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Characterization of the calcium signaling system in the submandibular cell line SMG-C6. 下颌下细胞系SMG-C6钙信号系统的表征。
Xiao-bing Liu, Xiuhua Sun, A. Mörk, Michael W. J. Dodds, J. Ricardo Martinez, Guo H. Zhang
Establishment of salivary cell lines retaining normal morphological and physiological characteristics is important in the investigation of salivary cell function. A submandibular gland cell line, SMG-C6, has recently been established. In the present study, we characterized the phosphoinositide (PI)-Ca2+ signaling system in this cell line. Inositol 1,4,5-trisphosphate(1,4,5-IP3) formation, as well as Ca2+ storage, release, and influx in response to muscarinic, alpha1-adrenergic, P2Y-nucleotide, and cytokine receptor agonists were determined. Ca2+ release from intracellular stores was strongly stimulated by acetylcholine (ACh) and ATP, but not by norepinephrine (NA), epidermal growth factor (EGF), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNFalpha). Consistently, 1, 4,5-IP3 formation was dramatically stimulated by ACh and ATP. ACh-stimulated cytosolic free Ca2+ concentration [Ca2+]i increase was inhibited by ryanodine, suggesting that the Ca2+-induced Ca2+ release mechanism is involved in the ACh-elicited Ca2+ release process. Furthermore, ACh and ATP partially discharged the IP3-sensitive Ca2+ store, and a subsequent exposure to thapsigargin (TG) induced further [Ca2+]i increase. However, exposure to TG depleted the store and a subsequent stimulation with ACh or ATP did not induce further [Ca2+]i increase, suggesting that ACh and ATP discharge the same storage site sensitive to TG. As in freshly isolated submandibular acinar cells, exposure to ionomycin and monensin following ACh or TG induced further [Ca2+]i increase, suggesting that IP3-insensitive stores exist in SMG-C6 cells. Ca2+ influx was activated by ACh, ATP, or TG, and was significantly inhibited by La3+, suggesting the involvement of store-operated Ca2+ entry (SOCE) pathway. These results indicate that in SMG-C6 cells: (i) Ca2+ release is triggered by muscarinic and P2Y-nucleotide receptor agonists through formation of IP3; (ii) both the IP3-sensitive and -insensitive Ca2+ stores are present; and (iii) Ca2+ influx is mediated by the store-operated Ca2+ entry pathway. We conclude that Ca2+ regulation in SMG-C6 cells is similar to that in freshly isolated SMG acinar cells; therefore, this cell line represents an excellent SMG cell model in terms of intracellular Ca2+ signaling.
建立保持正常形态和生理特征的唾液腺细胞系是研究唾液腺细胞功能的重要手段。最近建立了一种下颌腺细胞系SMG-C6。在本研究中,我们表征了该细胞系的磷酸肌苷(PI)-Ca2+信号系统。测定肌醇1,4,5-三磷酸(1,4,5- ip3)的形成,以及Ca2+的储存、释放和内流对毒蕈碱、α - 1-肾上腺素能、p2y -核苷酸和细胞因子受体激动剂的反应。乙酰胆碱(ACh)和ATP能强烈刺激细胞内Ca2+释放,但去甲肾上腺素(NA)、表皮生长因子(EGF)、白细胞介素-6 (IL-6)和肿瘤坏死因子- α (TNFalpha)不能。同样,乙酰胆碱和ATP显著刺激1,4,5 - ip3的形成。乙酰胆碱刺激的胞质游离Ca2+浓度[Ca2+]i升高被ryanodine抑制,提示Ca2+诱导的Ca2+释放机制参与了乙酰胆碱诱导的Ca2+释放过程。此外,ACh和ATP部分释放了ip3敏感的Ca2+储存,随后暴露于thapsigargin (TG)诱导了[Ca2+]i的进一步增加。然而,暴露于TG耗尽存储和随后的ACh或ATP刺激并没有诱导进一步的[Ca2+]i增加,这表明ACh和ATP释放了对TG敏感的同一存储位点。与新鲜分离的下颌腺泡细胞一样,在乙酰胆碱或TG后暴露于离子霉素和莫能菌素可诱导[Ca2+]i进一步增加,这表明SMG-C6细胞中存在ip3不敏感的储存。Ca2+内流可被ACh、ATP或TG激活,并被La3+显著抑制,提示参与储存操作的Ca2+进入(SOCE)途径。这些结果表明,在SMG-C6细胞中:(i)毒蕈碱和p2y -核苷酸受体激动剂通过形成IP3触发Ca2+释放;(ii) ip3敏感和ip3不敏感的Ca2+储存都存在;(iii) Ca2+内流是由储存操作的Ca2+进入途径介导的。我们得出结论,Ca2+在SMG- c6细胞中的调节与新分离的SMG腺泡细胞相似;因此,就细胞内Ca2+信号传导而言,该细胞系代表了一个优秀的SMG细胞模型。
