Hydrogen-rich saline protects against hepatic injury induced by ischemia-reperfusion and laparoscopic hepatectomy in swine

Background: Hydrogen-rich saline(HRS) has antioxidative, anti-inflammatory and anti-apoptotic properties. We investigated the effects of hydrogen on hepatic ischemia-reperfusion(I/R) and laparoscopic hepatectomy in swine. Methods: Twenty-one healthy Bama miniature pigs were randomly divided into the sham group, ischemia-reperfusion injury(IRI) group, HRS-5(5 m L/kg) group, and HRS-10(10 m L/kg) group. HRS was injected through the portal vein 10 min before reperfusion and at postoperative day 1, 2 and 3. The roles of HRS on oxidative stress, inflammatory response and liver regeneration were studied. Results: Compared with the IRI group, HRS treatment attenuated oxidative stress by increasing catalase activity and reducing myeloperoxidase. White blood cells in the HRS-10 group were reduced compared with the IRI group( P < 0.01). In the HRS-10 group, interleukin-1 beta, interleukin-6 and tumor necrosis factor alpha, C-reactive protein and cortisol were downregulated, whereas interleukin-10 was upregulated. In addition, HRS attenuated endothelial cell injury and promoted the secretion of angiogenic cytokines, including vascular endothelial growth factor, angiopoietin-1 and angiopoietin-2. HRS elevated the levels of hepatocyte growth factor, Cyclin D1, proliferating cell nuclear antigen, Ki-67 and reduced the secretion of transforming growth factor-beta. Conclusions: HRS treatment may exert a protective effect against I/R and hepatectomy-induced hepatic damage by reducing oxidative stress, suppressing the inflammatory response and promoting liver regeneration.

Hydrogen-rich saline protects against ultraviolet B radiation injury in rats

Exposure of skin to solar ultraviolet（UV） radiation induces photo-damage.Ultraviolet B（UVB） is the major component of UV radiation which induces the production of reactive oxygen species（ROS） and plays an impor-tant role in photo-damage.Hydrogen gas reduces ROS and alleviates inflammation.In this study,we sought to demonstrate that hydrogen-rich saline has the effect on skin injuries caused by UVB radiation.UVB radiation was irradiated on female C57BL/6 rats to induce skin injury.Hydrogen-rich saline and nitrogen-rich saline were ad-ministered to rats by intraperitoneal injection.Skin damage was detected by microscope after injury.UVB radia-tion had a significant affection in tumor necrosis factor alpha,interleukin（IL）-1β and IL-6 levels,tissue superox-ide dismutase,malondialdehyde and nitric oxide activity.Hydrogen-rich saline had a protective effect by altering the levels of these markers and relieved morphological skin injury.Hydrogen-rich saline protected against UVB radiation injury,possibly by reducing inflammation and oxidative stress.

Hydrogen-rich saline injection into the subarachnoid cavity within 2 weeks promotes recovery after acute spinal cord injury

Hydrogen can relieve tissue-damaging oxidative stress, inflammation and apoptosis. Injection of hydrogen-rich saline is an effective method for transporting molecular hydrogen. We hypothesized that hydrogen-rich saline would promote the repair of spinal cord injury induced by Allen＇s method in rats. At 0.5, 1, 2, 4, 8, 12 and 24 hours after injury, then once daily for 2 weeks, 0.25 mL/kg hydrogen-rich saline was infused into the subarachnoid space through a catheter. Results at 24 hours, 48 hours, 1 week and 2 weeks after injury showed that hydrogen-rich saline markedly reduced cell death, inflammatory cell infiltration, serum malondialdehyde content, and caspa se-3 immunoreactivity, elevated serum superoxide dismutase activity and calcitonin gene-related peptide immunoreactivity, and improved motor function in the hindlimb. The present study confirms that hydrogen-rich saline injected within 2 weeks of injury effectively contributes to the repair of spinal cord injury in the acute stage.

