冬虫夏草对免疫性肝损伤小鼠模型的保护作用研究

目的:观察冬虫夏草多糖(CP)对免疫性肝损伤小鼠模型的保护作用及其作用机制。方法:序贯注射卡介苗(BCG)和脂多糖(LPS)诱导小鼠产生免疫性肝损伤模型。造模过程中,小鼠每日灌胃(ig)冬虫夏草多糖(125、250、500 mg/kg),共12天。比色法测定血清中丙氨酸氨基转移酶(ALT)、天门冬氨酸氨基转移酶(AST)的含量、肝匀浆中超氧化物歧化酶(SOD)活力以及丙二醛(MDA)浓度,并作肝组织病理切片观察。采用ELISA法测定肝脏中TNF-α和IL-1的含量。结果:冬虫夏草多糖(125、250、500 mg/kg)ig给药明显降低BCG+LPS诱导的免疫性肝损伤后小鼠血清中升高的ALT和AST水平,抑制肝匀浆中上升的MDA水平和升高降低的SOD活性。显著降低肝脏中TNF-α和IL-1的含量。病理检查结果显示冬虫夏草多糖有明显的保肝作用。结论:冬虫夏草多糖对小鼠免疫性肝损伤有一定的保护作用,其机制可能与降低TNF-α、IL-1的含量、平衡细胞因子有关。     

天麻多糖GEP-2对BCG+LPS致小鼠免疫性肝损伤的保护作用

目的:观察天麻多糖GEP-2对卡介苗加脂多糖(BCG LPS)致小鼠免疫性肝损伤的影响.方法:制备BCG LPS致小鼠免疫性肝损伤模型,比色法测定血清中丙氨酸氨基转移酶(ALT)、天门冬氨酸氨基转移酶(AST)的含量,肝脏中超氧化物歧化酶(SOD)活力、丙二醛(MDA)浓度以及谷胱甘肽还原酶(GSH-Px)活力,酶联免疫法测定血清TNF-α、IL-1的含量,用MTT法测定脾T、B淋巴细胞增殖能力.结果:天麻多糖GEP-2(25、50、100 mg/kg)能明显降低小鼠血清中升高的ALT和AST水平以及TNF-α、IL-1的含量,抑制肝脏中上升的MDA水平和提高过低的SOD、GSH-Px活性,且各用药组均能提升脾T、B淋巴细胞增殖能力.结论:天麻多糖GEP-2对BCG LPS致小鼠免疫性肝损伤具有显著的保护作用.     

IFN-γ受体Ig融合蛋白对ConA诱导小鼠肝损伤的保护作用

本文研究γ 干扰素受体免疫球蛋白融合蛋白 (IFN γR Ig )对ConA诱导的小鼠细胞免疫性肝损伤的保护作用及机制。在Balb/c小鼠体内一次性静脉注射ConA 2 0mg/kg诱导细胞免疫性肝损伤模型 ,分别于模型建立前后不同时间腹腔注射 10mg/kgIFN γR Ig,观察该融合蛋白对小鼠血清谷丙转氨酶 (GPT )水平 ,细胞因子IFN γ、TNF α和IL 10分泌以及肝组织病理学变化的影响。结果表明IFN γR Ig预防给药明显改善肝脏损伤的组织学和血清学变化 ,降低GPT水平 ,减少肝脏中性粒细胞、单核细胞浸润 ;同时与模型对照小鼠相比血清IFN γ水平下降 ,TNF α分泌合成减少 ,IL 10水平明显增加。而IFN γR Ig通过早期结合并阻断内源性IFN γ ,提高IL 10的抗炎作用 ,减轻炎症细胞对肝脏的侵袭及IFN γ、TNF α的肝细胞破坏作用 ,保护免疫性肝损伤。     

乌索酸对小鼠免疫功能影响的实验研究

乌索酸((Ursolic acid又名熊果酸、乌苏酸)是从忍冬科接骨木属植物陆英(Sambucus Chinensis Lindl)中提取得到的单一化合物[1].研究表明, 乌索酸对BCG LPS免疫性肝损伤有明显的保护作用[2],本实验为进一步研究乌索酸的保肝作用机理,建立不同的小鼠免疫模型,从多角度研究乌索酸对小鼠免疫功能的影响.     

