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Urocortin protects against ischemic and reperfusion injury via a MAPK-dependent pathway

JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第12期275卷 8508-8514页

作者： Brar, BK Jonassen, AK Stephanou, A Santilli, G Railson, J Knight, RA Yellon, DM Latchman, DS Univ London Inst Child Hlth London WC1N 1EH England UCL Hosp & Med Sch Hatter Inst Cardiol London WC1E 6DB England Natl Heart & Lung Inst Dept Cyst Fibrosis London SW3 6LR England

Urocortin (UCN) is a peptide related to hypothalamic corticotrophin-releasing hormone and binds with high affinity to corticotrophin-releasing hormone receptor-2 beta, which is expressed in the heart. In this study, we report that UCN prevented cell death when administered to primary cardiac myocyte cultures both prior to simulated hypoxia/ischemia and at the point of reoxygenation after simulated hypoxia/ischemia. UCN-mediated cell survival was measured by trypan blue exclusion, 3'-OH end labeling of DNA (TUNEL), annexin V, and fluorescence-activated cell sorting. To explore the mechanisms that could be responsible for this effect, we investigated the involvement of MAPK-dependent pathways. UCN caused rapid phosphorylation of ERK1/2-p42/44, and PD98059, which blocks the MEK1-ERK1/2-p42/44 cascade, also inhibited the survival-promoting effect of UCN. Most important, UCN reduced damage in isolated rat hearts ex vivo subjected to regional ischemia/reperfusion, with the protective effect being observed when UCN was given either prior to ischemia or at the time of reperfusion after ischemia. This suggests a novel function of UCN as a cardioprotective agent that could act when given after ischemia, at reperfusion.

关键词：细胞死亡/药物作用细胞低氧/药物作用细胞培养的促肾上腺皮质素释放激素/药理学类黄酮物质/药理学心脏/药物作用 MAP激酶信号系统丝裂原激活蛋白激酶类/拮抗剂和抑制剂丝裂原激活蛋白激酶类/代谢心肌梗死/药物疗法心肌缺血/药物疗法心肌再灌注损伤/预防和控制心肌/细胞学心肌/酶学大鼠 Wistar 尿皮质素类动物男(雄)性大鼠

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Interleukin 1β protects mice from Fas-mediated hepatocyte apoptosis and death

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GASTROENTEROLOGY 1999年第3期117卷 661-668页

作者： Takehara, T Hayashi, N Tatsumi, T Kanto, T Mita, E Sasaki, Y Kasahara, A Hori, M Osaka Univ Grad Sch Med Dept Mol Therapeut Osaka 5650871 Japan Osaka Univ Grad Sch Med Dept Internal Med & Therapeut Osaka 5650871 Japan Osaka Univ Grad Sch Med Dept Gen Med Osaka 5650871 Japan

Background & Aims: Fas-mediated apoptosis is one of the major death processes of hepatocytes in liver diseases. The aim of this study was to determine whether interleukin (IL)-1 beta regulates the Fas-mediated apoptotic process of differentiated hepatocytes in vivo. Methods: IL-1 beta was injected into Balb/cA mice 5 hours before lethal challenge with agonistic anti-fas administration. Survival and hepatocyte apoptotic process of these mice were examined. Results: IL-1 beta pretreatment prolonged animal survival in a dose-dependent manner, and 500 ng of IL-1 beta completely protected mice from lethality. Both serum alanine aminotransferase value and hepatic DNA fragmentation were significantly suppressed by IL-1 beta pretreatment. IL-1 beta affected neither hepatic distribution of anti-fas antibody nor Fas expression levels on hepatocytes but significantly suppressed Fas-induced activation of hepatic caspase 3-like protease. Suppression of Fas-induced activation of the caspase by IL-1 beta was diminished by coadministration with D-galactosamine and reversed by coinjection with an excess amount of uridine. Conclusions: These results suggest that IL-1 beta suppresses Fas-mediated hepatocyte apoptosis by inducing molecule(s) that suppress the apoptosis control machinery upstream of caspase 3. This observation raises the possibility that IL-1 beta acts as a negative regulator of Fas-mediated hepatocyte apoptosis during liver injury.