The reason for the amelioration of N-methyl-N-nitrosourea-induced retinitis pigmentosa in rats by hydrogen-rich saline

AIM：To investigate the effects of hydrogen-rich saline（HRS）on microglia activation and Sirtuin type 1（Sirt1）in rats with N-methyl-N-nitrosourea（MNU）-induced retinitis pigmentosa（RP）.METHODS：Rats were divided into norm（N）group,model（M）group and HRS（H）group.Rats in M and H groups were given saline and HRS respectively prior to and after administration of MNU.At one day（d1）and d3 afterwards,electroretinogram and histological examination were performed to confirm the effects of HRS on retinal function and structure of MNU-induced RP.Immunofluorescence staining of anti-ionized calcium-binding adapter molecule 1（Iba1）,a maker of microglia cells,was performed,with quantitative real-time polymerase chain reaction（qRT-PCR）for its m RNA quantification.Moreover,Sirt1 m RNA and protein expression in the retinas were detected by Western blot and qRT-PCR.RESULTS：HRS preserved the retinal function and mitigated the reduction of photoreceptor degeneration in MNU-treated retinas.The presence of microglia cells was somewhat more obvious in H group than that in M group at d1.HRS suppressed the further activation of microglia cells,with the number of microglia cells less than that of M group at d3.Results of qRT-PCR of Iba1 were consistent with those of immunofluorescence staining,with the m RNA expression of Iba1 in H group more intensive than that of M group at d1（P〈0.05）,while less than that of M group at d3（P〈0.05）.Furthermore,the Sirt1 m RNA and protein expression decreased after MNU administration,while HRS mitigated the MNU-induced downregulation of Sirt1.CONCLUSION：HRS can effectively keep microglia activation induced by MNU to an appropriate extent,while upregulate Sirt1 in MNU-induced RP.

Protective effect of hydrogen-rich saline on ischemia/reperfusion injury in rat skin flap

Objective: Skin damage induced by ischemia/reperfusion (I/R) is a multifactorial process that often occurs in plastic surgery. The mechanisms of I/R injury include hypoxia, inflammation, and oxidative damage. Hydrogen gas has been reported to alleviate cerebral I/R injury by acting as a free radical scavenger. Here, we assessed the protective effect of hydrogen-rich saline (HRS) on skin flap I/R injury. Methods: Abdominal skin flaps of rats were elevated and ischemia was induced for 3 h; subsequently, HRS or physiological saline was administered intraperitoneally 10 min before reperfusion. On postoperative Day 5, flap survival, blood perfusion, the accumulation of reactive oxygen species (ROS), and levels of cytokines were evaluated. Histological examinations were performed to assess inflammatory cell infiltration. Results: Skin flap survival and blood flow perfusion were improved by HRS relative to the controls. The production of malondialdehyde (MDA), an indicator of lipid peroxidation, was markedly reduced. A multiplex cytokine assay revealed that HRS reduced the elevation in the levels of inflammatory cytokines, chemokines and growth factors, with the exception of RANTES (regulated on activation, normal T-cell expressed and secreted) growth factor. HRS treatment also reduced inflammatory cell infiltration induced by I/R injury. Conclusions: Our findings suggest that HRS mitigates I/R injury by decreasing inflammation and, therefore, has the potential for application as a therapy for improving skin flap survival.

Synergistic effect of hyperbaric oxygen preconditioning and hydrogen-rich saline in ameliorating rat flap ischemia/reperfusion injury

Aim:This study was conducted to evaluate the synergistic effects of hyperbaric oxygen(HBO)preconditioning and hydrogen-rich saline(HRS)treatment on skin flap survival and apoptosis in a rat ischemia/reperfusion(IR)skin flap model.Methods:Male Sprague-Dawley rats were randomly divided into five groups:one sham surgery group(sham group)and four surgery groups(IR group,HBO group,HRS group,and HBO+HRS group).An extended epigastric adipocutaneous flap(6 cm×9 cm)was raised over the abdomen in each animal of all five groups.The last four groups underwent 6 h of IR management and were treated,respectively,with normal saline,HBO,HRS(HRS,0.8 mmol/L),or a combined approach(HBO and HRS).On the 3rd postoperative day,flap survival rate and perfusion condition,apoptotic index,caspase-3 activity,protein expression of pASK1 and Bcl-2/Bax ratio,and Bcl-2 messenger RNA(mRNA)expression were assessed.Results:Prior studies have shown the protective effects of HBO and HRS,both of which have been associated with an increase in flap survival.Compared to the IR group,the flaps in the HBO,HRS,and HBO+HRS groups showed better perfusion and a larger survival area with a low number of apoptotic cells,low caspase-3 activity and pASK1 expression,and a high Bcl-2/Bax ratio and Bcl-2 mRNA expression.Of these groups,the HBO+HRS group showed the best flap survival.Conclusion:Both HBO and HRS treatments increase the rate of flap survival,while the synergistic application of HBO and HRS showed a higher survival rate as compared to individual treatments of each.The potential regulation of apoptosis with the use of these two modalities may improve skin flap survival.