CD38蛋白下调炎症因子的表达减轻脂多糖联合D-氨基半乳糖诱导的急性肝脏损伤

目的研究CD38蛋白在脂多糖联合D-氨基半乳糖(LPS/D-GalN)所诱发的小鼠急性肝损伤中的作用。方法野生型C57BL/6小鼠(WT)和CD38基因敲除小鼠(CD38 KO)随机分为正常对照组,模型早期组和模型晚期组。在造模后2 h和6 h处死动物,检测血清谷丙转氨酶(ALT)和谷草转氨酶(AST),实时荧光定量PCR检测肝脏组织炎症因子的表达,HE染色检测组织病理改变。结果在LPS/D-GalN诱导的模型小鼠中,与WT小鼠相比,CD38 KO小鼠血清ALT和AST水平显著升高,肝脏组织中炎性因子白细胞介素1β(IL-1β)、IL-6、肿瘤坏死因子α(TNF-α)以及γ干扰素(IFN-γ)的表达水平显著升高;病理组织学检测显示肝脏组织出血严重,肝实质细胞空泡变形明显增多,肝细胞死亡显著增加。结论 CD38蛋白通过下调炎症因子的表达,减少肝细胞死亡,减轻LPS/D-GalN诱导的急性肝脏损伤。     

沙棘多糖提取物对LPS/D-GalN诱导的小鼠肝损伤的保护作用及其对TLR4,SOCS3表达的调控北大核心CSCD

目的:研究沙棘多糖提取物对LPS联合D-Gal N诱导的肝损伤的保护作用以及对肝脏TLR4,SOCS3蛋白表达的调控。方法:将C57BL/6系雄性小鼠随机分为6组,即空白对照组、模型组、地塞米松阳性对照组、沙棘多糖低、中、高剂量组;沙棘多糖低、中、高剂量组分别以50、100和200 mg/kg沙棘多糖溶液连续灌胃14 d。通过腹腔注射LPS(10μg/kg)和DGal N(700 mg/kg)建立急性肝损伤模型,阳性药物组在建模前腹腔注射地塞米松(10 mg/kg)。建模4 h后采集血清和肝脏组织,检测血清ALT和AST水平,HE染色观察沙棘多糖提取物对肝损伤的影响。Western blot检测TLR4,SOCS3的表达情况。结果:沙棘多糖提取物显著降低了LPS/D-Gal N诱导的小鼠血清中ALT和AST水平(P<0.01,P<0.05);HE染色观察显示,沙棘多糖明显减轻了肝细胞损伤和炎性细胞浸润。Western blot检测表明,沙棘多糖提取物抑制了LPS/D-Gal N诱导的TLR4的表达,但是对SOCS3的表达影响不明显。结论:沙棘多糖提取物有效抑制了LPS/D-Gal N诱导的肝损伤,这种保护作用可能是通过抑制TLR4的表达来发挥作用的,而非通过调控SOCS3来实现的。     

