The Relaxant Effect of Propofol on Isolated Rat Intrapulmonary Arteries

Guangyan Zhang,Jianxiu Cui,Yijing Chen,Jue Ma 대한약리학회 2014 The Korean Journal of Physiology & Pharmacology Vol.18 No.5

Propofol is a widely used anesthetic. Many studies have shown that propofol has direct effects on bloodvessels, but the precise mechanism is not fully understood. Secondary intrapulmonary artery ringsfrom male rats were prepared and mounted in a Multi Myograph System. The following constrictorswere used to induce contractions in isolated artery rings: high K+ solution (60 mmol/L); U46619 solution(100 nmol/L); 5-hydroxytryptamine (5-HT; 3 μmol/L); or phenylephrine (Phe; 1 μmol/L). The relaxationeffects of propofol were tested on high K+ or U46619 precontracted rings. Propofol also was addedto induce relaxation of rings preconstricted by U46619 after pretreatment with the nitric oxide synthaseinhibitor NG-nitro-L-arginine methyl ester (L-NAME). The effects of propofol on Ca2+ influx via theL-type Ca2+ channels were evaluated by examining contraction-dependent responses to CaCl2 in theabsence or presence of propofol (10 to 300 μmol/L). High K+ solution and U46619 induced remarkablecontractions of the rings, whereas contractions induced by 5-HT and Phe were weak. Propofol induceddose-dependent relaxation of artery rings precontracted by the high K+ solution. Propofol also inducedrelaxation of rings precontracted by U46619 in an endothelium-independent way. Propofol at differentconcentrations significantly inhibited the Ca2+-induced contractions of pulmonary rings exposed to highK+-containing and Ca2+-free solution in a dose-dependent manner. Propofol relaxed vessels precontractedby the high K+ solution and U46619 in an endothelium-independent way. The mechanism forthis effect may involve inhibition of calcium influx through voltage-operated calcium channels (VOCCs)and receptor-operated calcium channels (ROCCs).

The Relaxant Effect of Propofol on Isolated Rat Intrapulmonary Arteries

Zhang, Guangyan,Cui, Jianxiu,Chen, Yijing,Ma, Jue The Korean Society of Pharmacology 2014 The Korean Journal of Physiology & Pharmacology Vol.18 No.5

Propofol is a widely used anesthetic. Many studies have shown that propofol has direct effects on blood vessels, but the precise mechanism is not fully understood. Secondary intrapulmonary artery rings from male rats were prepared and mounted in a Multi Myograph System. The following constrictors were used to induce contractions in isolated artery rings: high $K^+$ solution (60 mmol/L); U46619 solution (100 nmol/L); 5-hydroxytryptamine (5-HT; $3{\mu}mol/L$); or phenylephrine (Phe; $1{\mu}mol/L$). The relaxation effects of propofol were tested on high $K^+$ or U46619 precontracted rings. Propofol also was added to induce relaxation of rings preconstricted by U46619 after pretreatment with the nitric oxide synthase inhibitor $N^G$-nitro-L-arginine methyl ester (L-NAME). The effects of propofol on $Ca^{2+}$ influx via the L-type $Ca^{2+}$ channels were evaluated by examining contraction-dependent responses to $CaCl_2$ in the absence or presence of propofol (10 to $300{\mu}mol/L$). High $K^+$ solution and U46619 induced remarkable contractions of the rings, whereas contractions induced by 5-HT and Phe were weak. Propofol induced dose-dependent relaxation of artery rings precontracted by the high $K^+$ solution. Propofol also induced relaxation of rings precontracted by U46619 in an endothelium-independent way. Propofol at different concentrations significantly inhibited the $Ca^{2+}$-induced contractions of pulmonary rings exposed to high $K^+$-containing and $Ca^{2+}$-free solution in a dose-dependent manner. Propofol relaxed vessels precontracted by the high $K^+$ solution and U46619 in an endothelium-independent way. The mechanism for this effect may involve inhibition of calcium influx through voltage-operated calcium channels (VOCCs) and receptor-operated calcium channels (ROCCs).

