Macelignan attenuates LPS-induced inflammation and reduces LPS-induced spatial learning impairments in rats

Previous studies have shown that macelignan has anti-inflammatory and neuroprotective effects. Subsequently, in the current study, we demonstrate that oral administrations of macelignan reduce the hippocampal microglial activation induced by chronic infusions of lipopolysaccharide (LPS) into the fourth ventricle of Fisher-344 rat brains. A Morris water maze was used to evaluate the status of the hippocampal-dependent spatial learning in control rats with an artificial cerebrospinal fluid infusion, rats with chronic LPS infusions, and rats with chronic LPS infusions and oral administrations of macelignan. The rats with chronic LPS infusions showed spatial memory impairments relative to the control rats in the performance of the memory task. Daily administration of macelignan reduced the spatial memory impairments induced by the chronic LPS infusions. The results indicate that macelignan may possess therapeutic potential for the prevention of Alzheimer’s disease.     

糖皮质激素通过抑制p38MAPK信号通路缓解大鼠内毒素性急性肺损伤

目的： 研究糖皮质激素对内毒素导致的急性肺损伤的影响及作用机制。方法: 成年雄性SD大鼠被随机分为6组：对照组（control 组,n=6）;LPS组（n=24）;地塞米松＋LPS组（Dex＋LPS组,n=24）;糖皮质激素受体拮抗剂RU486组（RU486组,n=6）;RU486+LPS组（n=24）以及RU486＋Dex＋LPS组（n=24）。除对照组和RU486组外,其余4组在注射LPS后1、3、6、12 h又被分为4个亚组。分别检测各组大鼠支气管肺泡灌洗液（BALF）中TNF-α和IL-6的浓度,肺组织的病理变化,以及肺组织中p38MAPK的活化状态和MKP-1的表达情况。另外又分别比较了LPS组与RU486＋LPS组、Dex＋LPS组与RU486＋Dex＋LPS组大鼠48 h的死亡率。结果: 注射LPS后,BALF中TNF-α 和IL-6的浓度明显升高（P<0.05）,HE染色显示肺组织内广泛炎症反应。而这些现象在应用RU486后变得更加严重,并且RU486＋LPS组的死亡率也明显高于LPS组(P<0.05)。地塞米松能明显缓解LPS导致的肺损伤,糖皮质激素受体(GR)参与此作用。另外,在注射LPS后,肺组织中磷酸化的p38MAPK的表达明显升高,而MKP-1的表达则明显受到抑制。地塞米松能显著降低p38MAPK的磷酸化,这一作用也是GR依赖的。结论: 糖皮质激素活化GR诱导肺组织中MKP-1的表达,进而抑制p38MAPK的活化,从而发挥其抗炎作用,缓解LPS诱导的肺损伤。     

芍药苷减轻小鼠LPS性急性肺损伤的作用机制研究

目的: 观察芍药苷(Pae)对LPS诱导的小鼠急性肺损伤的影响及其作用机制。方法: 雄性 BALB/c小鼠随机分为对照组、脂多糖组(LPS)、芍药苷防治组(Pae+LPS)和芍药苷对照组(Pae),予以双蒸水或Pae(20 mg/kg)灌胃,1次/d,连续3 d,于实验第3 d灌胃后1 h,腹腔注射生理盐水或LPS (20 mg/kg)。观察各组小鼠肺组织形态学改变并进行肺损伤评分;用Western blotting检测肺组织髓过氧化物酶(MPO)、胞浆型磷脂酶A₂(cPLA₂)及磷酸化cPLA₂的含量。结果: 小鼠腹腔注射LPS后12 h,肺组织损伤明显,肺泡间隔增厚,大量炎症细胞浸润,可见明显肺出血及肺水肿;肺组织MPO含量、磷酸化cPLA₂水平显著升高。芍药苷防治组与LPS组相比,肺组织损伤明显减轻,炎症细胞浸润减少,肺出血、肺水肿显著减轻;肺MPO含量、磷酸化cPLA₂水平明显降低。芍药苷对照组与正常对照组相比,小鼠肺组织结构,MPO含量及磷酸化cPLA₂水平未见明显差别。结论: 芍药苷通过抑制肺组织中性粒细胞浸润、降低MPO含量和cPLA₂活性,减轻小鼠内毒素性肺损伤。     

