Comparison of hyperalgesia induced by capsaicin injection and controlled heat injury: effect on temporal summation

The relationship between induction of central sensitization and facilitation of temporal summation to repetitive stimulation is still unclear. The aim of this study was to investigate temporal summation before and after the induction of secondary hyperalgesia by two different experimental methods: capsaicin injection and controlled heat injury. The effect of each injury model was assessed on a separate day with an interval of at least 5 days. Twelve healthy volunteers participated. Each experiment was performed using electrical, radiant heat, mechanical impact, and punctuate stimuli consecutively. The pain threshold (PT) to a single stimulus and the summation threshold to five repetitive stimuli for electrical (2 Hz) and radiant heat (0.83 Hz) were assessed within the secondary hyperalgesic area. The degree of temporal summation for stimulus intensities of 0.8, 1.0, and 1.2 times the baseline pain thresholds were evaluated by the increase in visual analogue scale (VAS) scores from the first to the fifth stimulus of the train. Further, the degrees of temporal summation were assessed for mechanical impact and punctuate stimuli within the primary and secondary hyperalgesic areas. The contra-lateral forearm served as control (no injury). The pain threshold and the summation threshold to electrical and heat stimuli decreased significantly within the secondary hyperalgesic area after the injury induced by both heat injury or capsaicin injection. However, there was no temporal summation for heat and electrical stimuli in either model. In contrast, for the mechanical impact and punctuate mechanical stimuli the degree of temporal summation was significantly facilitated in the secondary hyperalgesic areas compared with the baseline and the control arm in both models. In the primary hyperalgesic area, the degree of temporal summation was facilitated to mechanical impact and punctuate stimuli but only following the capsaicin injection. In conclusion, the temporal summation mechanism for mechanical stimuli was facilitated in the secondary hyperalgesic area.     

Secondary heat hyperalgesia detected by radiant heat stimuli in humans: Evaluation of stimulus intensity and duration

Diverging observations on secondary hyperalgesia to heat stimuli have been reported in the literature. No studies have investigated the importance of heat stimulus intensity and duration for the assessment of secondary heat hyperalgesia. The present study was designed to investigate systematically (1) if pain sensitivity to radiant heat stimuli (focused Xenon light) is altered in the area of secondary punctuate hyperalgesia induced by intradermal injection of capsaicin and (2) if heat stimulus duration and intensity had an influence on the ability to detect secondary heat hyperalgesia.

Pain ratings to radiant heat stimuli from a focused xenon lamp were assessed within the area of secondary punctuate hyperalgesia in fifteen volunteers before and after intradermal injection of capsaicin. The stimulus conditions were systematically varied between three intensity levels (0.8, 1.0 and 1.2?×?heat pain threshold (PT)) and four duration steps (200, 350, 500 and 750?ms). The present study shows that long duration (350–750?ms) and low intensity (0.8 and 1.0 ×?PT) radiant heat stimuli were adequate to detect secondary heat hyperalgesia.     

The effect of heat conditioning of the primary area before and after induction of hyperalgesia by topical/intradermal capsaicin or by controlled heat injury

The aim of the present study was to test the effect of heat conditioning before and after the induction of hyperalgesia. Three different methods were used for induction of hyperalgesia, topical capsaicin, intradermal capsaicin injection, and a controlled heat injury. The vascular (blood flow and skin temperature) and sensory changes (area of secondary hyperalgesia and ongoing pain) associated with the cutaneous hyperalgesia were compared. Each experiment consisted of two randomized sessions separated by at least 2 days. In one session, pre-conditioning of the skin by heat was performed 30 min before the induction of hyperalgesia using a probe at 45°C for 5 min in the center of the expected primary hyperalgesic area. After the induction of hyperalgesia, heat conditioning was performed twice in the center of the primary hyperalgesic area using a temperature of 2°C above the present individual pain threshold. On the contra-lateral arm, no heat conditioning was applied while hyperalgesia was induced using the same method. This session was evaluated as a control. The preconditioning induced an increased skin temperature in the primary area for both topical capsaicin and the controlled heat injury. Postconditioning caused increased blood flow in the secondary hyperalgesic area for the topical capsaicin method and increased blood flow in the primary hyperalgesic area for the controlled heat injury method. However, conditioning with heat in an attempt to increase the C-fiber input did not have any effect on the ongoing pain ratings and sensory test results in any of the methods. The results of the present study suggest that there is still a need for a better experimental model with more stable allodynia both between sessions and between subjects while at the same time minimizing discomfort to the volunteer.     