LPS诱导的内毒素血症小鼠及重症联合免疫缺陷小鼠模型炎症反应的比较

目的:比较脂多糖(LPS)诱导的内毒素血症BALB/c小鼠及重症联合免疫缺陷(SCID)小鼠炎症反应的差异。方法:建立LPS诱导的BALB/c小鼠和SCID小鼠内毒素血症模型,观察小鼠的存活率。分别于诱导前、诱导后3h、6h、12h,取小鼠的血清及诱导后12h小鼠的肝脏、肺脏,用全自动生化分析仪检测两种小鼠血清谷丙转氨酶(ALT)、谷草转氨酶(AST)、尿素氮(BUN)水平;HE染色评价肝脏、肺脏的炎症病理改变;用流式细胞术微球阵列法检测两种小鼠血清TNF-α、IFN-γ、IL-6及MCP-1的水平。结果:(1)LPS诱导内毒素血症后,SCID小鼠于12～24h均死亡(8/8),BALB/c小鼠仅1只死亡(1/8)。(2)LPS诱导后12h,BALB/c小鼠及SCID小鼠血清ALT、AST、BUN的水平均明显升高(P<0.05),SCID小鼠前两项均高于BALB/c小鼠(P<0.05),但BUN两种小鼠无显著差异。(3)肺脏,肝脏炎症盲法的病理评分,SCID小鼠均高于BALB/c小鼠(P<0.05)。(4)SCID小鼠和BALB/c小鼠LPS诱导后3h、6h、12h,血清TNF-α,IFN-γ的水平,诱导后12h,IL-6,MCP-1的水平均显著升高(P<0.05),SCID小鼠明显高于BALB/c小鼠(P<0.05)。结论:LPS刺激SCID小鼠后,可分泌过量的炎性细胞因子,导致更严重的内毒素血症和脏器损伤,是造成小鼠死亡的重要原因。结果提示,缺乏适应性免疫应答细胞调控的情况下,异常增强的固有免疫应答,可能是危及机体生命的重症全身炎症反应综合征发生的重要原因。     

Lactobacillus casei Zhang 对扑热息痛诱导的小鼠急性肝损伤的保护作用

目的:研究益生菌Lactobacillus casei Zhang(Lcz)对扑热息痛(APAP)所致小鼠急性肝损伤的保护作用及其机制。方法:C57BL/6 小鼠被随机分为空白组(Ctrl)、APAP 诱导急性肝损伤模型组(Acetaminophen ,APAP)、阳性药物组(N-Acetylcysteine,NAC)、Lcz 预防组(Lcz/ APAP)和Lcz 对照组(Lcz)。Lcz(1伊109 CFU/ ml)连续灌胃30 d 后,NAC 组在APAP 处理前1 h 腹腔注NAC(150 mg/ kg)。APAP、NAC 以及Lcz/ APAP 组均腹腔注射APAP(300 mg/ kg)。APAP 作用18 h 后,采集血液和收集肝脏组织,检测血清中谷丙转氨酶(ALT)和谷草转氨酶(AST)的水平。通过Western blot 检测肝脏组织中血红素氧化酶(HO-1)、超氧化物歧化酶2(SOD2)、Bcl-2 以及TLR4 的表达水平。结果:Lcz 能抑制APAP 诱导的急性肝损伤血清中ALT 和AST 水平。Lcz 提高了HO-1、SOD2 和Bcl-2 的蛋白表达水平,而降低了APAP 诱导的TLR4 的表达。结论:益生菌Lcz对APAP 诱导的小鼠急性肝损伤有保护作用,其保肝作用机制可能与其抗氧化和抗炎活性有关。     

雷帕霉素对内毒素性肝损伤小鼠肝组织HIF-1表达的影响

目的探讨雷帕霉素对内毒素性肝损伤小鼠肝组织缺氧诱导因子-1(HIF-1)表达的影响。方法健康雄性昆明小鼠36只,随机分为正常组(12)、模型组(12)和雷帕霉素组(12)。应用脂多糖10 mg/kg腹腔注射小鼠诱导内毒素肝损伤模型。造模后6 h取血,检测小鼠血清谷丙转氨酶(ALT)和、谷草转氨酶(AST)活性,免疫组织化学方法和Western blot方法检测各组小鼠肝组织HIF-1的表达。结果模型组血清ALT、AST含量比正常组明显升高(0.01),而雷帕霉素组血清ALT、AST含量比模型组明显降低(0.05)。模型组小鼠肝组织HIF-1表达水平比正常组显著升高(0.01),而雷帕霉素组比模型组显著降低(0.01)。结论雷帕霉素能够下调内毒素性肝损伤小鼠肝组织HIF-1的表达。     