关键词：丙氨酸转氨酶/血液细胞凋亡/药物作用细胞凋亡/生理学半胱氨酸天冬氨酸蛋白酶3 半胱氨酸天冬氨酸蛋白酶/代谢细胞死亡/药物作用细胞死亡/生理学 DNA碎片裂酶前体/代谢流式细胞术白细胞介素1/药理学白细胞介素1/生理学肝/细胞学肝/药物作用肝/代谢小鼠近交BALBC 动物女(雌)性小鼠

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Photobiological properties of positively charged methylene violet analogs

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PHOTOCHEMISTRY AND PHOTOBIOLOGY 2000年第1期71卷 20-28页

作者： Houghtaling, MA Perera, R Owen, KE Wagner, S Kuhn, RJ Morrison, H Purdue Univ Dept Chem W Lafayette IN 47907 USA Purdue Univ Dept Sci Biol W Lafayette IN 47907 USA Amer Res Cross Biomed Serv Jerome H Holland Lab Med Sci Rockville MD USA

O-Methyl methylene violet (OMeMV), O-methyl bromomethylene violet (OMeBrMV) and O-methyl iodomethylene violet (OMeIMV) have been prepared in order to test their potential utility as anti-viral and anti-tumor phototoxic dyes. Rates of photosensitized toxicity of KB cells with 633 mn irradiation are (x10(-19) photon(-1)): 2.4, 2.2, 1.9 and 0.17 for OMeIMV, OMeBrMV, methylene violet (MV) and OMeMV, respectively. Rates of photosensitized inactivation of Sindbis virus in phosphate-buffered saline with 633 nn irradiation are (x10(-18) photon(-1)): 3.3, 1.8, 0.99, 0.15 for MV, OMeIMV, OMeBrMV and OMeMV, respectively, Quantum efficiencies for singlet oxygen formation were determined as OMeIMV, 0.64;OMeBrMV, 0.40;OMeMV, 0.054, Titration of the dyes with double-stranded (ds)DNA resulted in bathochromic shifts and hypochromic effects in the visible absorption spectra, Association constants for interaction of the methylated dyes with dsDNA of similar to 1 x 10(5) M-1 were determined by Scatchard analysis of equilibrium dialysis and UV absorption titration data. Photolysis of the halogenated dyes with DNA under argon led to covalent bond formation with the nucleic acid;there was no evidence of covalent binding in the dark.

关键词：抗病毒药/化学抗病毒药/药理学细胞死亡/药物作用 DNA/化学甲基化分子结构酚噻嗪类/化学酚噻嗪类/药理学光生物学光化学 Sindbis病毒/药物作用光谱分析

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Low-dose Carbicarb improves cerebral outcome after asphyxial cardiac arrest in rats

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ANNALS OF EMERGENCY MEDICINE 2002年第4期39卷 359-365页

作者： Katz, LM Wang, YF Rockoff, S Bouldin, TW Univ N Carolina Sch Med Dept Emergency Med Chapel Hill NC USA Univ N Carolina Sch Med Dept Pathol & Lab Med Chapel Hill NC USA Lake Erie Coll Osteopath Med Erie PA USA

Study objective: Controversy surrounds the use of buffers during cardiac arrest to correct acidosis. The objective of this study was to determine whether attenuation or neutralization of cerebral acidosis by Carbicarb alters hippocampal glutamate levels, neuronal cell death, and neurologic deficits after reperfusion from asphyxial cardiac arrest in rats. Methods: Bats were prospectively randomized to either a control (n=45), low-dose Carbicarb (LDC;3 mL/kg, n=45), or high-dose Carbicarb (HDC;6 mL/kg, n=45) group in a blinded fashion during resuscitation after 8 minutes of asphyxial cardiac arrest. Microdialysis was used to assess brain pH and glutamate. A neurologic deficit score and neuronal cell death in the hippocampus were determined at day 7. Results: Resuscitation was greatest in LDC rats (42/45) and least in HDC rats (28/45) versus that in control rats (34/45). Brain pH was higher in the LDC and HDC rats 10 minutes after resuscitation and remained higher than that of control rats for 120 minutes after resuscitation. Glutamate levels at 10 to 120 minutes after reperfusion were lowest in the LDC rats. LDC rats had the lowest neurologic deficit score (1 2) versus that of control rats (13 8) and HDC rats (19 6). Hippocampal neuronal cell death was lowest in LDC rats (30 20) versus that in control rats (86 47) and HDC rats (233 85). Conclusion: LDC administered during resuscitation from asphyxial cardiac arrest attenuated acidosis, improved resuscitation, and reduced neurologic deficits and the number of dead hippocampal neurons. Neutralization of cerebral acidosis with HDC increased the number of dead hippocampal neurons and neurologic deficits after resuscitation from cardiac arrest in rats.