Modulation of oral heat and cold pain by irritant chemicals

Common food irritants elicit oral heat or cool sensations via actions at thermosensitive transient receptor potential (TRP) channels. We used a half-tongue, 2-alternative forced-choice procedure coupled with bilateral pain intensity ratings to investigate irritant effects on heat and cold pain. The method was validated in a bilateral thermal difference detection task. Capsaicin, mustard oil, and cinnamaldehyde enhanced lingual heat pain elicited by a 49 degrees C stimulus. Mustard oil and cinnamaldehyde weakly enhanced lingual cold pain (9.5 degrees C), whereas capsaicin had no effect. Menthol significantly enhanced cold pain and weakly reduced heat pain. To address if capsaicin's effect was due to summation of perceptually similar thermal and chemical sensations, one-half of the tongue was desensitized by application of capsaicin. Upon reapplication, capsaicin elicited little or no irritant sensation yet still significantly enhanced heat pain on the capsaicin-treated side, ruling out summation. In a third experiment, capsaicin significantly enhanced pain ratings to graded heat stimuli (47 degrees C to 50 degrees C) resulting in an upward shift of the stimulus-response function. Menthol may induce cold hyperalgesia via enhanced thermal gating of TRPM8 in peripheral fibers. Capsaicin, mustard oil, and cinnamaldehyde may induce heat hyperalgesia via enhanced thermal gating of TRPV1 that is coexpressed with TRPA1 in peripheral nociceptors.     

人参皂苷Rg2对慢性坐骨神经损伤大鼠痛觉敏化和抑郁状态的影响*

目的:观察人参皂苷Rg₂对慢性坐骨神经损伤大鼠痛觉敏化、抑郁状态的影响。方法: 将50只 SD 大鼠随机分为 5组(n=10): 空白对照组(Normal+生理盐水腹腔注射)、假手术组(手术但不结扎+生理盐水腹腔注射) 、坐骨神经慢性压迫损伤(CCI)组(CCI +生理盐水腹腔注射) 、人参皂苷Rg₂低剂量组(CCI+ Rg₂ 5 mg/kg腹腔注射)、人参皂苷Rg₂高剂量组(CCI+ Rg₂ 10 mg/kg 腹腔注射)。CCI模型建立后,药物通过注射器进行腹腔内注射 5 ml/kg,每天1次,连续14 d。分别在术前1 d和术后 1、3、5、7、10、14 d测定大鼠的机械性缩足反射阈值(MWT)和热缩足潜伏期(TWL);术前1 d和术后第14日时检测明暗箱实验和强迫游泳试验。 结果:与假手术组比较,CCI组术后14 d机械痛阈值和热痛潜伏期明显缩短(P＜0.01),明箱内停留时间明显缩短(P＜0.01),穿梭次数明显减少(P＜0.01),游泳潜伏期明显延长(P＜0.01)。与CCI组比较,人参皂苷Rg₂组术后14 d机械痛阈和热痛潜伏期明显增加(P＜0.01),大鼠在明箱内时间明显延长(P＜0.01),穿梭次数明显增多(P＜0.01),且游泳潜伏期明显缩短(P＜0.01)。结论:人参皂苷Rg₂能抑制 CCI 大鼠的机械痛敏和热痛敏,同时改善其抑郁状态。     