猪肺表面活性物质对大鼠早期脂多糖性急性肺损伤的治疗作用

 目的： 观察猪肺表面活性物质（PPS）混悬液对大鼠早期脂多糖(LPS)性急性肺损伤（ALI）的治疗作用。方法： SD大鼠随机分为4组：生理盐水组、低、中、高3个不同剂量PPS给药组，各组动物均气道内滴注LPS 1.5 mg·kg-1,30 min后分别经气管滴注100 mg·kg^-1、150 mg·kg^-1、200 mg·kg-1PPS（PPS组）或等量生理盐水（对照组）。之后观察6 h，监测大鼠的PaO2和PaCO₂，计算各组大鼠存活率。大鼠处死后检测肺系数（LI），肺泡灌洗液（BALF）中总蛋白(TP)含量，白细胞（WBC）数和肿瘤坏死因子(TNF)-α的浓度，并观察肺病理组织学改变。结果： 与生理盐水组相比，LPS损伤大鼠早期气道内滴入外源性PPS可提高PaO₂，降低PaCO₂，提高存活率，减轻肺水肿及肺毛细血管膜的通透性，PPS150组、PPS200组的治疗效果优于PPS100组。结论： PPS早期给药对LPS气道内滴注致ALI具有明显的治疗作用。     

Previous heat shock treatment attenuates bicuculline-induced convulsions in rats

Exposure to elevated temperature provokes a sequence of events (heat shock response) in all living organisms. Through this response, heat shock proteins (HSPs) are induced and protect the cells against subsequent injury. We investigated the effect of heat treatment on bicuculline-induced convulsions, and analyzed a possible role of HSPs. Screw electrodes were implanted in the brain of mature male Wistar rats for electroencephalogram (EEG) recording. Experimental rats were subjected to whole-body hyperthermia at 41–42° C for 15 min. Fifteen hours later, bicuculline was injected intra peritoneally to induce convulsions in both experimental and control groups. The heated rats showed a significant attenuation of the convulsive response, in terms of both spike discharges in EEG and clinical seizures. Furthermore, induction of HSP72 was detected in the brain of heat-treated rats by immunoblotting, appearing at 4 h and reaching a maximal level 16–24 h after the heat shock. We conclude that the previous heat treatment stabilized neuronal excitability, most probably through the induction of HSP72.     

Long-term administration of tempol attenuates postinfarct ventricular dysfunction and sympathetic activity in rats

The purpose of this study was to determine whether the long-term administration of tempol attenuates postinfarct ventricular dysfunction and sympathetic activity in rats. Myocardial infarction (MI) was induced by left descending coronary artery ligation. Tempol was orally administered in drinking water (2 mmol/L), which was initiated 4 h after infarction and continued for 6 weeks. Tempol prevented not only the increases in left ventricular end-diastolic pressure and volume but also the decreases in ejection fraction and peak velocities of contraction in MI rats. The treatment normalized the increased renal sympathetic nerve activity (RSNA) and plasma norepinephrine level, as well as the enhanced cardiac sympathetic afferent reflex (CSAR; an excitatory cardiovascular reflex partially contributing to the sympathetic activation in chronic heart failure) and the RSNA responses to microinjection of angiotensin II into paraventricular nucleus in MI rats. Furthermore, tempol prevented the increased AT₁ receptor protein expression and superoxide anion level in both paraventricular nucleus and rostral ventrolateral medulla in MI rats. In conclusion, long-term administration of tempol attenuates ventricular dysfunction and normalizes sympathetic neural control in MI rats. The normalization of the CSAR, levels of superoxide anions and AT₁ receptor expression, and the response to angiotensin II in the paraventricular nucleus and rostral ventrolateral medulla may partially contribute to the beneficial effects of tempol on central sympathetic control.     