富氢液激活自噬减轻带状疱疹后神经痛大鼠痛敏并降低炎症因子的水平

目的探讨自噬在富氢液治疗带状疱疹后神经痛(PHN)中的作用。方法雄性SD大鼠100只,采用随机数字表法,将其分为5组(n=20):对照组、PHN组、富氢液处理的PHN组(PHN-H2组)、富氢液和3-MA同时处理的PHN组(PHN-H2-3-MA组)、富氢液和雷帕霉素(Rap)同时处理的PHN组(PHN-H2-Rap组)。通过水痘带状疱疹病毒(VZV)接种建立PHN大鼠模型。造模成功的大鼠给予腹腔注射15 mg/kg 3-MA或10 mg/kg Rap,隔日1次,连续3次。富氢液处理方式为于造模后每天2次,腹腔注射富氢液10 m L/kg,连续7 d。50只大鼠分别于造模后3、7、14、21 d,测定机械缩足反应阈(PWT);另50只大鼠,于造模后7 d,收集脊椎腰膨大处,ELISA测定肿瘤坏死因子α(TNF-α)、白细胞介素1β(IL-1β)和IL-6的含量,Western blot法测定自噬蛋白微管相关蛋白1轻链3、beclin 1、P62的水平。结果与对照组比较,PHN组大鼠PWT值减少,TNF-α、IL-1β、IL-6、LC3Ⅱ和beclin 1水平增加,P62含量减少;与PHN组比较,PHN-H2组和PHN-H2-Rap组大鼠PWT值增加,TNF-α、IL-1β和IL-6水平降低,LC3和beclin 1表达进一步增加,P62含量增加;与PHN-H2组比较,PHN-H2-3-MA组大鼠PWT值明显减少,TNF-α、IL-1β、IL-6水平增加、LC3和beclin 1水平降低、P62含量增加。结论富氢液可以通过激活自噬减轻PHN大鼠的机械痛敏和炎症因子的释放。

富氢液对大鼠全脑缺血再灌注损伤的影响

目的脑组织缺血缺氧后,过量自由基产生,破坏组织细胞,形成再灌注损伤。最近,学者研究报道氢气溶解在液体中可选择性中和培养细胞中的羟自由基和亚硝酸阴离子。文中观察腹腔注射富氢液对大鼠暂时性全脑缺血再灌注损伤的影响。方法雄性SD大鼠90只,建立四血管阻塞全脑缺血(15 min)再灌注损伤模型,分为3组:假手术组(n=30),模型组(再灌注同时腹腔注射等渗盐水5ml/kg,n=30)和治疗组(再灌注同时腹腔注射0.6mmol/L富氢液5ml/kg,n=30),检测各组再灌注24 h海马丙二醛(malondialdehyde,MDA)浓度、肿瘤坏死因子α(tumor necrosis factor-α,TNF-α)浓度、核因子-κB(nu-clear factor-kappaB,NF-κB)免疫组化阳性细胞数和活化caspase-3的表达水平以及再灌注72 h海马CA1区HE染色未损伤锥体细胞数。结果与模型组相比,治疗组海马MDA浓度、TNF-α浓度和NF-κB阳性细胞数活均显著下降(P<0.01);活化caspase-3蛋白表达显著降低(P<0.05);海马CA1区锥体细胞数显著增多(P<0.01)。结论腹腔注射富氢液能够有效减轻全脑缺血(15 min)后再灌注时大鼠脑的氧化应激和炎症反应,进而缓减再灌注损伤。

