强啡肽A（1－17）对大鼠脊髓组织钙调蛋白含量和磷酸二酯酶活性的影响

观察强啡肽Ａ（１－１７）经大鼠蛛网膜下腔注射后对胞内Ｃａ２＋受体钙调蛋白（ＣａＭ）含量及其依赖于Ｃａ２＋／ＣａＭ的磷酸二酯酶（ＰＤＥ）活性的影响。结果表明：强啡肽Ａ（１－１７）１０、２０ｎｍｏｌ给药１０ｍｉｎ可使脊髓组织ＣａＭ含量和ＰＤＥ活性明显下降，呈量效依赖关系，２ｈ后均有不同程度的恢复。选择性ｋ型阿片受体拮抗剂ｎｏｒ－ＢＮＩ３０ｎｍｏｌ、兴奋性氨基酸ＮＭＤＡ受体特异性拮抗剂ＡＰＶ１０ｎｍｏｌ可显著对抗强啡肽Ａ（１－１７）２０ｎｍｏｌ降低脊髓组织ＣａＭ含量的作用并完全阻断强啡肽Ａ（１－１７）对ＰＤＥ活性的抑制；Ｌ型Ｃａ２＋通道阻断剂异搏定１００ｎｍｏｌ亦可部分阻断强啡肽Ａ（１－１７）２０ｎｍｏｌ对脊髓组织ＣａＭ含量和ＰＤＥ活性的影响。     

绞股蓝总皂苷对NCTC11637株HP延缓大鼠实验性胃溃疡愈合的治疗作用及其机制

目的探讨绞股蓝总皂苷（ｇｙｐｅｎｏｓｉｄｅｓ,ＧＰ）对ＣａｇＡ（＋）,ＶａｃＡ（＋）ＮＣＴＣ１１６３７株幽门螺杆菌（Ｈｅｌｉｃｏｂａｃｔｅｒｐｙｌｏｒｉ,ＨＰ）延缓动物实验性胃溃疡愈合的治疗作用及其机制。方法用醋酸诱发大鼠实验性胃溃疡,以溃疡面积、溃疡面积占腺胃部百分比、粘膜组织内白细胞介素８（ＩＬ８）、ＰＧＥ２、ＭＤＡ、ＳＯＤ、·ＯＨ及溃疡愈合时间为指标,观察ｉｇ给予冻干ＮＣＴＣ１１６３７ＨＰ的影响及给予ＨＰ１ｈ后ｉｇＧＰ的治疗作用。结果单给ＨＰ组,溃疡面积加大,愈合延迟,粘膜组织内ＩＬ８、ＭＤＡ升高,ＳＯＤ活性下降;·ＯＨ生成无明显变化;损伤粘膜组织内ＩＬ８升高,ＰＧＥ２亦同时升高。ＨＰ＋ＧＰ组溃疡面积、溃疡面积百分率明显减小;粘膜内ＭＤＡ、·ＯＨ生成抑制,ＩＬ８、ＰＧＥ２平行下降,ＳＯＤ活性提高。结论ＮＣＴＣ１１６３７株ＨＰ可明显延缓醋酸性大鼠胃溃疡的愈合;绞股蓝总皂苷通过抑制炎症反应过程中ＩＬ８、ＭＤＡ、·ＯＨ生成,并通过提高ＰＧＥ２和ＳＯＤ活性增强胃粘膜保护机制,对感染ＮＣＴＣ１１６３７株ＨＰ大鼠实验性胃溃疡产生显著治疗作用。     