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引用次数: 24
Introduction: low-saturated fat, high-carbohydrate diets: effects on triglyceride and LDL synthesis, the LDL receptor, and cardiovascular disease risk. 前言:低饱和脂肪、高碳水化合物饮食:对甘油三酯和LDL合成、LDL受体和心血管疾病风险的影响
R. Knopp
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引用次数: 5
Cell death induction by CTL: perforin/granzyme B system dominantly acts for cell death induction in human hepatocellular carcinoma cells. CTL:穿孔素/颗粒酶B系统在诱导人肝癌细胞死亡中起主导作用。
M. Hayashida, H. Kawano, T. Nakano, K. Shiraki, A. Suzuki
Cell death induction by cytotoxic T lymphocytes (CTLs) is an important thesis for the understanding of tumor immunotherapy. In the current study we investigated the molecular machinery of CTL-induced cell death in human hepatocellular carcinoma cell lines (HCC lines). CTLs prepared from human peripheral blood induced cell death in all tested HCC lines. As the CTL-induced death system, the effectiveness of Fas ligand/Fas and/or Perforin/Granzyme B systems has been suggested, whereas cell death induction by CTLs was shown independently on Fas expression in the current study. Using various tetrapeptide inhibitors for caspase and its associated factor, we additionally demonstrated that inhibitors for caspase 3 (Ac-DEVD-CHO) and caspase 8/granzyme B (Ac-IETD-CHO) suppressed CTL-induced cell death, but an inhibitor for Fas-activated serine proteinase, which acts for the caspase 3 activator, did not, suggesting that CTL-induced cell death was initiated by the Perforin/Granzyme B system, rather than the Fas ligand/Fas system. On the basis of our current results, we report here that the Perforin/Granzyme B system acts dominantly for the cell death induction of HCC lines.
细胞毒性T淋巴细胞(ctl)诱导细胞死亡是理解肿瘤免疫治疗的重要课题。在本研究中,我们研究了ctl诱导人肝癌细胞系(HCC细胞系)细胞死亡的分子机制。从人外周血制备的ctl可诱导所有HCC细胞系的细胞死亡。作为ctl诱导的死亡系统,Fas配体/Fas和/或Perforin/Granzyme B系统的有效性已被提出,而目前的研究显示ctl诱导细胞死亡独立于Fas表达。利用各种caspase及其相关因子的四肽抑制剂,我们还证明了caspase 3 (Ac-DEVD-CHO)和caspase 8/颗粒酶B (Ac-IETD-CHO)抑制剂抑制了ctl诱导的细胞死亡,但Fas激活的丝氨酸蛋白酶抑制剂(caspase 3激活剂)却没有,这表明ctl诱导的细胞死亡是由穿孔素/颗粒酶B系统启动的,而不是Fas配体/Fas系统。基于我们目前的结果,我们在此报告穿孔素/颗粒酶B系统在诱导HCC细胞系细胞死亡中起主要作用。
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引用次数: 13
Role of nitric oxide and superoxide in acute cardiac allograft rejection in rats. 一氧化氮和超氧化物在大鼠急性异体心脏移植排斥反应中的作用。
E. Akizuki, T. Akaike, S. Okamoto, Shigemoto Fujii, Y. Yamaguchi, M. Ogawa, H. Maeda