雷帕霉素对内毒素性肝损伤小鼠肝组织Bcl-2表达的影响

目的探讨雷帕霉素对内毒素性肝损伤小鼠肝组织Bcl-2表达的影响。方法健康雄性昆明小鼠36只,随机分为正常组(12)、模型组(12)和雷帕霉素组(12)。应用脂多糖10mg/kg腹腔注射小鼠诱导内毒素肝损伤模型。造模后6h取血,检测小鼠血清谷丙转氨酶(ALT)和谷草转氨酶(AST)活性,免疫组织化学方法和Western blot方法检测各组小鼠肝组织Bcl-2的表达。结果模型组血清ALT、AST含量明显高于正常组(P0.01);雷帕霉素组血清ALT、AST含量明显降于模型组(P0.05)。与正常组相比,模型组小鼠肝组织Bcl-2表达显著降低(P0.01);而与模型组相比,雷帕霉素组小鼠肝组织Bcl-2表达显著升高高于(P0.01)。结论雷帕霉素能够上调内毒素性肝损伤小鼠肝组织Bcl-2的表达。     

Propolis Ameliorates Tumor Nerosis Factor-α, Nitric Oxide Levels,Caspase-3 and Nitric Oxide Synthase Activities in Kainic Acid Mediated Excitotoxicity in Rat Brain

Background

Increased nitric oxide (NO), neuronal inflammation and apoptosis have been proposed to be involved in excitotoxicity plays a part in many neurodegenerative diseases. To understand the neuro-protective effects of propolis, activities of Nitric oxide synthase (NOS) and caspase-3 along with NO and tumor necrosis factor-α (TNF-α) levels were studied in cerebral cortex (CC), cerebellum (CB) and brain stem (BS) in rats supplemented with propolis prior to excitotoxic injury with kainic acid (KA).

Materials and methods

Male Sprague-Dawley rats were divided into four groups (n=6 rats per group) as Control, KA, Propolis and KA+Propolis. The control group and KA group have received vehicle and saline. Propolis group and propolis + KA group were orally administered with propolis (150mg/kg body weight), five times every 12 hours. KA group and propolis +KA group were injected subcutaneously with kainic acid (15mg/kg body weight) and were sacrificed after 2 hrs. CC, CB and BS were separated, homogenized and used for estimation of NOS, caspase-3, NO and TNF-α by commercial kits. Results were analyzed by one way ANOVA, reported as mean + SD (n=6 rats), and p<0.05 was considered statistically significant.

Results

The concentration of NO, TNF-α, NOS and caspase-3 activity were increased significantly (p<0.001) in all the three brain regions tested in KA group compared to the control. Propolis supplementation significantly (p<0.001) prevented the increase in NOS, NO, TNF-α and caspase-3 due to KA.

Conclusion

Results of this study clearly demonstrated that the propolis supplementation attenuated the NOS, caspase-3 activities, NO, and TNF-α concentration and in KA mediated excitotoxicity. Hence propolis can be a possible potential protective agent against excitotoxicity and neurodegenerative disorders.     

Protective effects and antioxidant mechanism of bamboo leaf flavonoids on hepatocytes injured by CCl4

The protective effects and antioxidant mechanisms of bamboo leaf flavonoids (BLFs) on hepatocytes injured by CCl₄ were studied by establishing models of hepatocyte damage induced by CCl₄ and detecting the activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST), glutathione peroxidase (GSH-Px), superoxide dismurase (SOD), malondialdehyde (MDA) content and liver glycogen content. The degree of lesions in liver tissues between model and dosage groups was observed through paraffin sections. Results showed that BLFs significantly inhibit CCl₄-induced liver injury. The ALT and AST activities as well as MDA contents of cells decreased significantly after treatment with BLFs. GSH-Px and SOD activities as well as liver glycogen contents remarkably increased in the flavonoids groups, which exhibited dose-dependent relationships (P < 0.05). The degree of lesions in liver tissues in the BLF groups was microscopically better than that in the model group. BLFs also significantly suppressed hepatocellular injury and death of apoptotic cells. Therefore, BLFs have remarkable protective effects on acute liver injury, which is related to its strong antioxidant capacity to reduce damage in the liver caused by oxidative stress and cell (NCTC-1469) apoptosis. The results of this study provide pharmacological evidence to support the clinical application of BLFs.     