绞股蓝总皂苷对NCTC11637株HP延缓大鼠实验性胃溃疡愈合的治疗作用及其机制

目的探讨绞股蓝总皂苷（ｇｙｐｅｎｏｓｉｄｅｓ,ＧＰ）对ＣａｇＡ（＋）,ＶａｃＡ（＋）ＮＣＴＣ１１６３７株幽门螺杆菌（Ｈｅｌｉｃｏｂａｃｔｅｒｐｙ ｌｏｒｉ,ＨＰ）延缓动物实验性胃溃疡愈合的治疗作用及其机制。方法用醋酸诱发大鼠实验性胃溃疡,以溃疡面积、溃疡面积占腺胃部百分比、粘膜组织内白细胞介素 ８（ＩＬ ８）、ＰＧＥ２、ＭＤＡ、ＳＯＤ、·ＯＨ及溃疡愈合时间为指标,观察ｉｇ给予冻干ＮＣＴＣ１１６３７ＨＰ的影响及给予ＨＰ１ｈ后ｉｇＧＰ的治疗作用。结果单给ＨＰ组,溃疡面积加大,愈合延迟,粘膜组织内ＩＬ ８、ＭＤＡ升高,ＳＯＤ活性下降;·ＯＨ生成无明显变化;损伤粘膜组织内ＩＬ ８升高,ＰＧＥ２亦同时升高。ＨＰ＋ＧＰ组溃疡面积、溃疡面积百分率明显减小;粘膜内ＭＤＡ、·ＯＨ生成抑制,ＩＬ ８、ＰＧＥ２平行下降,ＳＯＤ活性提高。结论ＮＣＴＣ１１６３７株ＨＰ可明显延缓醋酸性大鼠胃溃疡的愈合;绞股蓝总皂苷通过抑制炎症反应过程中ＩＬ ８、ＭＤＡ、·ＯＨ生成,并通过提高ＰＧＥ２和ＳＯＤ活性增强胃粘膜保护机制,对感染ＮＣＴＣ１１６３７株ＨＰ大鼠实验性胃溃疡产生显著治疗作用。     

二甲基亚砜对原代培养大鼠肝细胞醋氨酚损伤的影响

醋氨酚（ＡＡＰ）引起肝细胞损伤时，肝细胞还原型谷胱甘肽（６ＳＨ）含量下降，胞浆游离Ｃａ２＋浓度（［Ｃａ２＋］）升高二甲亚砜（ＤＭＳＯ）对ＡＡＰ肝细胞损伤有明显的保护作用。对轻度损伤能完全拮抗，ＤＭＳＯ对ＧＳＨ含量下降有明显的拮抗作用，当ＧＳＮ维持在一定水平时，ＡＡＰ不引起［Ｃａ２＋］升高。提示ＤＭＳＯ可能通过保护ＧＳＨ等巯基物质而发挥拮抗ＡＡＰ肝细胞损伤的作用     

一氧化氮在顺铂致大鼠肾损害过程中的作用

目的 探讨一氧化氮在顺铂肾毒性氧化应激机制中的作用。方法 采用少量多次给大鼠腹腔注射顺铂（ＣＰ）及经口给予水飞蓟素（ＳＢ）预处理后给予ＣＰ模型,观察血尿素氮（ＢＵＮ）含量、一氧化氮合酶（ＮＯＳ）活性、丙二醛（ＭＤＡ）形成、超氧化物歧化酶（ＳＯＤ）活性等指标的变化。结果 ＣＰ可诱导ＮＯＳ活性增高,使ＮＯ生成量增多;ＢＵＮ含量与ＭＤＡ含量及ＳＯＤ活性的变化并不完全一致,而与ＮＯ含量的时相变化活性增高,     

槐定碱对实验性心衰豚鼠心功能的影响

对戊巴比妥钠所致实验性心力衰竭豚鼠，静注不同剂量的槐定碱（ＳＯＰ）可明显增加左心室内压力变化速率最大值）（ＬＶ＋ｄｐ／ｄｔｍａｘ），左心室内压力变化峰值（ＬＶＳＰ），平均动脉压（ＭＡＰ），加快心率（ＨＲ），降低左室舒张末压（ＬＶＥＤＰ），与不给药组、ＮＳ对照组比较差异显著。其作用于１ｍｉｎ左右达高峰。静脉注射毒毛旋花子甙Ｋ（９０μｇ／ｋｇ），对±ｄｐ／ｄｔｍａｘ，ＬＶＳＰ，ＭＡＰ，ＨＲ的影响较ＳＯＰ强，不同剂量ＳＯＰ可提高心肌组织Ｃａ２＋含量，但弱于毛旋花子甙Ｋ，与不给药组及ＮＳ对照组比较差异显著；结果表明ＳＯＰ能明显改善心衰豚鼠心脏功能，其作用机制可能与增加心肌组织Ｃａ２＋含量有关。     