The role of NO and superoxide (O(2)(-)) in tissue injury during cardiac allograft rejection was investigated by using a rat ex vivo organ perfusion system. Excessive NO production and inducible NO synthase (iNOS) expression were observed in cardiac allografts at 5 days after cardiac transplantation, but not in cardiac isografts, as identified by electron spin resonance spectroscopy and Northern blotting. Cardiac isografts or allografts obtained on Day 5 after transplantation were perfused with Krebs bicarbonate buffer with or without various antidotes for NO or O(2)-, including N(omega)-monomethyl-L-arginine (L-NMMA; 1 mM), 2-phenyl-4,4,5, 5-tetramethylimidazoline-1-oxyl 3-oxide (PTIO; 100 microM), 4-amino-6-hydroxypyrazolo[3,4-d]pyrimidine (AHPP; a xanthine oxidase inhibitor; 100 microM), and superoxide dismutase (SOD; 100 units/ml). Treatment of the cardiac allografts with PTIO showed most remarkable improvement of the cardiac injury as revealed by significant reduction in aspartate transaminase, lactate dehydrogenase, and creatine phosphokinase concentrations in the perfusate. Similar but less potent protective effect on the allograft injury was observed by treatment with L-NMMA, AHPP, and SOD. Immunohistochemical analyses for iNOS and nitrotyrosine indicated that iNOS is mainly expressed by macrophages infiltrating the allograft tissues, and nitrotyrosine formation was demonstrated not only in macrophages but also in cardiac myocytes of the allografts, providing indirect evidence for the generation of peroxynitrite during allograft rejection. Our results suggest that tissue injury in rat cardiac allografts during acute rejection is mediated by both NO and O(2)(-), possibly through peroxynitrite formation.
采用体外器官灌注系统研究了NO和超氧化物(O(2)(-))在同种异体心脏移植排斥反应中组织损伤中的作用。通过电子自旋共振光谱和Northern blotting检测,同种异体心脏移植物在心脏移植后5天观察到过量的NO产生和诱导NO合成酶(iNOS)表达,而在心脏同种异体移植物中则没有。移植后第5天获得的心脏同种异体或同种异体移植物灌注碳酸氢盐Krebs缓冲液,含或不含各种NO或O(2)-解毒剂,包括N(omega)-单甲基- l-精氨酸(L-NMMA);1 mM), 2-苯基- 4,4,5,5 -四甲基咪唑-1-氧基- 3-氧化物(PTIO;100微米),4-氨基-6-羟基吡唑[3,4-d]嘧啶(AHPP;黄嘌呤氧化酶抑制剂;100微米),超氧化物歧化酶(SOD;100单位/毫升)。同种异体心脏移植物经PTIO处理后,灌注液中天冬氨酸转氨酶、乳酸脱氢酶和肌酸磷酸激酶浓度显著降低,对心脏损伤的改善最为显著。L-NMMA、AHPP和SOD对同种异体移植物损伤的保护作用相似,但作用较弱。免疫组化iNOS和硝基酪氨酸分析表明,iNOS主要通过浸润同种异体移植物组织的巨噬细胞表达,并且硝基酪氨酸不仅在巨噬细胞中形成,而且在同种异体移植物的心肌细胞中也存在,这为同种异体移植物排斥反应中过氧亚硝酸盐的产生提供了间接证据。我们的研究结果表明,大鼠同种异体心脏移植在急性排斥反应期间的组织损伤是由NO和O(2)(-)介导的,可能是通过过氧亚硝酸盐的形成。
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引用次数: 26
Role of Sertoli cells in injury-associated testicular germ cell apoptosis. 支持细胞在损伤相关睾丸生殖细胞凋亡中的作用。
K. Boekelheide, Shawna L. Fleming, Kamin J. Johnson, Sutchin R. Patel, H. Schoenfeld
This review examines experimental models of Sertoli cell injury resulting in germ cell apoptosis. Since germ cells exist in an environment created by Sertoli cells, paracrine signaling between these intimately associated cells must regulate the process of germ cell death. Germ cell apoptosis may be signaled by a decrease in Sertoli cell pro-survival factors, an increase in Sertoli cell pro-apoptotic factors, or both. The different models of Sertoli cell injury indicate that spermatogenesis is susceptible to disruption, and that targeting critical Sertoli cell functions can lead to rapid and massive germ cell death.