Minus-C odorant binding protein TcasOBP7G contributes to reproduction and defense against phytochemical in the red flour beetle, Tribolium castaneum

Gao Shanshan,Zhang Xinyi,Zhou Can,Zhang Guangyan,Zhang Yong-lei,Li Rui-min,Zhang Kun-peng 한국응용곤충학회 2023 Journal of Asia-Pacific Entomology Vol.26 No.4

Insect odorant binding proteins (OBPs) paly an important role in the recognition and transmission signals. One odorant binding protein gene, TcasOBP7G, was significantly up-regulated after exposure to eucalyptol. Never theless, the causal role of TcasOBP7G in Tribolium castaneum is still unclear. Here, TcasOBP7G was cloned and characterized from T. castaneum, aligning with the typical characteristic of Minus-C OBPs. The analysis of gene expression profile showed that TcasOBP7G is highly expressed at late larval and adult stage, with particularly high expression levels in ovary and testis of adults, suggesting that TcasOBP7G might be associated with reproduction of T. castaneum. Furthermore, RNAi of TcasOBP7G led to a decrease in spawning, while the development of gonads was normal, suggesting that TcasOBP7G may medicate the reproduction of T. castaneum. Additionally, the mRNA level of TcasOBP7G was significantly increased after exposure to eucalyptol, and knockdown of TcasOBP7G resulted in an increased susceptibility of T. castaneum to eucalyptol, indicating that TcasOBP7G is associated with the tolerance of T. castaneum to eucalyptol. Altogether, these results indicate that TcasOBP7G is required for both reproduction and defense against phytochemical in T. castaneum. This study will provide a theoretical basis for the development of novel control strategies based on the olfaction of insects.

Synthesis of optically active chiral mesoporous molybdenum carbide film

Fusheng Zhang,Xintong Zheng,Cunli Wang,Dongdong Wang,Xingya Xue,Guangyan Qing 한국공업화학회 2021 Journal of Industrial and Engineering Chemistry Vol.94 No.-

A chiral nematic mesoporous molybdenum carbidefilm (CN-Mo2C) was fabricated through the selfassemblyof cellulose nanocrystal with peroxomolybdate. CN-Mo2C exhibits a tunable chiral nematicstructure by varying the ratio of constituents, enabling a surface area of 210 m2 g 1. Importantly, it showsa typical chiroptical feature through polarized optical microscopy and circular dichroism spectralanalysis. As it has an excellent conductivity of 2.410 2 S cm 1, we try to use CN-Mo2C in theelectrocatalytic HER production, presenting an efficient H2 production capacity. It is a versatile syntheticstrategy that can conveniently enable other large-area macroscopic chiral metal-based materials.

Dexmedetomidine inhibits vasoconstriction via activation of endothelial nitric oxide synthase

Lidan Nong,Jue Ma,Guangyan Zhang,Chunyu Deng,Songsong Mao,Haifeng Li,Jianxiu Cui 대한생리학회-대한약리학회 2016 The Korean Journal of Physiology & Pharmacology Vol.20 No.5

Despite the complex vascular effects of dexmedetomidine (DEX), its actions on human pulmonary resistance arteries remain unknown. The present study tested the hypothesis that DEX inhibits vascular tension in human pulmonary arteries through the endothelial nitric oxide synthase (eNOS) mediated production of nitric oxide (NO). Pulmonary artery segments were obtained from 62 patients who underwent lung resection. The direct effects of DEX on human pulmonary artery tension and changes in vascular tension were determined by isometric force measurements recorded on a myograph. Arterial contractions caused by increasing concentrations of serotonin with DEX in the presence or absence of L-NAME (endothelial nitric oxide synthase inhibitor), yohimbine (α₂-adrenoceptor antagonist) and indomethacin (cyclooxygenase inhibitor) as antagonists were also measured. DEX had no effect on endothelium-intact pulmonary arteries, whereas at concentrations of 10^–8~10^–6 mol/L, it elicited contractions in endothelium-denuded pulmonary arteries. DEX (0.3, 1, or 3×10^–9 mmol/L) inhibited serotonin-induced contraction in arteries with intact endothelium in a dose-dependent manner. L-NAME and yohimbine abolished DEX-induced inhibition, whereas indomethacin had no effect. No inhibitory effect was observed in endothelium-denuded pulmonary arteries. DEX-induced inhibition of vasoconstriction in human pulmonary arteries is mediated by NO production induced by the activation of endothelial α₂- adrenoceptor and nitric oxide synthase.