关键词：酸中毒/药物疗法酸中毒/病因学窒息/并发症脑/代谢脑缺血/药物疗法脑缺血/病因学脑缺血/代谢碳酸盐类/治疗应用细胞死亡/药物作用疾病模型动物复方合剂谷氨酸/药物作用谷氨酸/代谢心脏停搏/并发症海马/代谢神经元/药物作用功能恢复/药物作用再灌注损伤/药物疗法再灌注损伤/病因学碳酸氢钠/治疗应用治疗结果动物大鼠

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Chemotherapy for advanced hormone refractory prostate cancer

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UROLOGY 1999年第6A期54卷 30-35页

作者： Petrylak, DP Columbia Presbyterian Med Ctr Div Med Oncol Genitourinary Oncol Program New York NY 10032 USA

Men with metastatic prostate cancer treated with androgen ablation respond rapidly and often dramatically to therapy, with improvement of bone pain, regression of soft tissue metastases, and declines in serum prostate-specific antigen (PSA). Unfortunately, few treatment options are available to men who progress after hormone therapy. Recent studies in the mechanism of anticancer drug action have focused on the proteins that regulate apoptosis or programmed cell death as a target for the treatment of hormone-resistant prostate cancer. New treatments are now being designed with both resistance and apoptotic pathways in mind. US Food and Drug Administration (FDA) approval of the combination of mitoxantrone and prednisone for the palliation of bone pain in men with hormone refractory prostate cancer demonstrates that chemotherapy can be effective. Two randomized trials have demonstrated the superiority of mitoxantrone combined with a corticosteroid over corticosteroid therapy in alleviating bone pain. The combination of estramustine with vinblastine, or VP-16, is commonly used in clinical practice with both regimens demonstrating significant PSA declines. When estramustine is combined with either paclitaxel or docetaxel in vitro, greater than additive in vitro cytotoxicity is noted. Phase I and II studies of taxane-based therapy in hormone refractory prostate cancer demonstrate improved survival when compared with historical controls, but phase III studies are necessary to confirm these preliminary observations. (C) 1999, Elsevier Science Inc.

关键词：抗肿瘤药激素/治疗应用抗肿瘤联合化疗方案/治疗应用细胞死亡/药物作用临床试验(主题) 肿瘤激素依赖性/药物疗法肿瘤激素依赖性/死亡率肿瘤激素依赖性/病理学前列腺肿瘤/药物疗法前列腺肿瘤/死亡率前列腺肿瘤/病理学存活率人类男(雄)性

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RB-dependent S-phase response to DNA damage

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MOLECULAR AND CELLULAR BIOLOGY 2000年第20期20卷 7751-7763页

作者： Knudsen, KE Booth, D Naderi, S Sever-Chroneos, Z Fribourg, AF Hunton, IC Feramisco, JR Wang, JYJ Knudsen, ES Univ Cincinnati Dept Cell Biol Cincinnati OH 45267 USA Univ Calif San Diego Dept Biol La Jolla CA 92093 USA Univ Calif San Diego Ctr Canc La Jolla CA 92093 USA Univ Calif San Diego Sch Med La Jolla CA 92093 USA

The retinoblastoma tumor suppressor protein (RB) is a potent inhibitor of cell proliferation. RB is expressed throughout the cell cycle, but its antiproliferative activity is neutralized by phosphorylation during the G(1)/S transition. RB plays an essential role in the G(1) arrest induced by a variety of growth inhibitory signals. In this report, RB is shown to also be required for an intra-S-phase response to DNA damage. Treatment with cisplatin, etoposide, or mitomycin C inhibited S-phase progression in Rb+/+ but not in Rb-/- mouse embryo fibroblasts. Dephosphorylation of RB in S-phase cells temporally preceded the inhibition of DNA synthesis. This S-phase dephosphorylation of RB and subsequent inhibition of DNA replication was observed in p21(Cip1)-deficient cells. The induction of the RB-dependent intra-S-phase arrest persisted for days and correlated with a protection against DNA damage-induced cell death. These results demonstrate that RB plays a protective role in response to genotoxic stress by inhibiting cell cycle progression in G(1) and in S phase.

关键词：载体蛋白质类细胞周期蛋白质类细胞死亡/药物作用顺铂/药理学细胞周期蛋白A/拮抗剂和抑制剂细胞周期蛋白A/代谢周期素依赖激酶抑制剂p21 细胞周期蛋白类/缺乏细胞周期蛋白类/遗传学细胞周期蛋白类/生理学 DNA/生物合成 DNA损伤/药物作用 DNA复制/药物作用 DNA结合蛋白质类 E2F转录因子类依托泊甙/药理学成纤维细胞流式细胞术荧光抗体技术基因缺失小鼠基因敲除丝裂霉素/药理学诱变力试验磷酰化/药物作用视网膜母细胞瘤蛋白质/遗传学视网膜母细胞瘤蛋白质/代谢视网膜母细胞瘤结合蛋白1 S期/药物作用转录因子DP1 转录因子/拮抗剂和抑制剂转录因子/代谢动物小鼠大鼠