束缚应激对D-氨基半乳糖联合脂多糖诱导小鼠肝损伤的保护作用

目的探讨束缚应激对D-氨基半乳糖联合脂多糖（D–galactosamine and lipopolysaccharide combination,D＋L）诱导的小鼠肝损伤的保护作用。方法正常BALB/c小鼠随机分为正常对照组（con）、应激对照组（str）、模型组（D＋L）、束缚应激组（D＋L＋str）。con组小鼠常规饲养;str组小鼠给予定时定量的束缚应激;D＋L组小鼠腹腔注射D-氨基半乳糖和脂多糖的混合溶液,1次/2天;D＋L＋str组小鼠腹腔注射等量D＋L混合液后,给予与str组相同的束缚应激。第8周,各组小鼠取血检测血清AST、ALT,肝脏固定后HE及Masson染色观察小鼠肝脏结构、细胞形态及纤维化程度。结果第8周D＋L＋str组与D＋L组小鼠相比,血清ALT和AST显著降低（P〈0.01）,AST/ALT显著增高（P〈0.01）;HE及Masson染色显示,D＋L组小鼠肝小叶结构紊乱,出现结节性增生及大量上皮细胞核浓缩、溶解、坏死,枯否氏细胞浸润,而D＋L＋str组未见明显病理变化;纤维化程度评分显示,D＋L＋str组与D＋L组小鼠相比,病理评分与纤维显色吸光度值均显著降低（P〈0.05）。结论束缚应激对D＋L诱导的小鼠肝损伤具有一定保护作用。     

鸡矢藤注射液和野木瓜注射液对大鼠足底皮下化学组织损伤诱致自发痛、痛敏和炎症的作用

研究市售中药制剂鸡矢藤注射液和野木瓜注射液有无抗伤害及抗炎作用。采用两种持续性痛动物实验模型——蜜蜂毒(bee venom,BV)模型和福尔马林(formalin,F)模型,评价鸡矢藤注射液和野木瓜注射液系统给药对持续性自发痛反应、原发性热和机械痛敏及炎症反应的作用效果。成年清醒大鼠足底皮下注射BV(0．2％,50μl)不仅可诱发注射侧长达1h以上的、持续的、单相性的自发痛反应(其表现为自发缩足反射行为)和之后出现的持续3—4d的原发性热和机械痛敏现象,而且注射爪出现明显的红、肿等炎症反应。皮下注射F(2．5％,50μl)则产生双相性自发痛反应。与盐水组比较,致痛前系统给予0．32、1．6和9．0ml／kg三个剂量的500％鸡矢藤注射液或250％野木瓜注射液,对BV或F诱致的1h自发缩足反射次数具有剂量依赖性抑制作用;致痛5min后分别给予鸡矢藤或野木瓜注射液对BV或F诱发的自发痛反应也产生显著的抑制作用。然而,致痛前或致痛后静脉注射鸡矢藤注射液或野木瓜注射液对BV诱致的原发性热／机械痛敏及炎症反应均无明显的抑制作用。纳洛酮(一种非选择性的阿片受体拮抗剂)不能翻转鸡矢藤或野木瓜注射液对BV产生的自发痛反应的镇痛作用,提示其镇痛作用不是由内源性阿片受体介导。本研究结果证实鸡矢藤或野木瓜注射液能预防和缓解临床持续性自发痛,但是对原发性热／机械痛敏及炎症反应均无抗伤害效应和抗炎作用。在中药镇痛抗炎有效成分的筛选和评价中,BV模型是一个理想的实验动物模型。     

肌肽对低氧所致大鼠血管内皮细胞损伤的保护作用

目的：研究肌肽对低氧所致大鼠血管内皮细胞损伤的影响。方法：建立低氧条件下大鼠血管内皮细胞损伤模型,用MTT法观察肌肽对低氧损伤的血管内皮细胞活性的影响,测定细胞培养基中LDH活力,并对细胞骨架进行考马斯亮蓝R-250染色观测其细胞结构。结果：浓度为10mmol/L～20mmol/L肌肽孵育血管内皮细胞6h后,可以抑制缺氧12h和24h引起的血管内皮细胞活性下降,同时减少LDH的释放,保持细胞骨架完整。结论：肌肽对低氧所致的血管内皮细胞损伤具有保护作用。     