Montelukast, a leukotriene receptor antagonist abrogates lipopolysaccharide-induced toxicity and oxidative stress in rat liver

Endotoxemia-induced hepatotoxicity is characterized by disturbed intracellular redox balance, excessive reactive oxygen species (ROS) generation inducing DNA, proteins and membrane lipid damages. In the present study, the protective effects of montelukast (MNT) against Escherichia coli lipopolysaccharides (LPS)-induced oxidative stress were investigated in rat liver. LPS (10 mg/kg, i.p.) was injected and the animals were sacrificed 6 h after LPS challenge. MNT (10 mg/kg) was administered orally for seven successive days before endotoxemia induction. Blood samples were withdrawn for assessing the activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), lactate dehydrogenase (LDH) and levels of serum total bilirubin, total protein, tumor necrosis factor-alpha (TNF-α) and interleukin 1β (IL-1β). Livers were dissected out and used for histological examination or stored for the determination of malondialdehyde (MDA), protein carbonyl content (PCC), reduced glutathione (GSH) levels, enzymatic activities of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and myeloperoxidase (MPO). Sepsis significantly increased ALT, AST, ALP, LDH, total bilirubin, TNF-α and IL-1β, MPO, MDA and PCC levels and decreased total protein, GSH and enzymatic antioxidants (CAT, SOD and GSH-Px). MNT decreased the markers of liver injury (AST, ALT, ALP, LDH, and total bilirubin), inflammatory biomarkers (TNF-alpha, IL-1β), MDA, PCC and MPO after LPS challenge. In conclusion, MNT abrogates LPS-induced markers of liver injury and suppresses the release of inflammatory and oxidative stress markers via its antioxidant properties and enhancement enzymatic antioxidant activities.     

原卟啉钠对急性肝损伤小鼠肝组织SOD、MDA的影响

 目的 探讨原卟啉钠对四氯化碳（CCl4）致急性肝损伤小鼠血清转氨酶和肝组织超氧化物歧化酶（SOD）、脂质过氧化产物丙二醛（MDA）的影响。方法 60只ICR小鼠随机分为正常对照组、CCl4模型组、联苯双酯组、原卟啉钠低、中、高剂量组。各治疗组每天灌胃给药及造模16h后,摘眼球取血测定血清中谷丙转氨酶（ALT）和谷草转氨酶（AST）活性,剖腹取肝测定肝脏SOD活力和MDA含量。结果 CCl4模型组小鼠血清ALT和AST活力分别为（1879±1219）、（2210±1585）U/L,与正常对照组比较,降低显著（P<0.01）;联苯双酯组、原卟啉钠低、中、高剂量组的SOD活力和MDA含量分别为（207.61±16.02）、（184.35±13.42）、（190.88±17.77）、（199.38±14.43）U/mgprot和（1.08±0.15）、（1.35±0.26）、（1.07±0.16）、（0.92±0.18）nmol/mgprot,与CCl4模型组比较,差异有统计学意义（P<0.05～P<0.01）。结论 原卟啉钠能有效阻止CCl4致急性肝损伤小鼠肝组织SOD活性降低,脂质过氧化产物MDA含量升高,具有一定的保肝降酶作用。     