Long-term antioxidant supplementation attenuates oxidative stress markers and cognitive deficits in senescent-accelerated OXYS rats

Oxidative damage of biomolecules increases with age and is postulated to be a major causal factor of various neurodegenerative disorders. Consequently, the concept of neuroprotection by antioxidants has been developed. Recently we have shown that the behaviour of young senescent-accelerated OXYS rats is similar to the behaviour of old Wistar animals. To determine the role of oxidative stress in this phenomenon we investigated age-related changes in protein carbonyls (PrC), lipid peroxides (LP), reduced glutathione (GSH), alpha-tocopherol (TP) and SOD activity in the brain of OXYS and Wistar rats. We also studied the effect of long-term supplementation with bilberry extract (2g/kg of diet) and Vitamin E (140 mg/kg of diet) on oxidative stress markers and on learning in passive avoidance test. In both rat strains LP, PrC and TP increased with age and at 24 months PrC was significantly higher (p<0.0001) in OXYS rats. At 3 months GSH was higher and SOD activity was lower in OXYS rats than in Wistar rats. SOD activity decreased with age in OXYS whereas increased in Wistar rats. Cognitive impairments in OXYS rats were manifested earlier than significant differences in the level of brain oxidative stress markers between two strains. By contrast, differences in antioxidant systems of Wistar and OXYS rats were registered at 3 months. Antioxidants attenuated cognitive deficits in OXYS rats, providing evidence for therapeutic role of antioxidants. Nevertheless, the exact mechanisms of neuroprotective effects of antioxidants in vivo and the real impact of oxidative stress on the development of cognitive impairments in OXYS rats still needs to be further investigated.     

Tubeimoside-1 attenuates LPS-induced inflammation in RAW 264.7 macrophages and mouse models

Abstract

Context: Acute lung injury (ALI), characterized by severe hypoxemia, pulmonary edema and neutrophil accumulation in the lung, is a common clinical problem associated with significant morbidity and mortality in shock, sepsis, ischemia reperfusion, etc.

Objective: In this study, we aimed at investigating the protective effect of tubeimoside-1 (TBMS1) on inflammation in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells and a LPS-induced in vivo lung injury model.

Materials and methods: We evaluated the effect of TBMS1 on LPS-induced production of tumor necrosis factor (TNF)-α, interleukin (IL)-6 and IL-1β in the culture supernatants of RAW 264.7 cells by enzyme-linked immunosorbent assay. LPS (0.5?mg/kg) was instilled intranasally in phosphate-buffered saline to induce ALI, and the severity of pulmonary injury was evaluated 6?h after LPS challenge.

Results: TBMS1 significantly inhibited the production of the pro-inflammatory cytokines, TNF-α, IL-6 and IL-1β in vitro and in vivo. Pretreatment with TBMS1 markedly attenuated the development of pulmonary edema, histological severities and inflammatory cells infiltration in mice with ALI. In addition, we further demonstrated that TBMS1 exerts an anti-inflammatory effect in vivo model of ALI through suppression of IκB activation and p38/extracellular signal-regulated kinase mitogen-activated protein kinases signaling in a dose-dependent manner.

Discussion and conclusion: Overall, our data suggest that TBMS1 inhibits inflammation both in vitro and in vivo, and may be a potential therapeutic candidate for the prevention of inflammatory diseases.     

Hepatoprotective treatment attenuates oxidative damages induced by carbon tetrachloride in rats

The present study evaluated the hepatoprotective effect of an N-acetyl dl-methionine + choline chloride + caffeine + thiamine hydrochloride + nicotinamide + pyridoxine hydrochloride compound at doses of 0.2, 0.6 and 1.0 mL/kg of b.w., and the assessment was done by the investigation of serum-enzymatic activity, metabolic functions of the liver and histophatological changes in female Wistar rats, which were subjected to experimental intoxication with CCl₄. One hundred and nineteen rats were randomly distributed into 17 groups, performing five different treatments, being evaluated seven animals per treatment in four periods: 2, 4, 6 and 8 days after CCl₄-induced intoxication. Treated rats with the hepatoprotective medicine (HM) presented a significant reduction in infiltration of inflammatory cells, steatosis, necrosis and liver congestion when compared to non-treated rats (control). Beside these results, the treatment showed a positive effect on circulatory alterations in the intoxicated animals, with reduction of spleen and renal congestion, as well as, promotion of a significant improvement in ALT, AST, LDH, ALP, GGT enzymatic serum activity reduction and in recovering liver function regarding the metabolism of urea, triglycerides and glucose. These findings indicate therapeutic usefulness of the compound when administered at dose 0.6 and 1.0 mL/kg of b.w. in female Wistar rats.     