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Stability of oxygen deprivation in glass culture vessels facilitates fast reproducible cell death to cortical neurons under simulated ischemia

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ANALYTICAL BIOCHEMISTRY 2002年第1期306卷 149-152页

作者： Munns, SE Arthur, PG Univ Western Australia Dept Biochem Crawley WA 6009 Australia Western Australian Inst Med Res Perth WA Australia

Glass petri dishes provide tight control of oxygen concentration during continuous nitrogen gassing to cultured cells. This control has led to a quick and highly reproducible simulated ischemic model of cortical neuron death in vitro. Twenty-five minutes of simulated ischemia was required for 92% death in cortical neuron cultures on glass. The contamination of leached oxygen from plastic culture vessels, in comparative experiments, necessitates longer times of simulated ischemia (120 min) to achieve similar cell death. Steady-state release of oxygen from plastic petri dishes was observed for up to 60 min of nitrogen gassing, providing a metabolic environment contrary to that of anoxia. Further investigations with models of simulated ischemia in glass culture vessels could answer some criticisms of in vitro models and their relevance to in vivo situations (10).

关键词：脑缺血/代谢脑缺血/病理学细胞培养技术/仪器和设备细胞培养技术/方法细胞死亡/药物作用细胞低氧/生理学细胞存活/药物作用细胞培养的大脑皮质/药物作用大脑皮质/胚胎学大脑皮质/病理学玻璃糖酵解 L-乳酸脱氢酶/分析神经元/药物作用神经元/代谢神经元/病理学氧/代谢氧/药理学可重复性结果动物大鼠

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Areca nut extract up-regulates prostaglandin production, cyclooxygenase-2 mRNA and protein expression of human oral keratinocytes

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CARCINOGENESIS 2000年第7期21卷 1365-1370页

作者： Jeng, JH Ho, YS Chan, CP Wang, YJ Hahn, LJ Lei, D Hsu, CC Chang, MC Chang Gung Inst Nursing Team Biomed Sci Tao Yuan 33333 Taiwan Natl Cheng Kung Univ Med Ctr Grad Inst Environm Sci Tainan 70101 Taiwan Chang Gung Mem Hosp Dept Dent Taipei 10591 Taiwan Taipei Med Coll Inst Med Technol Taipei Taiwan Natl Taiwan Univ Grad Inst Clin Dent Sci Lab Dent Pharmacol & Toxicol Taipei 10764 Taiwan

There art! about 600 million betel quid (BQ) chewers in the world. BQ chewing is associated with increased incidence of oral cancer and submucous fibrosis, ill this study, areca nut (AN) extract (200-800 mu g/ml) induced the prostaglandin E-2 (PCE2) production by 1.4-3.4-fold and 6-keto-PGF(1 alpha) production by 1.1-1.7-fold of gingival keratinocytes (GK), respectively, Following 24 h of exposure. Exposure of GK to AN extract (>400 mu g/ml) led to cell retraction and intracellular vacuoles formation. At concentrations of 800 and 1200 mu g/ml, AN extract induced cell death at 21-24 and 32-52 % as detected by MTT assay and cellular lactate dehydrogenase release, respectively. Interestingly, AN-induced morphological changes of GK are reversible, GK can still proliferate following exposure to AN extract. Cytotoxicity of AN extract cannot be inhibited by indomethacin (1 mu M) and aspirin (50 mu M), indicating that prostaglandin (PG) production is not the major factor responsible for AN cytotoxicity, PGE(2) exhibited little effect on the growth of GK at concentrations ranging from 100-1000 pg/ml. Stimulating GK production of PGs by AN extract could be due to induction of cycloosygenase-2 (COX-2) mRNA expression and protein production. These results suggest that AN ingredients are critical in the pathogenesis of oral submucous fibrosis and oral cancer via their stimulatory effects on the PGs, COX-2 production and associated tissue inflammatory responses, AN cytotoxicity to CK is not directly mediated by COX-2 stimulation and PG production.