气候变暖对贺兰山东麓酿酒葡萄热量资源及冷冻害的影响

利用宁夏贺兰山东麓各地1981年以来气象资料,分析了气候变暖对酿酒葡萄生育关键期主要热量资源和冷冻害的影响。结果表明:1981年以来,随着气候变暖,贺兰山东麓酿酒葡萄发育期4—9月各地各月平均气温显著上升,1997年前后发生突变,突变后部分年份较常年同期偏高1℃以上,其中放条萌芽期4月平均气温上升显著,但月内波动幅度增大,酿酒葡萄遭受霜冻或强降温危害的风险增加;7—8月浆果生长和成熟期低温事件发生的可能性仍然较大;气候变暖使活动积温显著增加,中晚熟品种积温保证率达100%,4—9月3300℃(成熟度高,葡萄酒质量好的临界积温)的积温保证率明显提高;无霜期延长,晚熟品种的保证率提高,部分年份活动积温和无霜期满足极晚熟品需求;大部分地区冬季低温冻害相关要素变化趋势都不显著,其中出现持续低于-17℃(冬季受冻临界气温)日数减少,极端最低气温升高,但仍然低于-17℃,惠农、贺兰、平罗、银川20 cm深度-4℃以下日数减少;春季适宜放条期后出现霜冻的年份和日数增多,霜冻过程的最低气温明显降低,出现伴随霜冻的中等及以上强度冷空气频率和次数增加,强度增强。气候变暖对宁夏贺兰山东麓酿酒葡萄生产有利有弊,不同品种酿酒葡萄对气候的适用性不同,因此在酿酒葡萄生育各关键期,仍需加强极端天气气候事件和气象灾害的监测和防范工作,减轻或避免气候条件变化对酿酒葡萄产业发展的不利影响。     

热激处理对冷藏枇杷果实冷害的生理作用

枇杷(Eriobotrya japonica Lindl.)果实采后经48～52℃、10 min的热激处理,然后2～5℃贮藏,通过对贮藏期间果实冷害级别、呼吸速率、过氧化物酶、过氧化氢酶、苯丙氨酸解氨酶活性和质膜相对透性变化的分析,研究贮前热激处理对冷藏枇杷果实冷害的生理作用.结果表明,2～5℃低温可诱导枇杷果实呼吸速率和苯丙氨酸解氨酶活性异常升高,果实冷害程度与苯丙氨酸解氨酶活性之间呈正相关,相关系数r=0.926.热激处理能降低冷藏条件下(2～5℃)枇杷果实呼吸速率的异常升高,减轻由于低温胁迫造成的果肉细胞膜损伤,提高枇杷果实的过氧化物酶和过氧化氢酶活性,降低苯丙氨酸解氨酶的活性.贮前热激处理有推迟和减轻枇杷果实冷害症状发生、降低果肉低温劣变的作用.贮前热激处理结合低温冷藏是延长枇杷果实贮藏寿命的有效措施之一.     

The effect of in vivo heat treatments on blowfly flight muscle mitochondrial function: Effects on partial reactions of the respiratory chain

1. 1. The development of thermotolerance has been shown to protect blowfly flight muscle mitochondrial function from damage resulting from an LD₅₀ in vivo heat dose.

2. 2. The principal sites of the damage have been studied using specific inhibitors of the respiratory chain, rotenone and antimycin A, together with substrates that stimulate respiration through the different complexes.

3. 3. Complex I was identified as the primary site for heat damage. State III respiration was inhibited following the LD₅₀ in vivo heat dose, and uncoupling with FCCP did not restore respiration to control levels, indicating that the respiratory enzymes were inactivated. The development of thermotolerance protected this site from heat damage.

4. 4. In contrast, G3-P stimulated respiration was the same in control, LD₅₀ in vivo treated controls and LD₅₀, in vivo treated thermotolerant mitochondria, and significantly higher than state III respiration of LD₅₀ in vivo treated controls. This suggested that respiration through G3-P dehydrogenase, Co enzyme Q and Complex III is not damaged. However, as G3-P stimulated respiration of coupled mitochondria from LD₅₀ in-vivo treated flies was markedly reduced (El-Wadawi and Bowler, 1995. J. exp. Biol. 198: 2413–2421), phosphorylation at complex III may be inhibited also.

5. 5. Ferrocyanide stimulated respiration through cytochrome c-Complex IV was also inhibited in LD₅₀ in vivo treated flies, as compared with unheated control mitochondria. However, thermotolerance protected this site also from heat damage.