Pentoxifylline attenuates LPS-induced bronchial hyperresponsiveness but not the increase in exhaled nitric oxide

Background Inhaled endotoxin (LPS) may cause a transient increase in airway responsiveness, possibly through a cytokine-mediated airway inflammation, which is associated with an increase in nitric oxide synthesis and release. Objective We wondered whether pentoxifylline (PTX), which may attenuate cytokine release induced by LPS. could inhibit LPS-induced increase in airway responsiveness. Objective Methacholine (Mch) bronchial responsiveness was assessed 2 and 24 h after saline or LPS inhalation in eight subjects with bronchial hyperresponsiveness (PD20FEV1 610 ± 53 μg), treated with iv saline or PTX, in a double-blind crossover design. Nitric oxide (NO) in the exhaled air, which was expected to increase after LPS inhalation, and PEFR values were also measured at baseline, hourly for 6h and 24 h later. Results After LPS inhalation PEFR decreased significantly compared with placebo inhalation, reaching a maximum decrease of 11.25 ± 1.05 and 4.5 ± 0.84% of baseline, at 2h, respectively during saline and PTX infusion, P < 0.001. Exhaled NO were elevated after LPS compared with placebo inhalation at 1h (35.6 ± 4.8 vs 18 ± 2.8 ppb, P < 0.001), with no difference during saline or PTX infusion. Exhaled NO remained elevated until the 6th hour. PD20FEVI 2h after LPS inhalation was significantly lower than after placebo inhalation both during saline infusion (234 ± 29 vs 625 ± 62 μg, P < 0.001) and during PTX infusion (441 ± 47 vs 616 ± 48 μg, P < 0.001), the difference between saline and PTX being significant (P < 0.01). At 24 h no difference in PEFR, PD20FEV1 and exhaled NO was observed in comparison with pre-study values. Conclusion PTX attenuates both the decrease in airway patency and the increase in bronchial responsiveness induced by LPS inhalation, without any significant change in exhaled NO, which is increased by LPS inhalation.     

HSF1通过抑制中性粒细胞浸润减轻LPS诱导的小鼠急性肺损伤

目的:探讨热休克因子1(HSF1)是否通过抑制中性粒细胞浸润减轻LPS诱导的小鼠急性肺损伤(ALI)及其分子机制.方法:采用气管滴注脂多糖(LPS)的方法制备小鼠ALI模型,采用流式细胞术检测HSF1野生型(HSF1+/+)小鼠和HSF1敲除(HSF1-/-)小鼠LPS处理后12、24和36 h支气管肺泡灌洗液(BAL...     

莱菔硫烷减轻肾缺血再灌注大鼠肝损伤

目的：观察莱菔硫烷（ SFN）对肾缺血再灌注损伤（ RIRI）大鼠肝组织形态、功能、过氧化损伤及超氧化 物歧化酶（ SOD）表达变化的影响。方法：Wistar 大鼠随机分对照组、RIRI 组、SFN1 组和SFN2 组，RIRI 组大 鼠用夹闭左肾动脉45 min 的方法建立RIRI 模型，SFN1 组在夹闭左肾动脉后立即给予SFN，SFN2 组在RIRI 模型 恢复血液再灌注后给予SFN，对照组大鼠只分离左肾动脉并不夹闭。缺血再灌注24 h 后取血和肝，检测血清谷丙 转氨酶（ALT）活性；采用钼酸比色法、硫代巴比妥酸比色法及黄嘌呤氧化酶法测定肝组织H2O2、丙二醛（MDA） 含量及SOD 活性；H-E 染色观察肝组织形态结构改变；Real-time PCR 和免疫印迹法分别测定肝组织SOD mRNA 和蛋白表达水平。结果：与对照组相比，RIRI 组、SFN1 组和SFN2 组大鼠肝组织形态结构受损明显，SFN1 组和 SFN2 组受损程度轻于RIRI 组，SFN1 组又略轻于SFN2 组；RIRI 组、SFN1 组和SFN2 大鼠血清ALT 活性、肝组 织MDA和H2O2 含量升高明显；SFN1 组和SFN2 组的活性和含量均低于RIRI 组，SFN1 组又低于SFN2 组；RIRI 组、 SFN1 组和SFN2 大鼠肝组织SOD 活性明显低于对照组，SFN2 组、SFN1 组高于RIRI 组，SFN1 组又高于SFN2 组。 RIRI 组、SFN1 组、SFN2 组大鼠肝组织SOD mRNA和蛋白表达水平均高于对照组，SFN2 组和SFN1 组SOD的 表达水平又高于RIRI 组，但SFN2 组和SFN1 组差异无统计学意义。结论：大鼠RIRI 发生后，SFN 可能通过上调 SOD的表达增强机体对过氧化物的清除作用，降低了肝组织过氧化损伤程度；与再灌注后给予SFN 相比，缺血 后即刻给药更能有效降低肝组织氧化应激水平，改善肝的形态结构和功能改变。     

