米诺环素在下颌阻生牙拔除后干槽症预防中的应用

目的将米诺环素放入下颌阻生牙拔除后牙槽窝,评价其预防干槽症的效果。方法选择韶关学院医学院附属医院口腔门诊拔除下颌阻生牙的患者126例,随机分成两组,试验组在拔除阻生牙后放入米诺环素,对照组不放任何材料任其自行愈合,1周后复诊观察干槽症的发生情况。结果试验组有1例干槽症发生,对照组有8例干槽症发生,两组干槽症发生率的差异有统计学意义(P0.05)。结论复杂阻生牙拔除术,由于创伤大、操作时间长,在牙槽窝放入米诺环素可预防干槽症的发生。     

盐酸米诺环素软膏在感染渗出性根管封药中的应用

目的 评价盐酸米诺环素软膏作为根管消毒剂治疗感染渗出型慢性根尖周炎的临床疗效.方法 随机单盲对照研究,选择54例(患牙54颗)诊断为慢性根尖周炎合并根管渗液的患者,随机分为两组各27例.A组用盐酸米诺环素软膏作根管封药,B组常规用氢氧化钙甘油糊剂作根管封药;比较两组患者约诊间疼痛程度和复诊时根管渗液的变化,并对根管治疗术(RCT)半年后的临床疗效进行评价.结果 A组约诊间疼痛发生率约为7.4%,低于B组的33.3%(P<0.05);A组根管渗液减少程度优于B组(P<0.05);根管充填术后半年,A、B组间患者的治疗有效率分别为96.3%和88.89%,两组间比较差异无统计学意义(P>0.05).结论 盐酸米诺环素软膏在感染渗出性根管封药中应用短期疗效优于氢氧化钙甘油糊剂.     

米诺环素调控P2X7受体抑制BV-2细胞活化的研究*

 目的：探索P2X7受体在米诺环素(Mino)抑制脂多糖（LPS）刺激的BV-2细胞活化中的作用。方法：将体外培养的BV-2细胞分为5组：空白对照组、LPS处理组、LPS+ 0.1 μmol/L Mino组、LPS+ 1 μmol/L Mino组和LPS+ 10 μmol/L Mino组。分组处理8 h后行real-time PCR检测P2X7受体mRNA表达;处理24 h后观察各组细胞形态学变化,Western blotting检测P2X7受体蛋白表达,取细胞培养液上清行ELISA检测TNF-α和IL-1β的分泌情况。结果：经LPS处理后,BV-2细胞P2X7受体mRNA及蛋白的表达均升高,细胞培养液上清的TNF-α和IL-1β表达升高,同时伴有形态学的改变,而0.1～10 μmol/L Mino能抑制这一趋势,差异有统计学意义（P<0.01）。 结论： Mino抑制BV-2细胞活化的机制可能与抑制P2X7受体的活性相关。     

盐酸米诺环素软膏的释放度研究

目的探讨盐酸米诺环素缓释软膏的体外释放度及释药机制。方法制备盐酸米诺环素软膏供试品溶液和盐酸米诺环素标准品溶液。释放度采用桨法（《中国药典》2010版二部附录XD第二法）,以水为释放介质,体积为500 mL,转速为100 r/min,温度为（37.0±0.5）℃,检测波长为274 nm。采用紫外分光光度法测定释放介质中盐酸米诺环素的含量。结果盐酸米诺环素检测浓度在0.99～19.87μg/mL范围内具有良好的线性关系,线性回归方程为A=0.0301C＋0.0004,相关系素r=1,平均回收率为101.6%,相对标准偏差为1.5%。在1、4、7 h的释放度分别为13.91%、29.89%、40.76%,体外释放度有良好的缓释药物行为。体外释放特征显示该软膏制剂具有复合释药的规律,一级释放机制所占比例更大一些。结论盐酸米诺环素软膏制剂具有缓释作用,释放度测定方法操作简便、快速、准确度好。     

Spinal CCL2 and microglial activation are involved in paclitaxel-evoked cold hyperalgesia

The antineoplastic paclitaxel induces a sensory neuropathy that involves the spinal release of neuroinflammatory mediators and activation of glial cells. Although the chemokine CCL2 can evoke glial activation and its participation in neuropathic pain has been demonstrated in other models, its involvement in paclitaxel-evoked neuropathy has not been previously explored. Paclitaxel-evoked cold hypernociception was assessed in mice by the unilateral cold plate test and the effects on cold hyperalgesia of the CCR2 antagonist RS 504393, the CCR1 antagonist J113863, the microglial inhibitor minocycline or an anti-CCL2 antibody were tested. Furthermore, ELISA measurements of CCL2 concentration and immunohistochemical assays of Iba-1 and GFAP, markers of microglial and astroglial cells respectively, were performed in the lumbar spinal cord.Cold hypernociception measured 3 days after the administration of paclitaxel (10 mg/kg) was inhibited by the s.c. (0.3–3 mg/kg) or i.t. (1–10 μg) administration of RS 504393 but not of J113863 (3–30 mg/kg). CCL2 levels measured by ELISA in the lumbar spinal cord were augmented in mice treated with paclitaxel and the i.t. administration of an anti-CCL2 antibody completely suppressed paclitaxel-evoked cold hyperalgesia, strongly suggesting that CCL2 is involved in the hypernociception evoked by this taxane. Besides, the implication of microglial activation is supported by the increase in the immunolabelling of Iba-1, but not GFAP, in the spinal cord of paclitaxel-treated mice and by the inhibition of cold hyperalgesia produced by the i.t. administration of the microglial inhibitor minocycline (1–10 nmol). Finally, the neutralization of spinal CCL2 by the i.t. administration of a selective antibody for 3 days almost totally inhibited paclitaxel-evoked microglial activation.In conclusion, our results indicate that paclitaxel-evoked cold hypernociception depends on the activation of CCR2 due to the spinal release of CCL2 and the subsequent microglial activation.     

