替硝唑局部用药治疗牙周炎的临床效果及安全性评价简

目的 观察盐酸米诺环素软膏、替硝唑和碘甘油治疗牙周炎的临床效果.方法 选取2010年4月～2012年6月患有牙周炎的192例患者,将192例患者随机分成三组,即治疗一组（盐酸米诺环素软膏组）、治疗二组（替硝唑组）、对照组（碘甘油组）,每组64例,均给予局部药物治疗,疗程4周,记录菌斑指数（PLI）、龈沟出血指数（SBI）和牙周袋探诊的深度（PD）.对比每组患者治疗的总有效率.结果 治疗一组（PLI：1.06±0.42,SBI：0.73±0.37,PD：2.64±0.78）和治疗二组（PLI：1.04±0.43,SBI：0.79±0.38,PD：2.70±0.74）PLI、SBI、PD要比对照组小,差异有统计学意义（P＜0.05）;治疗一组（93.76％）和治疗二组（90.63％）的总有效率均高于对照组（81.25％）,差异有统计学意义（P＜0.05）,治疗一组与治疗二组总有效率比较,差异无统计学意义（P＞0.05）,这三组患者在相应的治疗后并没有明显的不良症状.结论 盐酸米诺环素软膏和替硝唑能够有效地改善牙周炎症状,且效果优于碘甘油.     

米诺环素软膏治疗慢性牙周炎疗效及对龈沟液中超敏C反应蛋白水平的影响

目的 探讨米诺环素软膏治疗慢性牙周炎疗效及对龈沟液中超敏C反应蛋白水平的影响.方法 选取74例慢性牙周炎患者随机分为观察组与对照组.两组均予以常规龈上洁治术和龈下刮治术等基础治疗.观察组牙周袋内放置米诺环素软膏,对照组牙周袋内放置2％碘甘油,每周放置1次,连用4周.观察两组治疗前后龈沟液中hs-CRP水平的变化,并比较牙周袋深度（PD）和牙龈指数（GI）的变化.结果 治疗4周后,两组龈沟液中hs-CRP水平较前明显下降（P＜0.05或P＜0.01）,且观察组下降幅度明显大于对照组（P＜0.05）;两组GI和PD均较前明显改善（P＜0.05或P＜0.01）,且观察组改善幅度明显大于对照组（P＜0.05）.结论 米诺环素软膏治疗慢性牙周炎具有较好效果,能降低龈沟液中hs-CRP水平,减少牙周袋深度,降低牙龈指数,从而消除牙周慢性炎症.     

口服米诺环素联合外用Derma光治疗重度寻常型痤疮临床观察

目的：探讨口服米诺环素联合外用Derma光治疗重度寻常型痤疮的临床疗效,为临床治疗提供理论依据。方法：选择符合标准的患者80例,采用随机数字的方法分为观察组和对照组各40例,对照组应用口服米诺环素,观察组应用口服米诺环素联合外用Derma光治疗,治疗8周后比较临床疗效。结果：治疗8周后观察组患者总有效率为97.50%,明显高于对照组的80.00%,差异有统计学意义（P〈0.05）。治疗前两组患者GAGS评分相似,差异无统计学意义（P〉0.05）;治疗后,两组患者GAGS评分较治疗前均下降,差异有统计学意义（P〈0.05）,但是观察组患者下降幅度更大（P〈0.05）。治疗期间观察组2例患者经红蓝光照射后面部皮肤出现轻度潮红、瘙痒和脱屑,对症处理1周后症状缓解。对照组未见不良反应。患者均随访3个月,观察组患者复发2例（5.00%）,对照组复发8例（20.00%）,差异有统计学意义（P〈0.05）。结论：口服米诺环素联合外用Derma光治疗重度寻常型痤疮的临床疗效确切,安全可靠,复发率低,值得临床推广使用。     

Minocycline-induced vasculitis fulfilling the criteria of polyarteritis nodosa

Abstract

A 47-year-old man who had been taking minocycline for palmoplantar pustulosis developed fever, myalgias, polyneuropathy, and testicular pain, with elevated C-reactive protein (CRP). Neither myeloperoxidase- nor proteinase-3-antineutrophil cytoplasmic antibody was positive. These manifestations met the American College of Rheumatology 1990 criteria for the classification of polyarteritis nodosa. Stopping minocycline led to amelioration of symptoms and normalization of CRP level. To our knowledge, this is the second case of minocycline-induced vasculitis satisfying the criteria. Differential diagnosis for drug-induced disease is invaluable even for patients with classical polyarteritis nodosa.     