厄贝沙坦减轻糖尿病肾病大鼠肾损伤

目的观察厄贝沙坦能否减轻糖尿病肾病(DN)大鼠的肾损伤。方法将大鼠随机分为对照组、DN模型组、厄贝沙坦治疗组。于22周测体质量、随机血糖、24 h尿微量白蛋白、血肌酐、尿素氮,观察肾脏形态改变。应用荧光定量PCR检测miR-192 mRNA在大鼠肾组织中的表达;蛋白免疫印迹法、免疫组织化学法检测肾组织TGF-β1、Zeb1、collagenⅠ蛋白的表达。结果与对照组比较,DN组大鼠体质量、随机血糖、血肌酐、尿素氮和24 h尿微量白蛋白显著增高(P<0.05);与DN组比较,厄贝沙坦治疗组大鼠体质量、随机血糖、血肌酐、尿素氮和24 h尿微量白蛋白显著降低(P<0.05)。厄贝沙坦治疗可以改善DN大鼠的一般情况和肾脏病理损害。与对照组相比,DN组miR-192 mRNA在DN大鼠肾脏的表达下调(P<0.05);与DN组相比,厄贝沙坦组miR-192 mRNA表达上调(P<0.05);与对照组大鼠相比,DN组肾组织的TGF-β1、ZEB1和collagenⅠ蛋白表达量明显增加(P<0.05);与DN组相比较,厄贝沙坦治疗可以减少TGF-β1、ZEB1和collagenⅠ蛋白的表达(P<0.05)。结论厄贝沙坦可减轻糖尿病肾病大鼠的肾损伤。     

L-硝基精氨酸对大鼠LPS性肺损伤的实验治疗研究

目的:观察一氧化氮(NO)和一氧化氮合酶抑制剂N^G-硝基-L-精氨酸(L-NA)对LPS性肺损伤的影响。方法:采用静脉注射脂多糖(LPS)复制急性肺损伤大鼠模型。将40只SD大鼠随机分为5组:空白对照组、LPS模型组、L-NA高剂量(20mg/kg)、中剂量(10mg/kg)、低剂量(5mg/kg)治疗组,经腹腔注射,实验过程中监测大鼠平均动脉压(MAP),定时取静脉血测定血浆中NO₂^-/NO₃^-含量,于规定时间处死大鼠,迅速取出肺脏,观察LPS引起大鼠急性肺损伤后肺系数、肺水肿情况和肺组织中丙二醛(MDA)含量、一氧化氮合酶(NOS)、超氧化物歧化酶(SOD)活性的变化,以及L-NA的治疗作用。结果:L-NA可明显升高MAP,降低肺系数和肺含水量,减少血浆中NO₂^-/NO₃^-含量,可显著降低肺组织中NOS活性,减少MDA含量,增强SOD活性,减轻肺损伤。结论:L-NA对LPS性肺损伤具有治疗作用,且随剂量增大作用增强。     

