pig papillary muscles.

Acta Physiologica Sinica.2002;54(1):83-87.

The cardiac electrophysiological effects of genistein (GST) were examined in guinea pig papillary muscle using intracellular microelectrode technique. The results obtained are as follows. (1) Duration of action potential (APD) in normal papillary muscles was decreased by GST (10 100 micromol/L) in a concentration-dependent manner. (2) In partially depolarized papillary muscles, 50 micromol/L GST not only reduced APD, but also decreased the amplitude of action potential, overshoot and maximal velocity of phase 0 depolarization. (3) Pretreatment with N( )-nitro-L-arginine (L-NNA, 5 mmol/L) failed to affect the above effects of GST (50 micromol/L)on papillary muscles. (4) 17beta-estradiol (E(2), 5 micromol/L) or GST (10 micromol/L) alone did not affect action potential, while GST combined with E(2) at the same doses shortened APD significantly. All these results indicate that the effects of GST on papillary muscles are likely due to a decrease of calcium inflow which is not mediated by NO and that GST has a facilitative or synergetic action with E(2).
Action Potentials ; drug effects ; Agmatine ; pharmacology ; Animals ; Dose-Response Relationship, Drug ; Drug Synergism ; Electrophysiology ; Estradiol ; pharmacology ; Estrogens, Non-Steroidal ; pharmacology ; Female ; Genistein ; pharmacology ; Guinea Pigs ; Isoflavones ; Male ; Papillary Muscles ; drug effects ; physiology ; Phytoestrogens ; Plant Preparations

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Recombinant human interleukin-10 inhibits vascular smooth muscle cell proliferation induced by TNF-alpha.

Ping OUYANG ; Li-Sheng PENG ; Hong YANG ; Wen-Yan WU ; An-Long XU

Acta Physiologica Sinica.2002;54(1):79-82.

Vessel injury provokes a release in proinflammatory cytokines that influence vascular smooth muscle cell (VSMC) proliferation. The purposes of this study was to determine the effects of recombinant human interleukin-10 (rhIL-10) on rat vascular smooth muscle cell proliferation and the activity of p44/p42 mitogen-activated protein kinase (MAPK) promoted by tumor necrosis factor-alpha (TNF-alpha). Rat aortic VSMCs were cultured and treated with rhIL-10 or TNF-alpha respectively, and then cotreated with rhIL-10 and TNF-alpha. The proliferation of VSMCs was quantified by colormetric assay. Cell cycle analysis was performed by flow cytometry. The p44/42 MAPK activity was evaluated by the immunoblotting technique using anti-p44/42 phospho-MAPK antibody. Compared to control group, TNF-alpha stimulated significantly VSMC proliferation in TNF-alpha group. rhIL-10 alone had no effect on VSMC growth, but significantly inhibited VSMC proliferation induced by TNF-alpha at a dose of 10 ng/ml. The cell number in G(0)/G(1) phase of TNF-alpha and rhIL-10 co-treatment group was higher than that of TNF- alpha group (P<0.01) by flow cytometry analysis. The p44/42 MAPK activity was significantly enhanced by TNF-alpha and the TNF-alpha effect was opposed by rhIL-10. It is suggested that rhIL-10 can inhibit TNF-alpha induced VSMC proliferation and phosphorylation of p44/42 MAPK.
Animals ; Cell Cycle ; drug effects ; Cell Division ; drug effects ; Cells, Cultured ; Interleukin-10 ; pharmacology ; Male ; Mitogen-Activated Protein Kinases ; biosynthesis ; Muscle, Smooth, Vascular ; cytology ; drug effects ; enzymology ; Rats ; Rats, Sprague-Dawley ; Recombinant Proteins ; pharmacology ; Tumor Necrosis Factor-alpha ; pharmacology

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Effect of angiotensin II on follicular atresia in mouse.

Yong CHENG ; Li-Hong JIAO ; Rui-Hua LIU ; Qing-Bin WANG ; Hong WANG ; Guo-Liang XIA

Acta Physiologica Sinica.2002;54(1):75-78.