美满霉素对MPP+诱导的PC12细胞凋亡的保护作用

目的在离体细胞培养中探讨美满霉素(Minocycline,MC)对1-甲基-4-苯基吡啶离子(MPP )诱导的帕金森病细胞凋亡模型的保护作用.方法将MC或MPP 加入培养的PC12细胞中,建立多巴胺神经元凋亡模型,四甲基偶氮唑盐法(MTT法)检测细胞代谢活性,电泳法检测细胞凋亡,流式细胞术检测细胞凋亡率.结果MPP 浓度为10μmol/L时建立多胺神经元凋亡模型;MC 100 μmol/L预处理可明显升高MPP 处理的PC12细胞活性;MC MPP 组细胞凋亡率显著低于MPP 组(P＜0.01),但仍明显高于阴性对照组(P＜0.05).结论MC对MPP 诱导的细胞凋亡有一定的保护作用.     

正常人口服盐酸二甲胺四环素胶囊的药代动力学及相对生物利用度

研究8名健康受试者随机交叉接受进口和国产盐酸二甲胺四环素(MINO·HCl)胶囊后的药代动力学和相对生物利用度。用反相HPLC-UV测定MINO·HCl血药浓度。单次口服上述胶囊200mg后,药时曲线符合二室模型。国产与进口胶囊的药代动力学和相对生物利用度参数是:t_(1/2log)0.31±0.05和0.30±0.19h;t_(1/2)ka0.67±0.25和0.65±0.33h;t_(1/2)α1.99±0.78和2.05±0.82h;t_(1/2)β20.61±3.22和25.50±5.27h;Vd42.01±11.97和42.19±9.51L;CL2.69±0.51和2.52±0.55L/h;MRT26.74±3.81和33.28±7.78h; AUC77.12±16.89和 82.87±19.48mg·h/L;C_(max)3.42±0.63和3.44±0.78μg/ml;t_p2.40±0.53和2.35±1.09h。国产MINO·HCl相对生物利用度97.75± 22.43％.结果表明三种胶囊所有药代动力学和生物利用度参数无明显差异。     

Curing human hybridomas infected with Mycoplasma hyorhinis

Tiamuline and minocycline were evaluated for the treatment of an IgM producing human-human hybridoma cell line infected with Mycoplasma hyorhinis. Tiamuline was used at a concentration of 10 μg/ml culture medium and minocycline at a concentration of 5 μg/ml culture medium. Both antibiotics were found to eliminate mycoplasma infection over a treatment period of 3 weeks, and the hybridoma cell line remained mycoplasma-free for 6 months after treatment. Tiamuline had no effect on either cell growth or IgM secretion. Whereas treatment with minocycline alternated the cell proliferation and completely inhibited IgM secretion. This effect on cell function was found to be reversible since both cell growth and IgM secretion returned to normal 1 week after the minocycline had been removed. Tiamuline as well as minocycline may be recommended for the treatment of human hybridomas infected with mycoplasma.     

Protection against oxaliplatin-induced mechanical hyperalgesia and intraepidermal nerve fiber loss by minocycline

Treatment with the chemotherapeutic agent oxaliplatin produces a robust painful neuropathy similar to various other neuropathic conditions which result in loss of nerve fibers innervating the skin. This loss of intraepidermal nerve fibers (IENFs) appears to play an important role in neuropathy, but has yet to be investigated in oxaliplatin-induced neuropathic pain. For this study, mechanical hyperalgesia and IENF density were measured in rats receiving oxaliplatin, given at a dosage of 2 mg/kg every other day for four injections. The immunomodulatory agent minocycline (25 mg/kg) was also administered and was given 24 h prior to the first dose of oxaliplatin and continued throughout oxaliplatin treatment. Immunohistochemistry using the pan-neuronal marker PGP9.5 was used to investigate IENF densities in hind paw skin on Day 15 and Day 30. The results show that a robust mechanical sensitivity developed in oxaliplatin treated animals, as did a pronounced decrease in epidermal nerve fibers, and these outcomes were effectively prevented by minocycline treatment. This is the first study to show changes in IENF density in oxaliplatin treated animals, and confirm not only a relationship between IENF loss and hypersensitivity but also prevention of both with minocycline treatment.     

Minocycline inhibits caspase-dependent and -independent cell death pathways and is neuroprotective against hippocampal damage after treatment with kainic acid in mice

Although minocycline has been generally thought to have neuroprotective properties, the neuroprotective role of minocycline has not been investigated in the animal model of epilepsy. In this study, we investigated whether minocycline is neuroprotective against kainic acid (KA)-induced cell death through the caspase-dependent or -independent mitochondrial apoptotic pathways. Adult male ICR mice were subjected to seizures by intrahippocampal KA injection with vehicle or with minocycline. For cell death analysis, TdT-mediated dUTP-biotin nick end labeling and cresyl-violet staining were performed. Western blot analysis and immunofluorescent staining for cytochrome c and apoptosis-inducing factor (AIF) were performed. Cell death was reduced in minocycline-treated mice. Cytosolic translocation of cytochrome c and subsequent activation of caspase-3 were diminished by minocycline treatment. AIF nuclear translocation and subsequent large-scale DNA fragmentation were also reduced in minocycline-treated mice. Thus, this study suggests that minocycline inhibits both caspase-dependent and -independent apoptotic pathways and may be neuroprotective against hippocampal damage after KA treatment.