虫草素预处理减轻SD大鼠心肌缺血再灌注损伤

目的:研究大鼠心肌缺血再灌注(IR)损伤中,虫草素(cordycepin,Cordy)能否通过调节微小RNA-455(miR-455)的表达和减少内质网应激(endoplasmic reticulum stress,ERS)引起的凋亡发挥心肌保护作用。方法:体重250~300 g的SD大鼠随机分为3组:对照(control)组,大鼠只进行开胸手术;IR组,大鼠心肌缺血30 min,再灌注120 min;虫草素治疗组(IR+Cordy组):大鼠缺血再灌注前给予虫草素(10 mg/kg)股静脉注射,每天1次,共注射1周。全自动化学分析法检测大鼠血清中乳酸脱氢酶(LDH)和肌酸激酶同工酶MB(CK-MB)活性。TUNEL试剂盒检测心肌内皮细胞(endothelial cells,EC)凋亡率,电镜观察EC超微结构的改变。RT-q PCR法检测心肌组织miR-455及ERS介导的细胞凋亡信号通路的标志物葡萄糖调节蛋白78(glucose-regulated protein 78,Grp78)和caspase-12的mRNA表达。结果:与control组比较,IR组EC的凋亡率明显升高(P0.05);与IR组比较,虫草素组EC的凋亡率明显下降(P0.05)。与control组比较,IR组的EC线粒体肿胀,膜不规整,内皱疏松有空泡,基粒消失,核膜不规整,染色质浓集、边集,核仁消失,甚至出现凋亡小体;IR+Cordy组与IR组比较症状大为改善。与control组比较,IR组心肌组织Grp78和caspase-12的mRNA及miR-455含量均升高(P0.05);与IR组比较,IR+Cordy组Grp78和caspase-12的mRNA及miR-455的含量均降低(P0.05)。结论:虫草素可有效减轻心肌IR后大鼠心肌EC凋亡,降低心肌组织miR-455表达,抑制内质网应激。     

Chronic treatment with melatonin attenuates serotonergic degeneration in the striatum and olfactory tubercle of zitter mutant rats

The effects of chronic treatment with the antioxidant hormone melatonin on degeneration of serotonergic fibers were studied in the striatum and olfactory tubercle of the zitter rat, which shows a loss-of-function mutation of the glycosylated transmembrane protein attractin. In these animals, serotonergic fibers in the striatum and olfactory tubercle undergo spontaneous and progressive degeneration as a result of abnormal metabolism of reactive oxygen species. Homozygous zitter (zi/zi) rats were provided ad libitum access to drinking water containing melatonin for 9 months (M) after weaning. High-performance liquid chromatography analysis revealed that melatonin treatment significantly increased serotonin in the caudate-putamen, (CPU), nucleus accumbens (NA) and olfactory tubercle (OT). Immunohistochemical staining for serotonin was consistent with the neurochemical data and further demonstrated substantially increased numbers of serotonergic nerve terminals in these areas. Aberrant serotonergic fibers characterized by swollen varicosities (>1 microm in diameter) were observed in the CPU and NA of 10 M zi/zi rats. The number of these fibers decreased after melatonin treatment ended. Furthermore, hyperinnervation of serotonergic fibers was observed in the OT of melatonin-treated zi/zi rats. These results suggest that melatonin protects serotonergic fibers and terminals in zitter rats and/or promotes their neuroplasticity.     

牙周炎对慢性细菌性前列腺炎大鼠前列腺的影响

目的研究牙周炎对慢性细菌性前列腺炎大鼠前列腺的影响。方法 80只SD大鼠随机分为4周组及8周组,每组40只,再将4周组和8周组分别随机分为空白对照组(N组)、慢性细菌性前列腺炎组(CBP组)、牙周炎组(PE组)和慢性细菌性前列腺炎合并牙周炎组(CBP+PE组),每组各10只。观察比较大鼠前列腺组织病理形态学改变、炎症评分、TNF-α、IL-1β的含量及牙周各项指标。结果在4周组中,PE组、CBP+PE组牙周各项指标高于N组、CBP组(P0.05),而PE组与CBP+PE组之间以及N组与CBP组之间牙周各项指标无明显差异(P0.05);CBP+PE组和CBP组前列腺组织病理、炎症评分、TNF-α、IL-1β比N组和PE组均高(P0.05),而N组与PE组之间以及CBP+PE组与CBP组之间前列腺组织病理、炎症评分、TNF-α、IL-1β无明显差异(P0.05)。在8周组中PE组、CBP+PE组牙周各项指标高于N组和CBP组(P0.05),而PE组与CBP+PE组之间以及N组与CBP组之间牙周各项指标无明显差异(P0.05);CBP+PE组、CBP组前列腺组织病理、炎症评分、TNF-α、IL-1β较N组、PE组高(P0.05),而N组与PE组之间前列腺组织病理、炎症评分、TNF-α、IL-1β无明显差异(P0.05),CBP+PE组前列腺组织病理、炎症评分、TNF-α、IL-1β则较CBP组高(P0.05)。4周组和8周组比较,N组各项观察指标无明显差异;8周PE组牙周各项指标高于4周PE组(P0.05),前列腺组织病理、炎症评分、TNF-α、IL-1β无明显差异(P0.05);8周CBP组前列腺组织病理、炎症评分、TNF-α、IL-1β较4周CBP组降低(P0.05),而牙周各项指标无明显差异(P0.05);8周CBP+PE组与4周CBP+PE组比较前列腺组织病理、炎症评分、TNF-α、IL-1β较低(P0.05),但8周CBP+PE组牙周各项指标较4周组高(P0.05)。结论慢性细菌性前列腺炎较长时间合并牙周炎,在大鼠模型上能抑制大鼠慢性细菌性前列腺炎的自愈倾向使其保持在慢性炎症阶段。     