The effect of angiotensin II (Ang II) on the follicular development was studied by using an animal model of follicular atresia induced by pregnant mare s serum gonadotropin (PMSG). The results showed that: (1) a large number of atretic follicles were found in the ovary of 24-day-old mouse after 6-day treatment of PMSG. Deoxyribonucleic acid (DNA) extracted from granulosa cells clearly showed a ladder band under agarose gel electrophoresis analysis. (2) the contents of Ang II in the ovary extremely increased with the development of follicular atresia. (3) Ang II significantly antagonized the stimulating effect of the follicle-stimulating hormone (FSH) on estradiol (E(2)) generation of granulosa cells. It is suggested that Ang II may be involved in the regulation of follicular atresia in mouse.
Angiotensin II ; pharmacology ; physiology ; Animals ; Cells, Cultured ; Estradiol ; biosynthesis ; Female ; Follicle Stimulating Hormone ; pharmacology ; Follicular Atresia ; physiology ; Gonadotropins, Equine ; pharmacology ; Granulosa Cells ; drug effects ; metabolism ; Mice

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Expression of intercellular adhesion molecule-1 in different organs of the mice with endotoxic shock induced by lipopolysaccharide.

Wen-Sheng YAN ; Wen-Hong KAN ; Qiao-Bing HANG ; Yong JIANG ; Shi-Wen WANG ; Ke-Sen ZHAO

Acta Physiologica Sinica.2002;54(1):71-74.

To investigate and compare the expression of intercellular adhesion molecule-1 (ICAM-1) in different organs of the mice with endotoxic shock induced by lipopolysaccharide (LPS), protein and mRNA of ICAM-1 were measured by Western blotting and RT-PCR respectively in different organs of BALB/c mice administered intraperitoneally with 5 mg/kg LPS. The results showed that the constitutive expression of ICAM-1 protein and mRNA was the greatest in the lungs, followed by the spleen, kidney and intestine. After LPS stimulation, the upregulation of ICAM-1 was still greatest in the lungs, followed by the liver, spleen, heart, kidney and intestine. Compared with the normal mice, the expression of ICAM-1 protein in endotoxic shocked mice increased by 4.5-fold in the lungs, 3.0-fold in the kidney, 1.5-fold in the spleen; the expression in the liver and heart was negative under normal condition and changed into positive during endotoxic shock; but ICAM-1 expression in the intestine did not change significantly. The expression of ICAM-1 mRNA also increased consistently. These data highlight that LPS can up-regulate ICAM-1 protein and mRNA expression in different tissues of the mice with endotoxic shock. The difference in ICAM-1 expression among the organs may lead to different sensitivity of organ damage in endotoxic shock. This suggests that inhibition of ICAM-1 expression may be a useful principle for prevention and treatment of endotoxic shock.
Animals ; Intercellular Adhesion Molecule-1 ; biosynthesis ; Kidney ; metabolism ; Lipopolysaccharides ; Lung ; metabolism ; Male ; Mice ; Mice, Inbred BALB C ; RNA, Messenger ; biosynthesis ; Shock, Septic ; chemically induced ; metabolism

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Role of melatonin in spatial learning and memory in rats and its mechanism.

Yin FENG ; Lie-Xiong ZHANG ; Dong-Man CHAO

Acta Physiologica Sinica.2002;54(1):65-70.

It has been suggested that melatonin is involved in learning and memory. In the present study, we investigated the effects of melatonin on spatial learning and memory in rats, using Morris water maze and electrophysiological methods. The results are as follows. (1) During a six-day water maze training, the mean escape latency of melatonin group in the last 4 days was 30.02+/-3.6 s, and that of control group was 18.44+/-2.7 s (P<0.01). The crossing annulus coefficient of melatonin group was 25.68+/-2.32%, and that of control group was 43.33+/-2.85% (P<0.01). (2) Microinjection of melatonin into CA1 area inhibited long-term potentiation (LTP). Sixty minutes after tetanus, the field excitory postsynaptic potentials (fEPSP) slope of group C (n=7 0.5 microliter saline) was 169.71+/-6.48 % of the baseline, and that of group M2 (n=6, 2 microgram melatonin) was 114.28+/-1.80% of the baseline. The difference is significant (P<0.01). (3) We also investigated the effects of melatonin on LTP after administration of scopolamine. Sixty minutes after tetanus, the fEPSP slope of group SM (n=6, 2 microgram scopolamine before 2 microgram melatonin) was 113.70+/-5.55% of the baseline. It showed a significant decrease compared with group C (P<0.01). However, there was no difference between groups SM and M2 (P>0.05, i.v.). The results obtained by applying melatonin after bicuculline were different from those after scopolamine. Sixty minutes after tetanus, the fEPSP slope of group BM (n=7, 1 microgram bicuculline before 2 microgram melatonin) was 162.29+/>10.52% of the baseline. Compared with group C, there is no significant difference (P>0.05); but compared with group M2, the difference is significant (P<0.01). Our results showed that application of melatonin in rats significantly inhibited not only spatial learning and memory, but also LTP in CA1 area. Furthermore, the results indicate that the inhibition of LTP by melatonin may not be mediated by cholinergic system, but may be through the modulation of GABAergic system.
Animals ; Bicuculline ; pharmacology ; Female ; Hippocampus ; drug effects ; physiology ; Learning ; drug effects ; Long-Term Potentiation ; drug effects ; Male ; Melatonin ; pharmacology ; Rats ; Rats, Sprague-Dawley ; Scopolamine Hydrobromide ; pharmacology ; Space Perception ; drug effects

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Propofol depresses c -fos expression of NOS neurons in the spinal cord of rats with inflammatory pain.