本文综述了支持细胞损伤导致生殖细胞凋亡的实验模型。由于生殖细胞存在于由支持细胞创造的环境中,这些密切相关细胞之间的旁分泌信号必须调节生殖细胞死亡的过程。生殖细胞凋亡的信号可能是支持细胞促存活因子的减少,支持细胞促凋亡因子的增加,或两者兼而有之。不同的支持细胞损伤模型表明,精子发生容易受到破坏,针对关键的支持细胞功能可导致快速和大量的生殖细胞死亡。
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引用次数: 114
Reduced natriuresis after oral sodium load in cholestatic rats: role of compartment volumes and ANP. 胆淤积大鼠口服钠负荷后尿钠减少:室容积和ANP的作用。
J. Casar, A. Valdivieso, J. A. Bravo, C. Chacón, M. Boric
The purpose of this study was to assess the participation of the atrial natriuretic peptide (ANP)-cGMP system in electrolyte and volume handling of cholestatic rats submitted to an acute oral sodium load. Cholestasis was induced by ligation and section of the common bile duct (n = 51). Control rats were sham operated (n = 56). Three weeks after surgery, 24-hr urinary volume, sodium, potassium, cGMP and creatinine excretion were measured. Three days later, animals received 10 mmol/kg NaCl (1 M) by gavage, and urinary excretion was measured for 6 hr. In parallel groups of rats, plasma volume, electrolytes and ANP concentration, extracellular fluid volume (ECFV), and renal medullary ANP-induced cGMP production were determined in basal conditions or 1 hr after oral sodium overload. As compared with controls, cholestatic rats had a larger ECFV and higher plasma ANP (67.2 +/- 5.2 vs 39.7 +/- 3.5 pg/ml), but lower hematocrit and blood volume, and were hyponatremic. Cholestatic rats showed higher basal excretion of sodium, potassium, and volume than controls, but equal urinary cGMP. After the NaCl overload, cholestatic rats showed a reduced sodium excretion but equal urinary cGMP. One hr after sodium overload, both groups showed hypernatremia, but whereas in control rats ECFV and ANP increased (50.7 +/- 4.1 pg/ml), in cholestatic rats ECFV was unchanged, and plasma volume and ANP were reduced (37.5 +/- 5.8 pg/ml). ANP-induced cGMP production in renal medulla was similar in cholestatic and control nonloaded rats (14.2 +/- 5.2 vs 13.4 +/- 2.6 fmol/min/mg). One hr after the load, medullary cGMP production rose significantly in both groups, without difference between them (20.6 +/- 3.1 vs 22.7 +/- 1. 7 fmol/min/mg). We conclude that the blunted excretion of an acute oral sodium load in cholestatic rats is associated with lower plasma ANP due to differences in body fluid distribution and cannot be explained by renal refractoriness to ANP.