异烟肼灌胃建立小鼠急性肝损伤模型的研究

 目的 探索应用异烟肼灌胃建立小鼠急性肝损伤模型，并初步阐明其机制。 方法 昆明种小鼠 50 只，随机分为异烟肼正常剂量造模组（常量组）、2 倍剂量造模组（2 倍量组）、5 倍剂量造模组（5 倍量组）、8 倍剂量造模组（8 倍量组）和空白对照组，每组各 10 只。各造模组分别以 90、180、450、720 mg/kg 剂量的异烟肼灌胃，18 h 后检测血清丙氨酸氨基转移酶（ALT）、天冬氨酸氨基转移酶（AST）水平并取肝组织进行光镜观察，探索导致明显急性肝损伤的相对合适剂量。另取昆明种小鼠 90 只，随机分为单纯造模组（40 只）、干预造模组（40 只）和空白对照组（10 只），各造模组以相对合适剂量异烟肼灌胃，其中干预造模组于造模前以甘利欣75 mg/kg 体重连续灌胃 5 d，18、36、54、72 h 后分别检测血清 ALT、超氧化物歧化酶（SOD）、丙二醛（MDA）、谷胱甘肽过氧物酶（GSH-Px）水平，并进行肝组织光镜和电镜观察，探索导致明显急性肝损伤的相对合适时间及可能机制。 结果 在探索相对合适剂量实验中，2 倍量组小鼠血清ALT、AST 分别为（101.6 ± 6.3）和（108.1 ± 14.9）U/L，明显高于空白对照组的（30.1 ± 3.6）、（35.3 ± 6.5）U/L 和常量组的（52.8 ± 5.3）、（53.9 ± 8.9）U/L，差异均有统计学意义（均P < 0.05），肝细胞出现广泛的脂肪变性和水肿，肝窦几乎消失；5 倍量组小鼠死亡 7 只，8 倍量组小鼠则全部死亡。在探索相对合适时间及发生机制实验中，应用2 倍剂量异烟肼灌胃后 18 h，单纯造模组小鼠血清 ALT、MDA 水平明显高于空白对照组，SOD、GSH-Px 水平明显低于空白对照组，肝细胞广泛损伤，细胞超微结构显著变化。 结论 应用 2 倍剂量（180 mg/kg）异烟肼灌胃可成功建立小鼠急性肝损伤模型。异烟肼所致急性肝损伤可能与自由基脂质过氧化反应密切相关。     

Restoration of Glutamine Synthetase Activity,Nitric Oxide Levels and Amelioration of Oxidative Stress by Propolis in Kainic Acid Mediated Excitotoxicity

Background

Propolis has been proposed to be protective on neurodegenerative disorders. To understand the neuroprotective effects of honeybee propolis, glutamine synthetase (GS) activity, nitric oxide (NO), thiobarbituric acid reactive substances (TBARS) and total antioxidant status (TAS) were studied in different brain regions-cerebral cortex (CC), cerebellum (CB) and brain stem (BS) of rats supplemented with propolis and subjected to kainic acid (KA) mediated excitotoxicity.

Materials and Methods

Male Sprague-Dawley rats were divided into four groups; Control group and KA group received vehicle and saline. Propolis group and propolis + KA group were orally administered with propolis (150mg/kg body weight), five times every 12 hours. KA group and propolis + KA group were injected subcutaneously with kainic acid (15mg/kg body weight) and were sacrificed after 2 hrs and CC, CB and BS were separated homogenized and used for estimation of GS activity, NO, TBARS, and TAS concentrations by colorimetric methods. Results were analyzed by one-way ANOVA, reported as mean + SD from 6 animals, and p<0.05 considered statistically significant.

Results

NO was increased (p< 0.001) and GS activity was decreased (p< 0.001) in KA treated group compared to control group as well as propolis + KA treated group. TBARS was decreased and TAS was increased (p< 0.001) in propolis + KA treated group compared KA treated group.

Conclusion

This study clearly demonstrated the restoration of GS activity, NO levels and decreased oxidative stress by propolis in kainic acid mediated excitotoxicity. Hence the propolis can be a possible potential candidate (protective agent) against excitotoxicity and neurodegenerative disorders.     