槲皮素对异丙肾上腺素所致大鼠心肌肥厚的影响

目的　研究槲皮素（ Ｑｕｅ） 对异丙肾上腺素（ Ｉｓｏ） 所致大鼠心肌肥厚的抑制作用及作用机制。方法　 Ｉｓｏ ００２ ｍｇ·ｋｇ－ １ ,每日两次,连续ｓｃ ６ ｗｋ ,形成大鼠心肌肥厚模型,分别测定心脏各重量参数、心肌过氧化脂质（ Ｌ Ｐ Ｏ） 含量、超氧化物歧化酶（ Ｓ Ｏ Ｄ） 活性及心肌 Ｃａ２ ＋ 和主动脉 Ｃａ２ ＋ 含量,培养乳鼠心肌细胞,应用 Ｆｕｒａ ２／ Ａ Ｍ 钙荧光指示剂技术测定心肌细胞内游离钙浓度。结果　 Ｉｓｏ 连续ｓｃ ６ ｗｋ 后,心肌和左心室重量明显增加,心肌 Ｌ Ｐ Ｏ 含量显著增加, Ｓ Ｏ Ｄ 活性下降,心肌 Ｃａ２ ＋ 和主动脉 Ｃａ２ ＋ 含量明显增加,给 Ｑｕｅ ７５ ｍｇ·ｋｇ－ １ ,１５０ ｍｇ·ｋｇ － １ 和维拉帕米１０ ｍｇ·ｋｇ － １ 后均能明显减轻心肌肥厚,降低 Ｌ Ｐ Ｏ 含量,增加 Ｓ Ｏ Ｄ 活性,降低心肌 Ｃａ２ ＋和主动脉 Ｃａ２ ＋ 的含量,应用 Ｆｕｒａ ２／ Ａ Ｍ 钙荧光指示剂技术发现 Ｉｓｏ 和 Ｈ２ Ｏ２ 能引起培养乳鼠心肌细胞内游离钙浓度明显升高。槲皮素对心肌细胞静息钙无明显影响,能抑制 Ｉｓｏ和 Ｈ２ Ｏ２ 致培养乳鼠心肌细胞内游离钙浓度的升高。结论　 Ｑｕｅ 能抑制 Ｉｓｏ 所引起的心肌肥厚, 该作用与清     

尼群地平对大鼠野百合碱性肺动脉高压的防治作用

目的：利用野百合碱（ＭＣＴ）引起的大鼠肺动脉高压（ＰＨ）模型，探讨尼群地平（ＮＩＴ）对ＭＣＴ性ＰＨ的防治作用。方法：给ＭＣＴ或ＭＣＴ＋ＮＩＴ（１０ｍｇ·ｋｇ－１ｉｐ，每日一次）４ｗｋ，测定肺血流动力学参数和静脉血浆及肺组织匀浆中内皮素样免疫反应物（ｉｒ－ＥＴ）、一氧化氮（ＮＯ）、超氧化物歧化酶（ＳＯＤ）和丙二醛（ＭＤＡ）的含量。结果：ＮＩＴ能有效地降低ＭＣＴ模型大鼠的肺动脉压（从４．５±０．９降至３．６±０．５ｋＰａ）和肺血管阻力（从１１８±１７降至７９±１８ｋＰａ·ｍｉｎ·Ｌ－１），能抑制ＭＣＴ引起的肺小动脉中膜增厚；ＮＩＴ能显著抑制ＭＣＴ模型大鼠的肺组织匀浆中ＮＯ含量的减少和血浆中ＳＯＤ活性的降低（Ｐ＜０．０５），明显阻止肺匀浆中ＭＤＡ的升高（Ｐ＜０．０１）。结论：长期使用ＮＩＴ可有效防治ＭＣＴ性ＰＨ，其作用可能与其Ｃａ２＋拮抗作用及保护ＳＯＤ活性和增加ＮＯ含量有关。     

山茱萸对致衰大鼠红细胞的抗氧化作用及钙与衰老的机制研究

本实验以Ｗｉｓｔａｒ大鼠颈背部注射Ｄ－半乳糖人为建立衰老模型,同时以山茱萸作为抗衰老药物观察自由基（ＦＲ）对机体组织的损伤作用,山茱萸的抗氧化能力,了解细胞内Ｃａ＾２＋在致衰前后的变化及在衰老中的作用。实验结果显示,模型组大鼠抗氧化能力下降,表现为ＲＢＣ内ＳＯＤ活力下降（Ｐ〉０．０５）。山茱萸给药组大鼠ＲＢＣ内ＳＯＤ活力、ＲＢＣ膜中ＭＤＡ含量及ＲＢＣ内Ｃａ＾２＋浓度无明显变化,实验结果证明,衰老大     