本研究的目的是评估心房利钠肽(ANP)-cGMP系统在急性口服钠负荷下胆汁淤积大鼠的电解质和体积处理中的作用。结扎和切开胆总管诱导胆汁淤积(n = 51)。对照组56只。术后3周,测定24小时尿量、钠、钾、cGMP、肌酐排泄量。3 d后,灌胃10 mmol/kg NaCl (1 M),测定尿排泄量6 h。在平行组大鼠中,在基础条件下或口服钠超载后1小时,测定血浆体积、电解质和ANP浓度、细胞外液体积(ECFV)和肾髓ANP诱导的cGMP产生。与对照组相比,胆汁淤积大鼠ECFV更大,血浆ANP更高(67.2 +/- 5.2 vs 39.7 +/- 3.5 pg/ml),但红细胞压积和血容量更低,且低钠血症。胆汁淤积大鼠的钠、钾排泄量和尿cGMP均高于对照组。NaCl超载后,胆汁淤积大鼠钠排泄量减少,但尿cGMP不变。钠超载1小时后,两组均出现高钠血症,但对照组大鼠ECFV和ANP升高(50.7 +/- 4.1 pg/ml),而胆固醇淤积大鼠ECFV不变,血浆容量和ANP降低(37.5 +/- 5.8 pg/ml)。anp诱导的肾髓质cGMP生成在胆固醇抑制大鼠和对照非负荷大鼠中相似(14.2 +/- 5.2 vs 13.4 +/- 2.6 fmol/min/mg)。负荷1小时后,两组的髓质cGMP产量均显著升高,两组间无差异(20.6 +/- 3.1 vs 22.7 +/- 1)。7 fmol /分钟/毫克)。我们的结论是,由于体液分布的差异,胆汁淤积大鼠急性口服钠负荷的钝化排泄与血浆ANP降低有关,而不能用肾脏对ANP的难耐性来解释。
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引用次数: 1
The effect of hyaluronan on elastic fiber injury in vitro and elastase-induced airspace enlargement in vivo. 透明质酸对体外弹性纤维损伤和体内弹性酶诱导的空气空间扩大的影响。
J. Cantor, J. Cantor, Bronislava Shteyngart, J. Cerreta, Ming Liu, G. Armand, G. Turino
This laboratory has previously described a method of preventing air-space enlargement in experimental pulmonary emphysema using aerosolized hyaluronan (HA). Although it was found that HA preferentially binds to elastic fibers (which undergo breakdown by elastases in emphysema), it remains to be shown that such attachment actually prevents damage to the fibers. In the current study, cell-free radiolabeled extracellular matrices, derived from rat pleural mesothelial cells, were used to test the ability of low molecular weight ( approximately 100 kDa) streptococcal HA to prevent elastolysis. Coating the matrices with HA significantly decreased elastolysis (P<0.05) induced by porcine pancreatic elastase (43%), human neutrophil elastase (53%), and human macrophage metalloelastase (80%). Concomitant in vivo studies examined the ability of an aerosol preparation of the streptococcal HA to prevent experimental emphysema induced by intratracheal administration of porcine pancreatic elastase. As seen with earlier studies involving bovine tracheal HA, a single aerosol exposure significantly decreased elastase-induced airspace enlargement, as measured by the mean linear intercept (107.5 vs 89.6 microm; P < 0. 05). Furthermore, repeated exposure to the HA aerosol for 1 month did not reveal any morphological changes in the lung. The results provide further evidence that aerosolized HA may be an effective means of preventing pulmonary emphysema and perhaps other lung diseases that involve elastic fiber injury.
该实验室先前描述了一种使用雾化透明质酸(HA)防止实验性肺气肿中空气空间扩大的方法。虽然发现透明质酸优先与弹性纤维结合(在肺气肿中,弹性纤维会被弹性蛋白酶分解),但仍有待证明这种附着实际上可以防止纤维受损。在目前的研究中,来自大鼠胸膜间皮细胞的无细胞放射性标记细胞外基质被用于测试低分子量(约100 kDa)链球菌HA防止弹性分解的能力。涂膜透明质酸可显著降低猪胰腺弹性酶(43%)、人中性粒细胞弹性酶(53%)和人巨噬细胞金属弹性酶(80%)诱导的弹性溶解(P<0.05)。同时进行的体内研究检测了链球菌透明质酸的气溶胶制剂预防猪胰腺弹性酶气管内注射引起的实验性肺气肿的能力。正如早期涉及牛气管HA的研究所见,通过平均线性截距(107.5 vs 89.6微米)测量,单次气溶胶暴露显著减少弹性酶引起的空域扩大;P < 0。05). 此外,反复暴露于HA气雾剂1个月未发现肺的任何形态学变化。结果进一步证明,雾化透明质酸可能是预防肺气肿和其他涉及弹性纤维损伤的肺部疾病的有效手段。
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引用次数: 62
Promotive effects of a silk film on epidermal recovery from full-thickness skin wounds. 蚕丝膜对全层皮肤创面表皮恢复的促进作用。
A. Sugihara, K. Sugiura, H. Morita, T. Ninagawa, K. Tubouchi, R. Tobe, M. Izumiya, T. Horio, N. Abraham, S. Ikehara