氢气生理盐水对创伤性胰腺炎大鼠氧化应激损伤作用的研究

目的研究氢气生理盐水(HS)抑制氧化应激,减轻大鼠创伤性胰腺炎(TP)损伤的作用。方法将24只雄性Wistar大鼠随机分为假手术组(sham组)、TP组、生理盐水处理组(TP+NS组)和氢气生理盐水处理组(TP+HS组),利用压缩气流冲击暴露的大鼠胰腺,建立大鼠TP模型,于术后12h取胰腺组织观察其病理学变化,并观察胰腺内超氧化物歧化酶(SOD)、丙二醛(MDA)、谷胱甘肽(GSH)变化。结果与TP+NS组比较,术后TP+HS组胰腺组织病理损伤情况明显改善(P<0.05),胰腺组织MDA水平较低(P<0.05),SOD活性和GSH含量较高(P<0.05)。结论 HS能减轻大鼠TP损伤,其机制可能与抑制胰腺创伤后氧化应激反应有关。

富氢液联合浅低温对大鼠脑缺血再灌注海马氧化应激水平的影响

目的在脑缺血再灌注过程中,富氢液和浅低温均可影响机体的氧化应激水平。探讨腹腔注射富氢液联合浅低温对大鼠脑缺血再灌注海马氧化应激水平的影响。方法 50只雄性SD大鼠随机分为5组(n=10):假手术组(S组)、四血管结扎模型组(C组)、富氢液+模型组(W组)、浅低温+模型组(P组)和低温+富氢液+模型组(WP组)。W和WP组在脑缺血再灌注即刻腹腔注射富氢液5 ml/kg,S、P和C组注射等容量等渗盐水。P和WP组通过全身物理降温15 min内将体温降至目标温度32～34℃,维持6 h,其余3组维持在37～38℃。所有大鼠在缺血再灌注6 h时处死,分离海马。苏木精-伊红染色(HE染色),观察海马神经元形态;免疫组化法观察血红素氧合酶-1(heme oxygenase-1,HO-1)的表达;化学分光光度计法测海马谷胱甘肽过氧化物酶(glutathion eperoxidase,GSH-Px)和髓过氧化物酶(myeloperoxidase,MPO)活性。结果与C组比较,P、W和WP组海马神经元结构排列紧凑、变性神经元减少;海马HO-1免疫阳性细胞增多。与C组比较,P、W、和WP组MPO含量降低(P<0.05),GSH-Px含量增高(P<0.05),WP组变化最明显。结论富氢液联合浅低温治疗可通过诱导海马HO-1蛋白表达、降低MPO和上调GSH-Px活性影响大鼠全脑缺血再灌注损伤氧化应激水平。

富氢生理盐水治疗相关疾病机制研究进展

氧化应激、炎症因子、细胞的凋亡参与多种疾病的发生、发展。近年来研究发现,富氢盐水可通过抗氧化应激反应、抗炎反应、抗凋亡作用治疗多种疾病,如缺血/再灌注引发的重要脏器的损伤、神经退行性疾病、脓毒血症、神经病理性痛、多器官衰竭等疾病。本文对富氢盐水治疗疾病的相关机制进行综述。

富氢液多次给药对大鼠全脑缺血再灌注损伤的影响

目的评价再灌注后多次给予富氢液对大鼠全脑缺血再灌注损伤的影响。方法成年雄性SD大鼠,随机分为3组:假手术组(S组)、脑缺血再灌注组(I/R组)和富氢液多次给药组(H组)。I/R组和H组采用四血管阻塞法制备全脑缺血再灌注损伤模型。H组大鼠于再灌注即刻及再灌注后2、4、6h分别腹腔注射0.6mmol/L富氢液5ml/kg。I/R组大鼠给予等容量的生理盐水。再灌注24h时,测定海马丙二醛(MDA)、肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)的含量;再灌注72h时,尼氏染色观察海马组织形态学变化。结果与I/R组比较,H组海马组织MDA、TNF-α、IL-6含量降低(P<0.05),尼氏染色见海马CA1区神经元、尼氏小体数目增多,细胞形态趋于正常。结论再灌注后多次给予富氢液可减轻大鼠全脑缺血再灌注损伤,其机制与抑制脂质过氧化反应和炎性反应有关。