Ming YAN ; Li-Cai ZHANG ; Ti-Jun DAI ; Yin-Ming ZHENG ; Shi-Ming DUAN

Acta Physiologica Sinica.2002;54(1):60-64.

In formalin pain model, the effect of propofol on Fos expression in the spinal cord was examined by means of c -fos oncogene immunohistochemistry and NADPH-d histochemistry. Fos-like immunoreactive (FLI) neurons were mainly found in the ipsilateral dorsal horn after injection of formalin, some of which were FLI/NOS double-labeled neurons. Most of the FLI or FLI/NOS double-labeled neurons were observed in the medial part of lamina and the outer lamina . Before or after injection of formain, i.p. injection of propofol significantly decreased the number of FLI and FLI/NOS double-labeled neurons in all laminae (P<0.05 or P<0.01). By single i.p. injection of propofol or normal saline, few FLI neurons were found in the spinal cord. The results suggest that the antinociceptive function of propofol is possibly involved in the depression of the NOS neurons in the spinal cord.
Animals ; Female ; Formaldehyde ; Male ; Neurons ; metabolism ; Nitric Oxide Synthase ; metabolism ; Pain ; chemically induced ; metabolism ; Propofol ; pharmacology ; Proto-Oncogene Proteins c-fos ; biosynthesis ; Rats ; Rats, Sprague-Dawley ; Spinal Cord ; metabolism

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Roles of entopeduncular nucleus in acupuncture analgesia and caudate-putamen nucleus stimulation-induced analgesia.

Guo-Ji WU ; Zheng-Qiu CHEN ; Hong SHI

Acta Physiologica Sinica.2002;54(1):55-59.

The present study was to investigate whether entopeduncular nucleus (EP) is involved in caudate-putamen nucleus (CPu) stimulation-induced analgesia and in acupuncture analgesia. It was found that the foot-withdrawal latency elicited by radiant heat exposure was increased after electroacupuncture analgesia (EA), and the nociceptive responses of neurons in parafascicular nucleus (Pf) were inhibited after EA or after excitation of CPu neurons in normal rats, but the foot-withdrawal latency and nociceptive responses of Pf neurons were unchanged by EA or excitation of CPu in the rats with lesion of EP by local application of kainic acid. The results obtained with microinjeciton of saline instead of kainic acid into the EP were the same with those in the nonlesioned control group. The differences in the results between the lesion group and the other groups were significant ( <0.05). It is suggested that EP is involved in acupuncture analgesia and also plays an important role in caudate-putamen nucleus stimulation-induced analgesia.
Acupuncture Analgesia ; Animals ; Caudate Nucleus ; physiology ; Electroacupuncture ; Electrophysiology ; Entopeduncular Nucleus ; physiology ; Female ; Male ; Rats ; Rats, Wistar

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Effects of intracarotid injection of 17beta-estradiol on electrical activity of rostral ventrolateral medullary neurons in male rats.

Sheng WANG ; Rui-Rong HE

Acta Physiologica Sinica.2002;54(1):47-54.

The purpose of this study was to determine the effects of 17beta-estradiol (E(2)) on electrical activity of the rostral ventrolateral medulla (RVLM) neurons in rats. Male Sprague-Dawley rats were anesthetized with urethane (1.0 g/kg) and subjected to sino-aortic denervation. Blood pressure, heart rate and spontaneous discharge of RVLM neurons were recorded simultaneously. Intracarotid injection of E(2) (10 ng/kg) decreased the discharge rate from 14.46+/-0.47 to 9.73+/-0.33 spikes/s (P<0.001) in 25 out of 30 RVLM neurons, while blood pressure and heart rate showed no significant change. The inhibitory effect of E(2) on RVLM neuronal activity was rapid at the onset (within 1 min) and long-lasting (>5 min). Prior administration of antiestrogen tamoxifen (TAM) did not affect the effect of E(2). However, pretreatment with N( )-nitro-L-arginine-methyl ester (L-NAME), an inhibitor of nitric oxide (NO) synthase, significantly attenuated the inhibitory effect of E(2). In addition, NO donor 3-morpholinosydnonimine (SIN-1) potentiated the effect of E(2). These results suggest that E(2) may inhibit spontaneous electrical activity of RVLM neurons, an effect which is mediated by the activation of NOS with the resultant of NO release via nongenomic actions.
Animals ; Carotid Arteries ; Electrophysiology ; Estradiol ; pharmacology ; Injections, Intra-Arterial ; Male ; Medulla Oblongata ; cytology ; drug effects ; physiology ; Neurons ; drug effects ; physiology ; Nitric Oxide ; metabolism ; Rats ; Rats, Sprague-Dawley