Effect of Croatian propolis on diabetic nephropathy and liver toxicity in mice

ABSTRACT: BACKGROUND: In the present study, we examined the antioxidant effect of water soluble derivative of propolis (WSDP) and ethanolic (EEP) extract of propolis on renal and liver function in alloxan-induced diabetic mice. In addition, we examined whether different extract of propolis could prevent diabetic nephropathy and liver toxicity by inhibiting lipid peroxidation in vivo. METHODS: Diabetes was induced in Swiss albino mice with a single intravenous injection of alloxan (75 mg kg-1). Two days after alloxan injection, propolis preparations (50 mg kg-1 per day) were given intraperitoneally for 7 days in diabetic mice. Survival analysis and body weights as well as hematological and biochemical parameters were measured. The renal and liver oxidative stress marker malonaldehyde levels and histopathological changes were monitored in the liver and kidney of treated and control mice. RESULTS: Administration of propolis to diabetic mice resulted in a significant increase of body weight, haematological and immunological parameters of blood as well as 100% survival of diabetic mice. Alloxan-injected mice showed a marked increase in oxidative stress in liver and kidney homogenate, as determined by lipid peroxidation. Histopathological observation of the liver sections of alloxan-induced diabetic mice showed several lesions including cellular vacuolization, cytoplasmic eosinophilia and lymphocyte infiltrations, but with individual variability.Treatment of diabetic mice with propolis extracts results in decreased number of vacuolized cells and degree of vacuolization; propolis treatment improve the impairment of fatty acid metabolism in diabetes. Renal histology showed corpuscular, tubular and interstitial changes in alloxan-induced diabetic mice. Test components did not improve renal histopathology in diabetic mice. CONCLUSIONS: Propolis preparations are able to attenuate diabetic hepatorenal damage, probably through its anti-oxidative action and its detoxification proccess as well as the potential to minimize the deleterious effects of free radicals on tissue. The protective role of propolis against the ROS induced damages in diabetic mice gives a hope that they may have similar protective action in humans.     

Effects of erdosteine on acetaminophen-induced hepatotoxicity in rats

We investigated the effects of erdosteine on acetaminophen (APAP)-induced hepatotoxicity in rats. Superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), AST (aspartate aminotransferase), and ALT (alanine transaminase) activities, and malonyldialdehyde (MDA) and nitric oxide levels as oxidant/antioxidant biochemical parameters were investigated with light microscopic evaluation in adult female Wistar Albino rats. APAP administration produced a decrease in hepatic SOD, CAT, and GSH-Px activities, and coadministration of erdosteine (150 and 300 mg/kg) resulted in increases in the activities. MDA and NO levels increased in the APAP group, and erdosteine treatments prevented these increases. Significant elevations in serum AST and ALT levels were observed in the APAP group, and when erdosteine and APAP were coadministered, their serum levels were close to those in the control group. Light microscopic evaluation of livers showed that there were remarkable centrilobular (zone III) hepatic necrosis and mild to moderate sinusoidal congestion in the APAP group, whereas in the erdosteine group, cellular necrosis was minimal and the hepatocytes maintained a better morphology when compared to the APAP group. Erdosteine prevented APAP-induced liver injury and toxic side effects probably through the antioxidant and radical scavenging effects of erdosteine.     

Effect of Brazilian propolis on sneezing and nasal rubbing in experimental allergic rhinitis of mice

We studied the effect of Brazilian propolis on sneezing and nasal rubbing in experimental allergic rhinitis of mice. A single administration of propolis caused no significant effect on both antigen-induced nasal rubbing and sneezing at a dose of 1000?mg/kg, but a significant inhibition was observed after repeated administration for 2 weeks at this dose. Propolis caused no significant inhibitory effect on the production of total IgE level after repeated administration of 1000?mg/kg. The drug also caused no significant inhibition of histamine-induced nasal rubbing and sneezing at a dose of 1000?mg/kg. On the other hand, propolis significantly inhibited histamine release from rat mast cells induced by antigen and compound 48/80 at a concentration of more than 10 μg/ml. These results clearly demonstrated that propolis may be effective in the relief of symptoms of allergic rhinitis through inhibition of histamine release.