We examined the effects of the transparent fibroin film (silk film) on full-thickness skin wounds. Full-thickness dermatotomies (15 mm x 9 mm) were prepared on the dorsal wall of CRJ:CD-1 nu/nu (ICR nu/nu) mice. The area of the wounds dressed with silk film was reduced to 10% of that made by the dermatotomy 14 days after the dermatotomy and were covered with regenerated epidermis 21 days after the dermatotomy. In contrast, less recovery and epidermal regeneration were found 14 days after dermatotomy in the wounds dressed with a conventional hydrocolloid dressing (Duro Active). Furthermore, only partial incomplete epidemal growth was obtained 21 days after dermatotomy. Most importantly, the healing time of wounds dressed with silk film was 7 days shorter than those dressed with DuoActive dressing. The silk film showed an almost similar or slightly better promotive effect as the lyophilized porcine dermis (Alloask D), which is used as a dressing for burns, ulcers, and decubitis. Histologic findings revealed that there was greater collagen regeneration and less inflammation and neutrophil-lymphocyte infiltration of the wounds dressed with silk film than with DuoActive dressing. It is clear that regeneration of the epidermis and dermis of the wound beds covered with silk film was faster than with DuoActive dressing. Finally, silk film is easily obtainable, sterilizable, and transparent, and it allows easy observation of tissue recovery. Therefore, silk film offers advantages over other dressings and may be clinically useful for wound treatment.
我们研究了透明丝素膜(蚕丝膜)对全层皮肤创面的影响。在CRJ:CD-1 nu/nu (ICR nu/nu)小鼠背壁制备全层皮肤切开术(15 mm × 9 mm)。术后14天,丝膜覆盖创面面积减少至创面面积的10%,术后21天创面覆盖再生表皮。相比之下,使用传统的水胶体敷料(Duro Active)敷料的创面在皮切术后14天恢复和表皮再生较少。此外,皮肤切开后21天仅获得部分不完整的表皮生长。最重要的是,与多活性敷料相比,丝膜敷料的愈合时间缩短了7 d。丝质薄膜表现出与冻干猪真皮(Alloask D)几乎相似或稍好一些的促进作用,冻干猪真皮被用作烧伤、溃疡和脱尿炎的敷料。组织学结果显示,与十二指肠活性敷料相比,丝膜敷料的创面胶原再生明显增加,炎症反应和中性粒细胞淋巴细胞浸润减少。结果表明,覆盖蚕丝膜的创面表皮和真皮的再生速度明显快于多活性敷料。最后,丝膜很容易获得,可消毒,透明,它可以很容易地观察组织恢复。因此,与其他敷料相比,丝膜具有优势,可能在临床上对伤口治疗有用。
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引用次数: 161
Acetaldehyde-stimulated PKC activity in airway epithelial cells treated with smoke extract from normal and smokeless cigarettes. 乙醛刺激正常和无烟香烟烟提取物处理的气道上皮细胞PKC活性。
T. Wyatt, S. Schmidt, S. Rennard, D. Tuma, J. Sisson
Previously, we have found that acetaldehyde, a volatile component of cigarette smoke, stimulates the protein kinase C (PKC) pathway and inhibits ciliary motility. A "smokeless" cigarette (Eclipse) now exists in which most of the tobacco is not burned, reducing the pyrolyzed components in the extract. We hypothesized that acetaldehyde is a component of cigarette smoke that activates PKC in the airway epithelial cell, and therefore the Eclipse cigarette would not activate epithelial cell PKC. In this study, bovine bronchial epithelial cells (BBEC) were incubated with cigarette smoke extract (CSE) or Eclipse smoke extract (ESE). We found that PKC activity was significantly higher in cells exposed to 5% CSE than cells exposed to 5% ESE or media. When acetaldehyde levels of both extracts were measured by gas chromatography, CSE was found to have 15-20 times greater concentration (microM) of acetaldehyde than ESE. When BBEC were treated with 5% CSE, ciliary beating was further decreased from baseline levels. This decrease in ciliary beating was not observed in cells treated with ESE, suggesting that acetaldehyde contained in CSE slows cilia. These results suggest that volatile components such as acetaldehyde in cigarette smoke may inhibit ciliary motility via a PKC-dependent mechanism.