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Effects of regulatory peptides on adhesion of eosinophil to bronchial epithelial cells.

Yong TAN ; Xiao-Qun QIN ; Cha-Xiang GUAN ; Chang-Qing ZHANG

Acta Physiologica Sinica.2002;54(1):43-46.

To explore the roles of regulatory peptides in the process of various anaphylactic inflammation of the airway, we observed the influence of four peptides, i.e., vasoactive intestinal peptide (VIP), epidermal growth factor (EGF), endothelin-1 (ET-1), and calcitonin gene-related peptide (CGRP), on the adhesion of eosinophil (EOS) to unstimulated and O(3)-stressed bronchial epithelial cells (BEC). From the experiments we observed that VIP and EGF decreased EOS adherence to O(3)-stressed BEC and downregulated airway inflammation; ET-1 and CGRP increased the adhesion of EOS to BEC in the inflammatory process; and CGRP aggravated O(3)-stressed reactions. The effects of ET-1 and CGRP were inhibited by W(7)and H(7). Anti-ICAM-1 antibody inhibited the adhesion of EOS to BEC, which brings to light that EOS adherence to BEC may be related to the expression of ICAM-1 of BEC.
Animals ; Antibodies ; pharmacology ; Bronchi ; cytology ; Cell Adhesion ; drug effects ; physiology ; Cells, Cultured ; Endothelin-1 ; pharmacology ; Eosinophils ; physiology ; Epidermal Growth Factor ; pharmacology ; Epithelial Cells ; physiology ; Female ; Intercellular Adhesion Molecule-1 ; immunology ; physiology ; Male ; Rabbits ; Vasoactive Intestinal Peptide ; pharmacology

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Vasodilative action of carbon monoxide on rat pulmonary artery in vitro.

Xue-Qin DING ; Gui-Ming LIU ; Jun-Ke WANG ; Zhuo-Ren SHENG

Acta Physiologica Sinica.2002;54(1):38-42.

The present study investigates the vasodilative action of carbon monoxide on rat pulmonary artery in vitro. After isolation of the pulmonary artery rings (PAR) from Wistar rats, an ACh concentration-response curve was generated; the PARs were incubated with the NOS inhibitor L-NAME (30 micromol/L, n=10) or the heme oxygenase inhibitor ZnPPIX (10 micromol/L)+L-NAME (30 micromol/L, n=10) for 30 min. After that, a second ACh concentration-response curve was elicited. Other isolated PARs were randomly divided into two groups: endothelium-intact group (n=8) and endothelium-denuded group (n=8). The effect of exogenous carbon monoxide (CO) on pulmonary arterial vessel tone was observed. The results showed that ACh induced a concentration-dependent pulmonary vasorelaxation. This relaxation disappeared after endothelium was denuded. The ACh induced relaxation was attenuated after pretreatment with 30 micromol/L L-NAME, and attenuated further after pretreatment with 10 micromol/L ZnPPIX+30 micromol/L L-NAME. Exogenous carbon monoxide relaxed pulmonary artery in both the endothelium-intact group and the endothelium-denuded group. These data suggest that ZnPPIX inhibits ACh induced endothelium-dependent pulmonary artery relaxation and that CO is an endothelium-derived relaxation factor, and exogenous CO can relax pulmonary artery.
Acetylcholine ; pharmacology ; Animals ; Carbon Monoxide ; pharmacology ; Dose-Response Relationship, Drug ; Endothelium, Vascular ; drug effects ; Heme Oxygenase (Decyclizing) ; antagonists & inhibitors ; In Vitro Techniques ; NG-Nitroarginine Methyl Ester ; pharmacology ; Nitric Oxide Synthase ; antagonists & inhibitors ; Protoporphyrins ; pharmacology ; Pulmonary Artery ; drug effects ; Rats ; Rats, Wistar ; Vasodilation ; drug effects

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