     

注射硫代乙酰胺及饲喂不同油脂水平饲料建立草鱼肝损伤实验模型

目的通过注射硫代乙酰胺(TAA)及饲喂不同油脂水平饲料建立草鱼肝损伤实验模型。方法 实验草鱼分模型组和对照组,每组分别投喂2.8%油脂组、4.8%油脂组和6.8%油脂组,模型组腹腔注射TAA 300mg/kg,1次/日,注射1 d,共计6个实验组,饲养10周。养殖过程中,于2周、4周和6周对每组实验鱼采血,测定天门冬酸氨基转移酶(AST)、丙氨酸氨基转移酶(ALT)和AST/ALT。结果①模型组特定生长率显著降低了30.5%(P<0.01),成活率平均为73.33%。模型组草鱼肌肉粗脂肪含量显著降低了17.6%,而肝胰脏粗脂肪含量显著增高了13.38%(P<0.01)。②模型组2周、4周和6周时,模型组血清AST/ALT分别为对照组的1.94倍、1.38倍和1.31倍。10周时,模型组草鱼血清AST/ALT增高了10.10%(P>0.05),而血清胆碱酯酶(CHE)降低了6.38%(P>0.05)。模型组草鱼血清超氧化物歧化酶(SOD)活力显著低于对照组8.56%(P<0.05)。③与对照组相比,模型组肝细胞肿胀且边界模糊,肝细胞部分脂肪病变,有部分炎症浸润,并均出现肝纤维化。结论注射TAA及饲喂不同油脂水平饲料可以诱导草鱼肝损伤实验模型,实验模型具备脂肪肝和肝纤维化病理特征。     

牛磺酸对失血性休克再灌注肺损伤的防护作用及其机制探讨

目的:探讨失血性休克再灌注肺损伤与一氧化氮的关系及牛磺酸对其的影响.方法:健康家兔24只随机分为三组:对照组、单纯休克组、牛磺酸治疗组.采用失血性休克再灌注后肺损伤模型.测定肺组织及血浆中一氧化氮合酶(NOS)活性、一氧化氮代谢产物(NO2-/NO3-)含量、超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量、肺湿重/肺干重、肺水含量、肺通透指数(LPI)、肺泡灌洗液(PALF)中蛋白含量等指标的变化,并常规留取肺标本进行病理形态观察.结果:①再灌注3 h时肺组织及血浆中SOD活性显著下降,而上述其它指标均显著升高,与对照组相比差异有显著性(均P<0.01).②血浆、肺组织中NO2-/NO3-含量与MDA含量均呈正相关,且肺组织中NO2-/NO3-含量和肺损伤指标呈显著正相关.③牛磺酸(40 mg*kg-1,iv)可减轻上述指标的变化.结论:NO在休克再灌注肺损伤中起重要作用,牛磺酸可减少NO的生成、增强自由基的清除从而使肺组织损伤减轻.     

Aloperine attenuated neuropathic pain induced by chronic constriction injury via anti-oxidation activity and suppression of the nuclear factor kappa B pathway

Objective

To investigate whether aloperine (ALO) has antinociceptive effects on neuropathic pain induced by chronic constriction injury, whether ALO reduces ROS against neuropathic pain, and what are the mechanisms involved in ALO attenuated neuropathic pain.

Methods

Mechanical and cold allodynia, thermal and mechanical hyperalgesia and spinal thermal hyperalgesia were estimated by behavior methods such as Von Frey filaments, cold-plate, radiant heat, paw pressure and tail immersion on one day before surgery and days 7, 8, 10, 12 and 14 after surgery, respectively. In addition, T-AOC, GSH-PX, T-AOC and MDA in the spinal cord (L4/5) were measured to evaluate anti-oxidation activity of ALO on neuropathic pain. Expressions of NF-κB and pro-inflammatory cytokines (TNF-α, IL-6, IL-1β) in the spinal cord (L4/5) were analyzed by using Western blot.

Results

Administration of ALO (80 mg/kg and 40 mg/kg, i.p.) significantly increased paw withdrawal threshold, paw pressure, paw withdrawal latencies, tail-curling latencies, T-AOC, GSH-PX and T-SOD concentration, reduced the numbers of paw lifts and MDA concentration compared to CCI group. ALO attenuated CCI induced up-regulation of expressions of NF-κB, TNF-α, IL-6, IL-1β at the dose of 80 mg/kg (i.p.). Pregabalin produced similar effects serving as positive control at the dose of 10 mg/kg (i.p.).

Conclusion

ALO has antinociceptive effects on neuropathic pain induced by CCI. The antinociceptive effects of ALO against neuropathic pain is related to reduction of ROS, via suppression of NF-κB pathway.     