富氢液对糖尿病大鼠周围神经病变血红素氧合酶1表达的影响

目的探讨富氢液对糖尿病大鼠周围神经病变血红素氧合酶1（HO-1）表达的影响。方法健康雄性SD大鼠36只,体重180~200g,采用随机数字表法将其均分为三组：健康对照组（C组）、糖尿病神经病变组（DPN组）和富氢液组（HRS组）。DPN组与HRS组大鼠采用腹腔注射1%链脲佐菌素（STZ）65mg/kg的方法制备糖尿病模型。HRS组于注射STZ 14d后腹腔注射富氢液5ml·kg^-1·d^-1,连续14d,C组和DPN组注射等容量生理盐水。分别于STZ注射前2d（T0,C组注射生理盐水）、注射后7d（T1）、14d（T2）、21d（T3）和28d（T4）测定机械刺激缩足阈值（PWT）和热刺激缩足阈值（PWL）,观察三组大鼠疼痛行为学变化;在T4时测定右后肢运动神经传导速度（MNCV）和神经传导潜伏期。测定结束后,采用HE染色观察三组大鼠坐骨神经损伤情况,采用免疫组化法与Western blot法检测HO-1在坐骨神经中的表达,同时检测丙二醛（MDA）含量和过氧化氢酶（CTA）活性。结果与C组比较,DPN组和HRS组T1~T4时PWT明显降低,T2~T4时PWL明显缩短,T4时MNCV明显减慢,神经传导潜伏期明显延长,DPN组和HRS组坐骨神经中HO-1阳性细胞率与HO-1表达明显升高,MDA含量明显增加,CAT活性明显降低（P〈0.05）。与DPN组比较,HRS组T3、T4时PWT明显增高,PWL明显延长,T4时MNCV明显增快,神经传导潜伏期明显缩短,坐骨神经中HO-1阳性细胞率与HO-1表达明显增高,MDA含量明显降低,CAT活性明显升高（P〈0.05）。结论富氢液可能通过上调HO-1表达,产生抗氧化作用对糖尿病大鼠周围神经损伤发挥保护作用。

氢生理盐水对梗阻性黄疸大鼠肝功能的保护作用

目的研究氢生理盐水对梗阻性黄疸大鼠肝功能的保护作用并探讨其可能机制。方法将雄性SD大鼠随机分为3组(n=14),除假手术组外,均采用双重结扎胆总管造成阻黄模型,不同组大鼠分别给予等量生理盐水和氢生理盐水(5ml/kg,i.p.),10天后检测血清肝功能、内毒素及HMGB1水平,肝组织MDA、HMGB1、TNF-α、IL-1β、IL-6含量及MPO活性,并用光镜观察肝细胞变性、死亡和炎细胞浸润情况。结果胆总管结扎后,对照组大鼠肝功能水平明显降低,血清内毒素、HMGB1及肝组织MDA、HMGB1、TNF-α、IL-1β、IL-6含量及MPO活性明显升高,光镜下肝细胞大量变性坏死伴炎性细胞浸润。氢生理盐水治疗组大鼠肝功能显著好转,各指标明显低于对照组(P<0.01)。结论氢生理盐水能显著减轻梗阻性黄疸大鼠肝损伤,并能有效抑制氧化应激及炎性反应。

富氢盐水对严重烫伤延迟复苏大鼠肠道损伤的影响

目的:探讨富氢盐水对严重烫伤延迟复苏大鼠肠道损伤的影响及机制。方法:48只SD大鼠随机分成假烫伤组(S组)、烫伤+0.9%氯化钠注射液处理组(B+N组)、烫伤+富氢盐水处理组(B+H组)、烫伤+维生素C处理组(B+C组),各12只。制作大鼠背部全层皮肤烫伤30%TBSA模型,伤后6 h按Parkland公式用林格液补液复苏。在伤后6、18、30、42 h各组大鼠腹腔分别注射0.9%氯化钠注射液(5 ml/kg)、0.9%氯化钠注射液(5 ml/kg)、富氢盐水(5 ml/kg)、维生素C(9 ml/kg)(250mg/kg)。观察伤后24、48 h的肠道病理改变,并检测肠道组织中丙二醛、二胺氧化酶、白细胞介素1β的变化及肠绒毛上皮细胞凋亡率。结果:与B+N组相比,B+C组和B+H组24、48 h时相点大鼠肠道病理形态改变均显著减轻(P<0.01);二胺氧化酶均显著升高(P<0.01);而丙二醛、白细胞介素1β、肠黏膜上皮细胞凋亡率均显著降低(P<0.01)。结论:富氢盐水可有效减轻严重烫伤延迟复苏肠道的缺血-再灌注损伤,其保护作用可能与富氢盐水减轻再灌注损伤引起的氧化应激反应、炎性因子介导的炎症反应以及抑制肠道上皮细胞凋亡等机制有关。