Dexmedetomidine inhibits vasoconstriction via activation of endothelial nitric oxide synthase

Nong, Lidan,Ma, Jue,Zhang, Guangyan,Deng, Chunyu,Mao, Songsong,Li, Haifeng,Cui, Jianxiu The Korean Society of Pharmacology 2016 The Korean Journal of Physiology & Pharmacology Vol.20 No.5

Despite the complex vascular effects of dexmedetomidine (DEX), its actions on human pulmonary resistance arteries remain unknown. The present study tested the hypothesis that DEX inhibits vascular tension in human pulmonary arteries through the endothelial nitric oxide synthase (eNOS) mediated production of nitric oxide (NO). Pulmonary artery segments were obtained from 62 patients who underwent lung resection. The direct effects of DEX on human pulmonary artery tension and changes in vascular tension were determined by isometric force measurements recorded on a myograph. Arterial contractions caused by increasing concentrations of serotonin with DEX in the presence or absence of L-NAME (endothelial nitric oxide synthase inhibitor), yohimbine (${\alpha}_2$-adrenoceptor antagonist) and indomethacin (cyclooxygenase inhibitor) as antagonists were also measured. DEX had no effect on endothelium-intact pulmonary arteries, whereas at concentrations of $10^{-8}{\sim}10^{-6}mol/L$, it elicited contractions in endothelium-denuded pulmonary arteries. DEX (0.3, 1, or $3{\times}10^{-9}mmol/L$) inhibited serotonin-induced contraction in arteries with intact endothelium in a dose-dependent manner. L-NAME and yohimbine abolished DEX-induced inhibition, whereas indomethacin had no effect. No inhibitory effect was observed in endothelium-denuded pulmonary arteries. DEX-induced inhibition of vasoconstriction in human pulmonary arteries is mediated by NO production induced by the activation of endothelial ${\alpha}_2$-adrenoceptor and nitric oxide synthase.

The bifunctional effect of propofol on thromboxane agonist (U46619)-induced vasoconstriction in isolated human pulmonary artery

Ning Hao,Zhaojun Wang,Sujuan Kuang,Guangyan Zhang,Chunyu Deng,Jue Ma,Jianxiu Cui 대한생리학회-대한약리학회 2017 The Korean Journal of Physiology & Pharmacology Vol.13 No.3

Propofol is known to cause vasorelaxation of several systemic vascular beds. However, its effect on the pulmonary vasculature remains controversial. In the present study, we investigated the effects of propofol on human pulmonary arteries obtained from patients who had undergone surgery. Arterial rings were mounted in a Multi-Myograph system for measurement of isometric forces. U46619 was used to induce sustained contraction of the intrapulmonary arteries, and propofol was then applied (in increments from 10-300 μM). Arteries denuded of endothelium, preincubated or not with indomethacin, were used to investigate the effects of propofol on isolated arteries. Propofol exhibited a bifunctional effect on isolated human pulmonary arteries contracted by U46619, evoking constriction at low concentrations (10-100 μM) followed by secondary relaxation (at 100-300 μM). The extent of constriction induced by propofol was higher in an endothelium-denuded group than in an endothelium-intact group. Preincubation with indomethacin abolished constriction and potentiated relaxation. The maximal relaxation was greater in the endothelium-intact than the endothelium-denuded group. Propofol also suppressed CaCl₂-induced constriction in the 60 mM K⁺-containing Ca²⁺-free solution in a dose-dependent manner. Fluorescent imaging of Ca²⁺ using fluo-4 showed that a 10 min incubation with propofol (10-300 μM) inhibited the Ca²⁺ influx into human pulmonary arterial smooth muscle cells induced by a 60 mM K⁺-containing Ca²⁺-free solution. In conclusion, propofol-induced arterial constriction appears to involve prostaglandin production by cyclooxygenase in pulmonary artery smooth muscle cells and the relaxation depends in part on endothelial function, principally on the inhibition of calcium influx through L-type voltage-operated calcium channels.

The bifunctional effect of propofol on thromboxane agonist (U46619)-induced vasoconstriction in isolated human pulmonary artery

Hao, Ning,Wang, Zhaojun,Kuang, Sujuan,Zhang, Guangyan,Deng, Chunyu,Ma, Jue,Cui, Jianxiu The Korean Society of Pharmacology 2017 The Korean Journal of Physiology & Pharmacology Vol.21 No.6

Propofol is known to cause vasorelaxation of several systemic vascular beds. However, its effect on the pulmonary vasculature remains controversial. In the present study, we investigated the effects of propofol on human pulmonary arteries obtained from patients who had undergone surgery. Arterial rings were mounted in a Multi-Myograph system for measurement of isometric forces. U46619 was used to induce sustained contraction of the intrapulmonary arteries, and propofol was then applied (in increments from $10-300{\mu}m$). Arteries denuded of endothelium, preincubated or not with indomethacin, were used to investigate the effects of propofol on isolated arteries. Propofol exhibited a bifunctional effect on isolated human pulmonary arteries contracted by U46619, evoking constriction at low concentrations ($10-100{\mu}m$) followed by secondary relaxation (at $100-300{\mu}m$). The extent of constriction induced by propofol was higher in an endothelium-denuded group than in an endothelium-intact group. Preincubation with indomethacin abolished constriction and potentiated relaxation. The maximal relaxation was greater in the endothelium-intact than the endothelium-denuded group. Propofol also suppressed $CaCl_2$-induced constriction in the 60 mM $K^+$-containing $Ca^{2+}$-free solution in a dose-dependent manner. Fluorescent imaging of $Ca^{2+}$ using fluo-4 showed that a 10 min incubation with propofol ($10-300{\mu}m$) inhibited the $Ca^{2+}$ influx into human pulmonary arterial smooth muscle cells induced by a 60 mM $K^+$-containing $Ca^{2+}$-free solution. In conclusion, propofol-induced arterial constriction appears to involve prostaglandin production by cyclooxygenase in pulmonary artery smooth muscle cells and the relaxation depends in part on endothelial function, principally on the inhibition of calcium influx through L-type voltage-operated calcium channels.