鞘内注射孤啡肽对大鼠足底注入蜜蜂毒诱致长时程自发痛、痛敏和炎症的不同效果

为进一步了解孤啡肽在脊髓水平是否具有抗伤害及抗炎作用,本实验在具有多种痛行为表现的蜜蜂毒模型上观察了鞘内注射孤啡肽对大鼠一侧后足底注入蜜蜂毒所诱致的同侧自发缩足反射、原发热和机械性痛敏以及注射部位炎症反应的影响,同时观察了新的高选择性孤啡肽受体拮抗剂CompB的作用.结果表明与生理盐水对照组比较,鞘内注射孤啡肽(3、10、30 nmol/10μl)对蜜蜂毒诱发的自发缩足反射次数的抑制作用随剂量提高而增大,抑制率分别为37±7,43±6and57±11%(三个剂量vs对照,P＜0.05);而对蜜蜂毒诱发的注射部位炎症反应(爪体积、爪背腹厚度和蛋白渗出的增加)无显著影响.CompB(30 nmo1)可完全翻转10 nmol孤啡肽对自发缩足反射的抑制作用.鞘内单次或重复注射孤啡肽(10 nmol/10μl)对蜜蜂毒诱致的原发性热和机械性痛敏的发生和维持均无作用.本实验结果提示,外源性孤啡肽在脊髓通过孤啡肽受体的介导产生一定的镇痛作用,但是它可能仅对持续性自发痛有抑制作用,而对热和机械性痛敏及炎症反应均无影响.     

稻纵卷叶螟幼虫驯化产生的热适应能力的继代效应

摘要: 【目的】在全球不断变暖背景下,昆虫受到热胁迫的频率不断增加。短期内反复受到热胁迫会使昆虫产生热适应性,但是昆虫热驯化所产生的耐热能力的传代效应还不完全清楚。稻纵卷叶螟Cnaphalocrocis medinalis是水稻上的重要害虫,对其幼虫在特定温度下进行几代热锻炼可提高其对高温的适应能力。本研究旨在摸清稻纵卷叶螟热适应的传代能力,为在全球变暖形势下以温度因子预测其种群发展趋势提供指导。【方法】将实验室内分别经39℃和41℃连续锻炼30代建立的稻纵卷叶螟热锻炼品系HA39和HA41以及非锻炼品系HA27的1-5龄期幼虫在不同温度(36℃和41℃)下进行不同时长(1~144 h)的暴露处理,调查幼虫的存活率,确定热锻炼品系幼虫的耐热能力;采用两品系间杂交实验测定HA39和HA27各交配组合的繁殖力及后代3龄幼虫的耐热能力;对HA39停止高温锻炼,并测定停止锻炼2代后3龄幼虫的耐热能力。【结果】稻纵卷叶螟3龄幼虫经历多代次短期热锻炼不仅可提高该龄幼虫的高温适应力,而且可提高其他龄期幼虫对特定高温的耐受能力,表现为HA39和HA41在36或41℃下处理特定时长的存活率显著高于HA27。锻炼高温的不同,幼虫获得的热耐受能力也有差异。39℃下锻炼可提高4龄幼虫在36℃下暴露2和4 d以及5龄幼虫在41℃下暴露5和6 h时的存活率,但41℃下锻炼则不可。HA39和HA27的自交及杂交后代的繁殖力之间均无显著差异,杂交后代3龄幼虫在41℃下处理5和6 h时的存活率与HA39自交后代的相当,并且显著高于HA27自交后代的,幼虫通过热锻炼获得的耐热能力可从亲本遗传给后代。停止热锻炼2代后,在39℃下处理4 h时HA39 3龄幼虫的存活率显著高于HA27的,但39℃下其余处理时间以及36和41℃下处理1~7 h HA39 3龄幼虫的存活率均与HA27的无显著差异,表明幼虫热锻炼产生的耐热能力在停止锻炼后2代仍可部分保持。【结论】稻纵卷叶螟幼虫的热适应能力具有继代效应。经过长期的气候变暖适应后,稻纵卷叶螟种群的热适应能力很可能在不断增强,从而夏季高温对其种群的抑制作用减弱,其种群暴发频率增加。     

Absence or presence of glucose in growth medium and its effect on heat injury inStaphylococcus aureus