氢饱和盐水对阿尔茨海默病模型大鼠氧化应激损伤的影响

目的探索氢饱和盐水对阿尔茨海默病(AD)模型大鼠氧化应激的影响。方法选用280~320 g Sprague-Dawley(SD)大鼠,随机分为模型组、假手术组、氢饱和盐水治疗组;利用立体定向技术侧脑室注射Aβ1~42建立AD模型大鼠,腹腔注射氢饱和盐水。给药14 d后采用生物化学法检测各组大鼠的脑海马组织匀浆的MDA含量,利用免疫组织化学法检测各组大鼠脑海马组织氧化应激标志物HNE及8-OH-d G蛋白的表达。结果模型组大鼠脑组织MDA含量为(6.65±1.07)nmol/mgprotein,与假手术组相比显著升高(P=0.000),而氢饱和盐水治疗组大鼠脑组织的MDA含量较模型组大鼠显著降低(P=0.016)。模型组大鼠海马齿状回显现较多的HNE阳性细胞,假手术组大鼠鲜见HNE阳性细胞,而氢饱和盐水治疗组大鼠海马齿状回HNE阳性细胞较模型组大鼠显著减少(P=0.011)。海马齿状回呈现棕黄色8-OH-d G染色阳性细胞,与假手术组大鼠相比,模型组大鼠海马齿状回出现明显增多的8-OH-d G染色阳性细胞(P=0.000),而经氢饱和盐水治疗后的模型大鼠海马齿状回8-OH-d G染色阳性细胞明显减少(P=0.000)。顶叶皮层呈现棕黄色8-OH-d G染色阳性细胞,与假手术组大鼠相比,模型组大鼠顶叶皮层出现明显增多的8-OH-d G染色阳性细胞(P=0.000),而经氢饱和盐水治疗后的模型大鼠顶叶皮层8-OH-d G染色阳性细胞明显减少(P=0.000)。结论氢饱和盐水可显著减少Aβ诱导的氧化应激损伤蛋白及核酸标志物的表达。

氢气生理盐水对大鼠创伤性胰腺炎的保护作用

目的探讨一种抗氧化剂——氢气生理盐水(hydrogen-rich saline,HS)对大鼠创伤性胰腺炎(traumatic pancreatitis,TP)的保护作用。方法将雄性Wistar大鼠随机分为假手术组(sham组)、创伤性胰腺炎组(TP组)、生理盐水处理组(TP+NS组)和HS处理组(TP+HS组),其中80只分4组,观察各组7 d生存率;另有24只大鼠同上分为4组,分别于术后12 h取胰腺组织观察组织病理学变化及观察细胞因子、血清脂肪酶、淀粉酶变化。结果 TP+HS组术后7 d生存率明显高于TP+HS组(P<0.05);术后TP+HS组胰腺组织病理损伤较TP+NS组轻;与TP+NS组相比,TP+HS组炎症因子TNF-α和IL-1β明显下降(P<0.05);术后TP+HS组与TP+NS组血清淀粉酶和脂肪酶无明显改变。结论 HS能降低组织中炎性因子,减轻大鼠胰腺损伤,是一种治疗TP的可行方法。