Minocycline attenuates testicular damages in a rat model of ischaemia/reperfusion (I/R) injury

Testicular torsion is a serious urological disease leading to testicular damage. This study aimed to assess the effect of minocycline on testicular ischaemia/reperfusion (I/R) injury caused by testicular torsion/detorsion. Male adult Wistar rats (n = 32) were assigned into four groups of sham, I/R, I/R + minocycline and minocycline. I/R injury was induced by two sets of surgical operations, including the rotation of the left testis (720°, counterclockwise), followed by detorsion after 4 hr. The administration of minocycline was carried out 30 min before detorsion and then continued for 8 weeks. At the end of the 8th week, rats were killed and sampling was done. Johnson's score, the height of seminiferous tubule epithelium, the mean seminiferous tubule diameter, as well as biochemical parameters, SOD, GPx and CAT, were significantly enhanced in the I/R + minocycline group compared with the I/R group. The administration of minocycline led to a marked decrease in expression levels of Caspase-3, Bax, IL-1β and TNF-α genes, and a remarkable increase in expression levels of Bcl-2, 3β-HSD and 17β-HSD3 genes compared with the I/R group. Administration of minocycline could also reduce the rate of germ cell apoptosis (TUNEL staining). Hence, minocycline was useful in the management of testicular torsion/detorsion.     

2型糖尿病合并牙周病应用盐酸米诺环素联合替硝唑治疗的效果分析

目的探索2型糖尿病合并牙周病应用盐酸米诺环素联合替硝唑治疗的效果分析。方法在2018年12月—2019年12月选取120例2型糖尿病合并牙周病患者为研究对象,选择单双号随机分组,每组60例,对照组采用盐酸米诺环素,观察组采用盐酸米诺环素联合替硝唑治疗,随后对比两组总有效率、PD(牙周探诊深度)、SBI(龈沟出血指数)、PLI(菌斑指数)、GI(牙龈指数)。结果观察组PD(1.11±0.08)mm、SBI(1.06±0.45)分、PLI(0.41±0.59)分、GI(0.22±0.05)分优于对照组,差异有统计学意义(t=20.284、23.295、13.272、7.064,P<0.05);观察组总有效率(96.67%)高于对照组,差异有统计学意义(χ²=12.810,P<0.05);观察组HbAIc(6.96±0.54)%、餐后2 h血糖(7.15±1.66)mmol/L、空腹血糖(4.89±0.43)mmol/L低于对照组,差异有统计学意义(t=12.052、6.684、19.749,P<0.05)。结论盐酸米诺环素联合替硝唑治疗用于2型糖尿病合并牙周病患者中效果显著,可改善牙周环境,促进牙周组织再生。     

中西医结合治疗口腔扁平苔藓的临床疗效观察

目的观察盐酸米诺环素和维A酸乳膏联合用药在治疗寻常痤疮中的疗效,探讨其应用价值。方法将60例寻常痤疮患者随机分为实验组和对照组,观察治疗前后皮损改善情况,按4级评分法进行评估。结果实验组有效率为71．4％,对照组有效率为38．9％。结论盐酸米诺环素联合维A酸乳膏治疗寻常痤疮疗效显著,安全可靠,值得临床推广应用。     

米诺环素对慢性脑缺血大鼠脑内Notch信号通路的影响

目的 观察慢性脑缺血后米诺环素是否可以通过调节Notch信号通路而发挥脑保护作用。方法 将健康雄性SD大鼠40只随机分为5组(n=8):假手术(Sham)组、缺血模型(Model)组、DAPT组、米诺环素(Min)组、DAPT+米诺环素(DAPT+Min)组; 双侧颈总动脉永久性结扎(2-VO)建立慢性脑缺血模型,给药1月后行为学检测大鼠的学习记忆能力,免疫组化和Western blot检测VEGF及Notch信号通路下游物质Hes1的表达水平。结果 与假手术组比较,缺血模型组大鼠的学习记忆能力降低(P<0.05); 米诺环素组与DAPT组比较,VEGF及Hes1的表达水平存在显著差异(P<0.01); 米诺环素组分别于与缺血模型组和DAPT+米诺环素组比较,DAPT+米诺环素组与DAPT组比较,学习记忆能力、VEGF及Hes1的表达水平存在显著差异(P<0.05)。结论 米诺环素可能通过对慢性脑缺血大鼠脑内Notch信号通路的调节来促进脑缺血后血管的新生,进而发挥脑保护作用。     

抑制病理性疼痛相关胶质细胞活化药物的研究进展

背景 病理性疼痛的产生和持续机制十分复杂.近些年越来越多的研究者关注到脊髓胶质细胞在病理性疼痛中所发挥的作用,其中胶质细胞活化和增殖的抑制剂成为了研究的重点.目的 系统阐述胶质细胞在病理性疼痛中的作用和部分胶质细胞抑制剂的作用机制及研究进展.内容 胶质细胞不仅具有营养和支持作用,还参与了病理性疼痛,已有许多实验证实了应用胶质细胞抑制剂可以减弱胶质细胞的激活从而削弱疼痛反应.趋向 期望能为进一步的药物实验研究提供有价值的思路和借鉴.