Summary Staphylococcus aureus 196E, when grown in a glucose (0.25% wt./vol.)-containing medium, produced cells that would undergo injury when subjected to sublethal heat conditions (45 min at 50°C); however, if glucose was omitted from the growth medium, the extent of injury was greatly reduced. Media containing glucose sterilized by filtration or by separate autoclaving produced cells equal in injury susceptibility to medium in which glucose was autoclaved as part of the medium components. Injury also occurred when other sugars such as fructose, mannose, maltose, or lactose were substituted for glucose. Sugar-containing media that producedStaphylococcus aureus of maximal susceptibility to heat injury reached a pH of approximately 6 or lower during growth of the cells. Incubation of staphylococci in growth medium acidified with acetic or lactic acids or HCl did not lead to cells that would undergo injury under the stated conditions. The stimulatory effect of glucose on injury appears to be related to the metabolism of the sugar byStaphylococcus aureus.Agricultural Research Service, U.S. Department of Agriculture. Reference to brand or firm name does not constitute endorsement by the U.S. Department of Agriculture over others of a similar nature not mentioned.     

碱性成纤维生长因子对大鼠成肌细胞氧化应激损伤的作用及其机制

目的：探讨碱性成纤维生长因子（bFGF）下调氧自由基水平在大鼠成肌细胞氧化应激中的保护作用。方法：采用对数生长期大鼠成肌细胞,随机分为四组（n=6）：正常对照组（control）,单纯bFGF组（bFGF）,氧化应激组（H₂O₂）,干预组（bFGF+H₂O₂）。氧化应激组采用含100μmol/L H₂O₂的培养基继续孵育4 h。免疫组化检测B淋巴细胞瘤-2基因（Bcl-2）阳性沉积颗粒;免疫荧光观察活性氧自由基（ROS）水平、Bcl-2、B淋巴细胞瘤-2基因相关X蛋白（Bax）及细胞色素C（Cyt.C）表达;Western blot检测Cyt.C、聚腺苷二磷酸核糖聚合酶（PARP）蛋白表达情况。结果：与正常组比较,氧化应激组成肌细胞Bcl-2表达降低,ROS、Cyt.C表达显著增加（P < 0.05）。与氧化应激组比较,bFGF干预后的成肌细胞Bcl-2表达增加,ROS及Cyt.C表达减少（P < 0.05）。结论：bFGF对成肌细胞氧化应激具有保护作用,其机制可能与bFGF下调氧自由基水平、Bcl-2蛋白增加、Cyt.C表达减少有关。     

维生素K2对四氯化碳诱导的急性大鼠肝损伤的保护作用

探讨枯草芽胞杆菌产物维生素K2(MK-7)对四氯化碳诱导的急性肝损伤的保护作用及机制。

选取SPF级实验用6~8周龄SD雄性大鼠30只, 体质量200~220 g, 随机分为5组(每组6只): 空白组、肝损伤模型组、模型+溶剂组、模型+水飞蓟素组和模型+维生素K2组。空白组不做额外处理, 其余各组均予四氯化碳染毒, 溶剂组给予与维生素K2组相同体积的大豆油, 水飞蓟素组添加水飞蓟素100 mg/100 g体质量, 维生素K2组用维生素K2每日灌胃(给药剂量为2 μg/100 g体质量)。1周后观察大鼠体征和肝脏外观、肝脏炎症及微肉芽肿、肝细胞空泡化结构, 检测血液AST、ALT、MDA、SOD、TNF-α和IL-6含量。

与肝损伤模型组大鼠比, 模型+维生素K2组肝脏指数下降(t=3.250 0, P=0.031 4)。HE染色结果显示, 与肝损伤模型组大鼠比, 模型+维生素K2组空泡化程度明显降低, 损伤较为弥散。与肝损伤模型组大鼠比, 模型+维生素K2组肝功、氧化应激指标及相关炎症因子水平降低[AST(t=4.283 0, P=0.012 8)、ALT(t=2.582 0, P=0.041 6)、MDA(t=7.028 0, P=0.005 9)、SOD(t=3.384 0, P=0.011 7)、TNF-α(t=3.459 0, P=0.013 5)、IL-6(t=2.422 0, P=0.041 8)]。

维生素K2可减轻大鼠急性肝损伤程度, 其作用可通过改善抗氧化酶体系、抑制氧化应激反应及降低炎性因子水平而实现。