过氧化氢亚急性吸入毒性研究

本研究应用Ｈ２Ｏ２蒸气（５．４，３２．１ｍｇ／ｍ３）进行大鼠亚急性吸入染毒。大鼠吸入Ｈ２Ｏ２蒸气后，发现血清ＡＫＰ和ＡＣＰ活性增高，全血ＣＡＴ及肺组织ＳＤＨ活性降低。同时还发现肺组织ＧＳＨ含量明显降低，ＭＤＡ含量显著升高。Ｈ２Ｏ２对呼吸系统不仅有刺激作用还可诱发对肺脏的氧化性损伤。     

N-乙酰半胱氨酸联合维生素E对大鼠急性出血坏死性胰腺炎NF-κB的作用研究

目的 研究抗氧化剂N-乙酰半胱氨酸(NAC)联合维生素E(VitE)对大鼠急性胰腺炎动物模型胰腺组织NF-κB的作用,探讨两药的联合使用对急性胰腺炎的影响.方法 40只SD大鼠随机分为假手术(SO)组、出血坏死性胰腺炎(AHNP)组、NAC治疗组、NAC+ VitE治疗组,4组各10只.造模后12h取材,同时观察大鼠胰腺病理评分、血清淀粉酶(AMY)、丙二醛(MDA)、胰腺组织髓过氧化物酶(MPO)及胰腺组织中核因子-κB(NF-κB)的表达.结果 AHNP组胰腺病理评分、AMY、丙二醛、MPO及胰腺组织NF-κB的表达明显高于其他组(P＜0.01),NAC治疗组上述指标均低于AHNP组(P＜0.01),但仍高于SO组(P＜0.01),NAC+ VitE治疗组上述指标均低于AHNP组(P＜0.01)及NAC治疗组(P＜0.01),高于SO组(P＜0.01).结论 在AHNP时应用NAC+ VitE能明显减轻胰腺组织病理损伤,降低胰腺炎时血清AMY、丙二醛的浓度和胰腺组织MPO的活性,抑制胰腺组织中核因子-κB(NF-κB)的表达.     

血小板激活因子在大鼠肝脏缺血预处理中的作用

目的探讨缺血预处理(IP)在肝组织缺血再灌注(I/R)损伤的保护机制及血小板激活因子(PAF)在其中的作用。方法采用大鼠原位半肝缺血再灌注和缺血预处理模型,缺血前通过肠系膜静脉分别注入PAF(3μg/kg)和PAF拮抗剂BN52021(5 mg/kg),观察分析血清丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)、乳酸脱氢酶(LDH)、肝组织脂质过氧化物产物丙二醛(MDA)、超氧化物歧化酶(SOD)含量、肝组织病理改变、中性粒细胞(PMN)计数及电镜观察等各项指标。结果I/R导致明显的肝损伤,IP减轻肝I/R损伤,BN52021能模拟IP的保护作用,大剂量PAF可以抵消IP的保护作用。结论IP对鼠肝I/R有明显的保护作用,IP期间产生一定量的自由基,对随后的I/R的保护作用具有重要意义。PAF参与了肝IP的作用过程,其作用是通过影响氧自由基产生和PMN与血管内皮的黏附而实现的。PAF的降低可能是肝IP的保护机制。     

牛磺酸对2型糖尿病大鼠胰腺线粒体氧化应激的影响

目的探讨牛磺酸对糖尿病大鼠胰腺线粒体氧化应激的影响。方法将30只Wistar大鼠随机分为正常对照组、糖尿病组(DM组)和牛磺酸治疗组(Tau组,采用20g.L-1牛磺酸生理盐水溶液治疗,200mg·kg-1),前两组注射等体积的生理盐水溶液。8wk后,测3组大鼠血浆葡萄糖、胰岛素、丙二醛(MDA),胰腺线粒体MDA、Ca2+、超氧化物歧化酶(SOD)及Na+,K+-ATP酶(Na+,K+-ATPase)和Ca2+,Mg2+-ATP酶(Ca2+,Mg2+-ATPase)的活性。结果①DM组大鼠血糖、MDA和胰腺线粒体MDA、Ca2+含量明显高于对照组(P<0.01),而血浆胰岛素水平、SOD、Na+,K+-AT-Pase和Ca2+,Mg2+-ATPase活性明显降低(P<0.05)。②Tau组大鼠血糖、MDA及胰腺线粒体Ca2+、MDA含量较DM组明显降低(P<0.05),血浆胰岛素水平、SOD、Na+,K+-ATPase和Ca2+,Mg2+-ATPase活性明显升高(P<0.05)。结论牛磺酸可减轻2型糖尿病大鼠胰腺线粒体氧化应激水平。     