The bifunctional effect of propofol on thromboxane agonist (U46619)-induced vasoconstriction in isolated human pulmonary artery

Jianxiu Cui,Zhaojun Wang,Sujuan Kuang,Guangyan Zhang,Chunyu Deng,Jue Ma,Jianxiu Cui 대한약리학회 2017 The Korean Journal of Physiology & Pharmacology Vol.21 No.6

Propofol is known to cause vasorelaxation of several systemic vascular beds. However, its effect on the pulmonary vasculature remains controversial. In the present study, we investigated the effects of propofol on human pulmonary arteries obtained from patients who had undergone surgery. Arterial rings were mounted in a Multi-Myograph system for measurement of isometric forces. U46619 was used to induce sustained contraction of the intrapulmonary arteries, and propofol was then applied (in increments from 10-300 μM). Arteries denuded of endothelium, preincubated or not with indomethacin, were used to investigate the effects of propofol on isolated arteries. Propofol exhibited a bifunctional effect on isolated human pulmonary arteries contracted by U46619, evoking constriction at low concentrations (10-100 μM) followed by secondary relaxation (at 100-300 μM). The extent of constriction induced by propofol was higher in an endothelium-denuded group than in an endothelium-intact group. Preincubation with indomethacin abolished constriction and potentiated relaxation. The maximal relaxation was greater in the endothelium-intact than the endothelium-denuded group. Propofol also suppressed CaCl2-induced constriction in the 60 mM K+-containing Ca2+-free solution in a dose-dependent manner. Fluorescent imaging of Ca2+ using fluo- 4 showed that a 10 min incubation with propofol (10-300 μM) inhibited the Ca2+ influx into human pulmonary arterial smooth muscle cells induced by a 60 mM K+- containing Ca2+-free solution. In conclusion, propofol-induced arterial constriction appears to involve prostaglandin production by cyclooxygenase in pulmonary artery smooth muscle cells and the relaxation depends in part on endothelial function, principally on the inhibition of calcium influx through L-type voltage-operated calcium channels.

Tissue Inhibitor of Metalloproteinase-1 Pro-motes NIH3T3 Fibroblast Proliferation by Activating p-Akt and Cell Cycle Progression

Yang Lu,Shuxin Liu,Shujia Zhang,Guangyan Cai,Hongwei Jiang,Huabin Su,Xiaofan Li,Quan Hong,Xueguang Zhang,Xiangmei Chen 한국분자세포생물학회 2011 Molecules and cells Vol.31 No.3

Tissue inhibitor of metalloproteinase-1 (TIMP-1) plays various roles in cell growth in different cell types. However, few studies have focused on TIMP-1’s effect on fibroblast cells. In this study, we investigated the effects of TIMP-1 overexpression on NIH3T3 fibroblast proliferation and potential transduction signaling pathways involved. Overexpression of TIMP-1, by transfection of the pLenti6/ V5-DESTTIMP-1 plasmid, significantly promoted NIH3T3 proliferation as determined by the BrdU array. Neither 5 nor 15 nM GM6001 (matrix metalloproteinase system inhibitor) affected NIH3T3 proliferation, but 45 nM GM6001 inhibited proliferation. TIMP-1 overexpression activated the p-Akt pathway, but not the p-ERK or p-p38 pathway. In TIMP-1-transfected cells, cyclinD1 was upregulated and p21CIP1 and p27^(KIP1) were downregulated, which promoted cell entry into the S and G2/M phases. The PI3-K inhibitor LY294002 abolished the TIMP-1-induced effects. Overexpression of intracellular TIMP-1 stimulated NIH3T3 fibroblast proliferation in a matrix metalloproteinase (MMP)-independent manner by activating the p-Akt pathway and related cell cycle progression.