关键词： 6-酮前列腺素F1α/生物合成印迹法蛋白质细胞死亡/药物作用细胞大小/药物作用细胞培养的环氧化酶2 地诺前列酮/生物合成剂量效应关系药物牙龈/细胞学牙龈/药物作用牙龈/酶学牙龈/代谢同工酶类/生物合成同工酶类/遗传学角蛋白细胞/药物作用角蛋白细胞/酶学角蛋白细胞/代谢膜蛋白质类植物提取物/毒性植物药用前列腺素内过氧化物合酶类/生物合成前列腺素内过氧化物合酶类/遗传学 RNA 信使/生物合成 RNA 信使/代谢增量调节/药物作用空泡/药物作用动物牛人类

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Neuronal apoptosis induced by β-amyloid is mediated by caspase-8

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NEUROBIOLOGY OF DISEASE 1999年第5期6卷 440-449页

作者： Ivins, KJ Thornton, PL Rohn, TT Cotman, CW Univ Calif Irvine Inst Brain Aging & Dementia Irvine CA 92697 USA

The Alzheimer disease-associated beta-amyioid peptide has been shown to induce apoptotic neuronal death. In the present study, we test the hypothesis that the apoptotic pathway activated by beta-amyloid is similar to the pathway activated by the Fas/TNFR family of death receptors, which requires caspase-8 activity and adaptor proteins such as FADD. We demonstrate that the selective caspase-8 inhibitor IETD-fmk blocks neuronal death induced by beta-amyioid. Furthermore, using viral-mediated gene delivery, we show that neurons expressing dominant-negative FADD are protected from apoptosis induced by beta-amyloid. Together these results indicate that the apoptotic pathway activated by beta-amyloid requires both caspase-8 activity and FADD. These findings further support the hypothesis that beta-amylold might initiate apoptosis by cross-linking death receptors of the Fas/TNFR family. (C) 1999 Academic Press.

关键词：衔接蛋白质类信号转导淀粉样β蛋白/毒性细胞凋亡/药物作用细胞凋亡/生理学载体蛋白质类/代谢半胱氨酸天冬氨酸蛋白酶8 半胱氨酸天冬氨酸蛋白酶9 半胱氨酸天冬氨酸蛋白酶/拮抗剂和抑制剂半胱氨酸天冬氨酸蛋白酶/代谢细胞死亡/药物作用细胞培养的酶抑制剂/药理学 Fas相关死亡结构域蛋白质海马/细胞学海马/生理学模型神经学神经元/细胞学神经元/药物作用神经元/生理学肽碎片/毒性信号传导星状孢子素/药理学动物人类大鼠

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A longitudinal study of the effects of prenatal ethanol exposure on neuronal acquisition and death in the principal sensory nucleus of the trigeminal nerve: interaction with changes induced by transection of the infraorbital nerve

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JOURNAL OF NEUROCYTOLOGY 1999年第12期28卷 999-1015页

作者： Miller, MW Vet Affairs Med Ctr Res Serv Iowa City IA 52246 USA Univ Iowa Coll Med Dept Psychiat Iowa City IA 52242 USA Univ Iowa Coll Med Dept Pharmacol Iowa City IA 52242 USA

The present study determines (1) whether ethanol-induced microencephaly results from reductions in neuronal acquisition (i.e., cell proliferation and neuronal migration) and/or increases in neuronal death and (2) whether ethanol exacerbates death by the same mode as that for naturally occurring or lesion-induced neuronal death. Pregnant rats were exposed to a diet containing 6.7% (v/v) ethanol or an isocaloric control diet during the last two weeks of gestation. At birth, the right infraorbital nerves of the pups were transected. The numbers of neurons in the principal sensory nucleus of the trigeminal nerve (PSN) on both sides of the pons were examined at various prenatal and early postnatal timepoints. The numbers of pyknotic and argyrophilic PSN cells were also counted. Ethanol delayed and reduced (19.9%) the prenatal acquisition of PSN neurons. The postnatal decline in neuronal number (indicative of neuronal death) was significantly increased (10.6%) by ethanol. Likewise, the numbers of pyknotic and silver-stained cells were significantly higher in ethanol-treated rats. Lesion of the infraorbital nerve induced significant transsynaptic neuronal death in the control rats. Ethanol increased the amount of death caused by the lesion;however, it altered neither the timing of the neuronal loss nor the incidence of pyknosis or silver-staining. Therefore, ethanol affects both neuronal acquisition and survival;the greater effect being on neuronal acquisition. The timing and morphology of dying cells indicate that regardless of the cause (natural processes, ethanol-induced, or lesion-induced), neurons die in the developing PSN by the same mode.

关键词：年龄因素轴突切断术细胞计数细胞死亡/药物作用中枢神经系统抑制药/药理学乙醇/药理学纵向研究上颌神经/细胞学上颌神经/生理学神经元传入/细胞学神经元传入/药物作用产前暴露迟发效应大鼠 Sprague-Dawley 三叉神经核/细胞学动物女(雌)性妊娠大鼠

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