Pinealectomy aggravates acute pancreatitis in the rat

Melatonin, a pineal indoleamine, protects the pancreas against acute damage; however, the involvement of the pineal gland in the pancreatoprotective action of melatonin is unknown. The primary aim of this study was to determine the effects of pinealectomy on the course of acute caerulein-induced pancreatitis (AP) in rats. AP was induced by a subcutaneous infusion of caerulein (25 μg/kg) into pinealectomized or sham-operated animals. Melatonin (5 or 25 mg/kg) was given via intraperitoneal (ip) injection 30 min prior to the induction of AP. The pancreatic content of the lipid peroxidation products malondialdehyde and 4-hydroxynonenal (MDA + 4HNE) and the activity of an antioxidative enzyme, glutathione peroxidase (GSH-Px), were measured in each group of rats. Melatonin blood levels were measured by radioimmunoassay (RIA). In the sham-operated rats, AP was confirmed with histological examination and manifested as pancreatic edema and an increase in the blood lipase level (by 1,500%). In addition, the pancreatic content of MDA+ 4HNE was increased by 200%, and pancreatic glutathione peroxydase (GSH-Px) activity was reduced by 40%. Pinealectomy significantly aggravated the histological manifestations of AP, reduced the GSH-Px activity and markedly augmented the levels of MDA+ 4HNE in the pancreas of rats with or without AP as compared to sham-operated animals. Melatonin was undetectable in the blood of the pinealectomized rats with or without AP. Treatment with melatonin (25 mg/kg, ip) prevented the development of AP in the sham-operated rats and significantly reduced pancreatic inflammation in the animals previously subjected to pinealectomy. In conclusion, pineal melatonin contributes to the pancreatic protection through the activation of the antioxidative defense mechanism in pancreatic tissue as well as its direct antioxidant effects.     

Cellular electrophysiological effects of platelet-activating factor (PAF) and its antagonist BN 52021 in cardiac preparations.

The effects of PAF and its antagonist BN 52021 were studied on the transmembrane action potential (AP) in atrial and ventricular papillary muscles of guinea-pig. PAF (10(-11)-10(-7) M) did not modify the resting membrane potential (RP) nor the maximum rate of depolarization (Vmax) either in atrial or in ventricular fibres. At 10(-11) M, PAF increased the amplitude of AP both in atrial and ventricular muscles. the repolarization phase was dose-dependently shortened in the case of atrium, while the duration of ventricular AP was somewhat increased. The K+ channel blocker 4-aminopyridine (10(-3) M) prevented the effect of PAF on the duration of atrial AP. BN 52021 (10(-7) M to 10(-5) M) produced a significant shortening of the duration of atrial AP and did not modify the other parameters. In papillary muscle up to 10(-6) M, it increased both RP and the amplitude of AP and caused a dose-dependent shortening of the repolarization. Neither PAF (10(-11) to 10(-7) M) nor BN 52021 (10(-5) M) was able to induce slow AP in guinea-pig atrial and ventricular preparations depolarized by 25 mM K+ Tyrode solution. PAF did not modify the slow AP elicited by isoprenaline (5 x 10(-7) M). The present findings suggest that neither PAF nor BN 52021 affects slow inward Ca2+ current but their effects on other ionic currents, e.g. K+ currents, may be important.     

The effects of PAF-acether on the cardiovascular system and their inhibition by a new highly specific PAF-acether receptor antagonist BN 52021

BN 52021, a new specific PAF-acether receptor antagonist, was evaluated on several cardiovascular models. BN 52021 antagonized PAF-acether-induced extravasation in rats. Inhibition of the hypotensive action of PAF-acether was obtained by administration of the antagonist, given preventively or curatively. In isolated guinea-pig hearts, BN 52021 inhibited the vasoconstriction induced by PAF-acether whereas a small inhibition was observed with papaverine. On the other hand, phosphodiesterase inhibitors were very effective against coronary vasoconstriction induced by vasopressin while BN 52021 was without effect. PAF-acether increased the tonus of rat isolated portal vein; this effect was inhibited by BN 52021, without any reduction in basal myogenic activity. In this model Ca2+ antagonists (D 600, diltiazem) showed a small inhibitory effect but they strongly reduced basal myogenic activity. Neither PAF-acether nor BN 52021 modified phenylephrine-induced contraction of the isolated rabbit aorta with or without endothelium demonstrating that endothelium-dependent relaxing factor is not related to PAF-acether. Our results suggest that BN 52021 specifically block the cardiovascular effects of PAF-acether. This agent may thus be an useful tool for a better understanding of the role of PAF-acether in hemodynamic changes involved in anaphylaxis or shock.     