在此之前,我们发现香烟烟雾中的挥发性成分乙醛刺激蛋白激酶C (PKC)途径并抑制纤毛运动。现在有一种“无烟”香烟(Eclipse),其中大部分烟草不燃烧,减少了提取物中的热解成分。我们假设乙醛是香烟烟雾中激活气道上皮细胞PKC的成分,因此Eclipse香烟不会激活上皮细胞PKC。在本研究中,牛支气管上皮细胞(BBEC)与香烟烟雾提取物(CSE)或Eclipse烟雾提取物(ESE)孵育。我们发现,暴露于5% CSE的细胞的PKC活性明显高于暴露于5% ESE或培养基的细胞。当用气相色谱法测量两种提取物的乙醛水平时,发现CSE的乙醛浓度(微米)比ESE高15-20倍。当BBEC用5%的CSE治疗时,纤毛搏动从基线水平进一步降低。在用ESE处理的细胞中没有观察到纤毛跳动的减少,这表明CSE中含有的乙醛减缓了纤毛。这些结果表明,香烟烟雾中的乙醛等挥发性成分可能通过pkc依赖机制抑制纤毛运动。
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引用次数: 68
Antioxidative effects of melatonin in protection against cellular damage caused by ionizing radiation. 褪黑素在保护细胞免受电离辐射损伤中的抗氧化作用。
M. Karbownik, Russel J. Reiter
Ionizing radiation is classified as a potent carcinogen, and its injury to living cells is, to a large extent, due to oxidative stress. The molecule most often reported to be damaged by ionizing radiation is DNA. Hydroxyl radicals (*OH), considered the most damaging of all free radicals generated in organisms, are often responsible for DNA damage caused by ionizing radiation. Melatonin, N-acetyl-5-methoxytryptamine, is a well-known antioxidant that protects DNA, lipids, and proteins from free-radical damage. The indoleamine manifests its antioxidative properties by stimulating the activities of antioxidant enzymes and scavenging free radicals directly or indirectly. Among known antioxidants, melatonin is a highly effective scavenger of *OH. Melatonin is distributed ubiquitously in organisms and, as far as is known, in all cellular compartments, and it quickly passes through all biological membranes. The protective effects of melatonin against oxidative stress caused by ionizing radiation have been documented in in vitro and in vivo studies in different species and in in vitro experiments that used human tissues, as well as when melatonin was given to humans and then tissues collected and subjected to ionizing radiation. The radioprotective effects of melatonin against cellular damage caused by oxidative stress and its low toxicity make this molecule a potential supplement in the treatment or co-treatment in situations where the effects of ionizing radiation are to be minimized.
电离辐射被列为强致癌物,其对活细胞的损伤在很大程度上是由于氧化应激。据报道,最常被电离辐射破坏的分子是DNA。羟基自由基(*OH)被认为是生物体产生的所有自由基中最具破坏性的,通常是电离辐射引起DNA损伤的原因。褪黑素,n -乙酰-5-甲氧基色胺,是一种众所周知的抗氧化剂,可以保护DNA、脂质和蛋白质免受自由基的损害。吲哚胺通过直接或间接地刺激抗氧化酶的活性和清除自由基来表现其抗氧化特性。在已知的抗氧化剂中,褪黑激素是*OH的高效清除剂。褪黑素在生物体中无处不在,据我们所知,它存在于所有的细胞区室中,并能迅速穿过所有的生物膜。褪黑素对电离辐射引起的氧化应激的保护作用已经在不同物种的体外和体内研究以及使用人体组织的体外实验中被记录下来,以及当褪黑素被给予人体,然后收集组织并受到电离辐射。褪黑素对氧化应激引起的细胞损伤具有辐射保护作用,其低毒性使其成为治疗或协同治疗中电离辐射影响最小化的潜在补充。
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引用次数: 351
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Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine
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