高压氧疗法对大鼠心理应激条件下的牙周炎治疗效果观察

目的:探讨心理应激对大鼠实验性牙周炎的影响,观察高压氧(hyperbaric oxygen,HBO)治疗对心理应激相关牙周炎的疗效。方法:清洁级4周龄雄性Wistar大鼠80只,随机分为4组:(1)正常对照组;(2)牙周炎组:用浸有牙龈卟啉单胞菌株的丝线结扎左侧上颌第2磨牙牙颈部,复制实验性牙周炎模型;(3)单纯应激组;(4)牙周炎+应激组。于实验后第9周停止应激刺激,对除正常对照组外其它各组大鼠每组选取4只进行HBO治疗。于实验后2、4和8周末分批处死动物,每组处死4只,于实验后10周末处死动物,每组处死8只。采血检测血糖浓度、血浆促肾上腺皮质激素(ACTH)、皮质类固醇和肾上腺素含量。测量术区的牙周附着情况,制作牙体牙周联合切片,观察牙周的组织学改变。结果:检测应激标记物的变化可见单纯应激组的血糖及血浆ACTH、皮质类固醇和肾上腺素含量在实验后第2、4周明显高于正常对照组和牙周炎组(P0.01),第8周时血糖降至正常水平,但血浆ACTH、皮质类固醇和肾上腺素含量仍高于正常对照组和牙周炎组(P0.05);牙周炎+应激组在实验后第2、4和8周血糖及血浆ACTH、皮质类固醇和肾上腺素含量均高于正常对照组和牙周炎组(P0.05);HBO治疗组牙周炎+应激组血糖明显低于非治疗组(P0.01),单纯应激组和牙周炎+应激组血浆ACTH、皮质类固醇和肾上腺素水平显著下降(P0.01)。大体观察可见正常对照组及单纯应激组牙周附着位置正常;牙周炎组出现牙龈萎缩,附着丧失明显;牙周炎+应激组附着丧失明显,根分叉暴露,HBO治疗后,牙龈水肿减轻,牙周袋变浅。单纯应激组与正常对照组在各时点的牙周附着水平的差异不显著(P0.05);牙周炎+应激组附着丧失程度在各时点均明显高于牙周炎组(P0.01);HBO治疗结束后牙周炎组及牙周炎+应激组牙周附着丧失程度减轻(P0.01)。组织学观察可见牙周炎+应激组牙周组织破坏程度在各时点均重于牙周炎组;经HBO治疗后,牙周组织炎症程度减轻,炎症细胞浸润减少。结论:心理应激可加重牙周炎进程。HBO对大鼠实验性牙周炎及心理应激相关牙周炎均有治疗效果。     

骨质疏松性牙周炎大鼠左归丸与雌激素治疗后颌骨结构和骨量的变化

背景：有研究表明经典补肾方剂左归丸可用于治疗绝经后女性的骨质疏松。 目的：观察骨质疏松性牙周炎大鼠左归丸与雌激素治疗后颌骨结构和骨量的变化。 方法：将SD大鼠麻醉下结扎上颌第一磨牙建立牙周炎模型、摘除大鼠卵巢建立骨质疏松模型,去势3个月后分别用左归丸和戊酸雌二醇治疗3个月。 结果与结论：左归丸、戊酸雌二醇治疗均能促进大鼠牙槽骨的新生,减轻牙周附着丧失(P < 0.05),使破骨细胞数量减少 (P  < 0.05),牙周组织中骨保护素水平升高(P < 0.01),降低了血清中的碱性磷酸酶水平(P  < 0.01)。结果证实,左归丸、戊酸雌二醇在改善骨质疏松性牙周炎大鼠牙槽骨结构的基础上,促使颌骨骨量增加。