川芎嗪对急性胰腺炎大鼠胰腺血流量影响与治疗作用

应用牛磺胆酸钠诱发大鼠急性胰腺炎(AP)模型.观察了川芎嗪(TMP)对AP大鼠胰腺血流量和存活率的影响.发现TMP显著增加胰腺相对血流量及灌注量.减轻胰腺病理形态损伤.提高大鼠存活率。通过测定血浆TXB_2、6-酮PGF_la及血小板聚集率.显示TMP能纠正AP时TXA_2-PGI_2失衡.降低血小板聚集率。提示TMP的治疗作用可能系通过调节TXA_2-PGI_2平衡而改善AP时胰腺血液循环紊乱而实现。     

银杏苦内酯B对豚鼠心室肌细胞动作电位及L-型钙通道的影响

目的　研究银杏苦内酯B(BN 5 2 0 2 1)对豚鼠心室肌细胞动作电位 (AP)和L 型钙通道的影响。方法　全细胞膜片箝技术。AP记录采用电流箝方式 ,电流记录采用电压箝方式。结果　BN 5 2 0 2 1明显缩短动作电位时程 (APD) ,在10 -6mol·L-1浓度 ,APD90 缩短 9% (P <0 0 5 )。在 10 -5mol·L-1浓度 ,APD90 缩短 12 % (P <0 0 1)。 10 -6mol·L-1以上浓度BN 5 2 0 2 1还明显缩短APD50 ,最大缩短达 14% (P <0 0 5 )。较高浓度 (10 -5mol·L-1)的BN 5 2 0 2 1可使静息电位增加 (P <0 0 5 )。BN 5 2 0 2 1浓度依赖性减少L 型钙电流(L ICa)。 10 -6mol·L-1浓度下 ,峰值L ICa降低 2 4 7% (P<0 0 1) ,10 -5mol·L-1浓度下 ,峰值L ICa降低 36 9% (P <0 0 1)。随着药物浓度的增加 ,I U关系曲线逐渐上移 ,但其峰值电压保持不变。结论　BN 5 2 0 2 1明显缩短APD ,抑制L ICa,且具有明显的浓度依赖关系。     

Effect of tiron on remote organ injury in rats with severe acute pancreatitis induced by <Emphasis Type="SmallCaps">l</Emphasis>-arginine

Acute pancreatitis (AP) is an acute inflammatory disorder of the pancreas that can be complicated by involvement of other remote organs. Oxidative stress is known to have a crucial role in the development of pancreatic acinar damage and one of the main causes in multisystem organ failure in experimental AP. The aim of the study was to determine the effect of tiron on pancreas and remote organ damage in l-arginine (L-Arg) induced AP rat model. Thirty-two male rats were divided in random into four groups: control, tiron, L-Arg, and tiron with L-Arg. At the end of the experiment, blood samples were withdrawn for biochemical analysis. The pancreas, lung, kidney, and liver were collected for histopathological examination. Estimation of pancreatic water content was done. Analysis of pulmonary, hepatic, renal, and pancreatic lipid peroxide levels (MDA), superoxide dismutase (SOD), and reduced glutathione (GSH) were carried out. Finally, nuclear factor kappa B (NF-κB) and transforming growth factor β1 (TGF-β1) expression in pancreatic tissue was determined. Results indicated that treatment with tiron significantly decreased lipid peroxide levels and markedly increased both SOD activity and GSH level. Moreover, histopathological analysis further confirmed that administration of tiron relatively ameliorates pancreatic acinar cells and remote organ damage. Increased immunoreactivity of NF-κB and TGF-β1 were reduced also by tiron treatment. These findings pointed out the protective role of the mitochondrial antioxidant, tiron against AP induced by L-Arg.