大鼠全脑缺血再灌注损伤富氢液不同时间点给药的疗效比较

目的:评价再灌注后富氢液不同时间点给药,对大鼠全脑缺血再灌注损伤的影响。方法:清洁级成年雄性SD大鼠72只,随机均分为4组:假手术组(S组)、全脑缺血再灌注损伤组(I/R组)、再灌注即刻给药组(H1组)、再灌注期间给药组(H2组)。I/R组、H1组、H2组按照四血管阻塞法制作全脑缺血再灌注损伤模型。H1组大鼠在再灌注即刻,经腹腔注射富氢液5m L/kg(浓度0.6 mmol/L)。H2组大鼠在再灌注后6 h,经腹腔注射富氢液5 m L/kg(浓度0.6 mmol/L)。I/R组大鼠经腹腔注射等容量的生理盐水。再灌注24 h后,分别测定海马组织丙二醛(MDA)、肿瘤坏死因子-α(TNF-α)和白细胞介素-6(IL-6)的含量。结果:与I/R组相比较,H1组和H2组海马组织的MDA含量、TNF-α、IL-6水平降低(P<0.05)。H1组与H2组海马组织的MDA含量、TNF-α和IL-6水平无显著差异(P>0.05)。结论:再灌注后不同时间点给予富氢液均能改善大鼠全脑缺血再灌注损伤,但两种给药方法之间无明显差异。

氢饱和生理盐水对小鼠重症急性胰腺炎及胰腺局部p38MAPK表达的影响

目的观察氢饱和生理盐水（hydrogen—richsaline，HRS）对小鼠重症急性胰腺炎（severe acute pancreatitis，SAP）的作用，并探讨其对SAP小鼠胰腺局部p38丝裂原活化蛋白激酶（1,38MAPK）表达的影响。方法雄性C57BIM6小鼠180只，随机分为空白对照组、HRS对照组、SAP组和HRS组，腹腔注射雨蛙素和脂多糖诱导小鼠SAP模型，分别于造模后2、12、24和48h处死各组小鼠；HE染色观察胰腺组织病理学变化，从水肿、腺细胞坏死、炎症及出血等四项指标对胰腺损伤进行病理学评分；生化方法测定血清淀粉酶水平；ELISA法检测血清肿瘤坏死因子-α（TNF-α）、白细胞介素-1β（IL-1β）、IL-6和IL-10；qRT—PCR检测胰腺组织p38MAPK的mRNA表达量。结果HRS不影响SAP小鼠48h生存率；与同时间点SAP组比较，I-IRS组小鼠血清淀粉酶水平12h显著降低（P〈0．05），其余各时间点差异无统计学意义；HRS能减轻SAP小鼠胰腺病理变化，胰腺水肿、腺细胞坏死、炎症及出血评分均显著低于SAP组（P〈0．05）；与SAP组比较，HRS组血清IL-1β、TNF-α水平显著降低（P〈0．05），血清IL-6、IL-10差异无统计学意义；HRS组小鼠胰腺组织p38MAPKmRNA表达24h时间点显著低于SAP组（P〈0．05），其余各时点差异无统计学意义。结论HRS对SAP小鼠48h生存率无影响，能减轻SAP小鼠胰腺病理变化及炎症反应，可能与其下调胰腺局部p38MAPK表达有关。

富氢液通过PI3K通路减轻大鼠脑缺血再灌注损伤

目的探讨富氢液对大鼠脑缺血再灌注致海马神经元凋亡及PI3K/Akt/FoxO1信号通路表达的影响。方法采用线栓法阻塞大鼠大脑中动脉,建立大鼠局灶性脑缺血/再灌注(I/R)模型,SD大鼠随机分为假手术组(Sham组)、缺血/再灌注组(I/R组)和富氢液处理组(HRS组),每组10只;各组于再灌注后24 h,ELISA检测血清中炎症因子IL-6、TNF-α及IL-1β的变化;HE染色观察海马变化,TUNEL法观察脑组织细胞凋亡情况;Western blot法检测海马p-PI3K、Akt、caspase-3和FoxO1蛋白表达变化。结果与Sham组相比,I/R组锥体细胞排列疏松,大量锥体细胞死亡,海马凋亡细胞增多,血清炎症因子IL-1β、IL-6、TNF-α、表达显著增加(P<0.05),脑组织中pPI3K、Akt、caspase-3表达显著升高,FoxO1蛋白降低,两组间比较均具有统计学差异(P<0.05);与I/R组相比,HRS组炎症因子显著降低;p-PI3K、Akt、caspase-3表达水平均显著降低,,FoxO1蛋白升高(P<0.05)。结论富氢液可以减轻缺血再灌注导致的脑损伤,其机制可能与PI3K/Akt/FoxO1信号通路相关。