中药颈椎Ⅰ号治疗模拟颈神经根炎病理学观察

目的　为了观察中药颈椎 号对模拟颈神经根炎的疗效及作用机理。方法　将 96只模拟颈神经根炎 Wistar大鼠随机分为 4组 :颈椎 号中剂量组、颈椎 号高剂量组、颈复康组及空白对照组 ,分别给予颈椎 号中剂量、高剂量、颈复康及凉开水 ,于造模后 3天、 7天、 14天、 4 2天 ,取神经根进行病理学观察。结果　颈椎 号中剂量、高剂量可以明显减轻模型鼠颈神经根的充血、水肿、淋巴细胞浸润等炎症反应 ,减轻成纤维细胞和胶原纤维的增多 ,减轻瘢痕化 ,促使神经功能恢复。结论　颈椎 号对模拟颈神经根炎具有良好的疗效     

中药颈椎I号治疗模拟颈神经根炎病理学观察

目的 为了观察中药颈椎Ｉ号对模拟颈神经根炎的疗效及作用机理，方法 将９６只模拟颈神经根炎Ｗｉｓｔａｒ大鼠随机分为４组：颈椎Ｉ号中剂量组，颈椎Ｉ号高剂量组，颈复康组及空白对照组，分别给予颈椎Ｉ号中剂量，高剂量，颈复康及凉开水，于造模后３天，７天，１４天，４２天，取神经根进行病理学观察，结果 颈椎Ｉ号中剂量，高剂量可以明显轻模型鼠颈神经根的充血，水肿，淋巴细胞浸润等炎症反应，减轻成纤维细胞和胶原纤维的     

实验性胰腺炎大鼠血浆ET和PGI2水平的改变及川芎嗪？…

目的 探讨内皮素（ＥＴ）与前列环素（ＰＧＩ２）在急性出血坏死性胰腺炎（ＡＨＮＰ）病理生理中的作用及川芎嗪（ＴＭＰ）治疗意义。方法 动态测定ＡＨＮＰ大鼠血浆ＥＴ和ＰＧＩ２水平,观察胰腺组织形态及大鼠的存活率,并观察ＴＭＰ对它们的影响。结果 ＡＨＮＰ大鼠术后随时间延长,血浆ＥＴ含量及ＥＴ／ＰＧＩ２比值递增,胰腺组织病理形态损害加重,均较假手术组有显著性差异（Ｐ〈０．０５）;胰腔注射ＴＭＰ组血浆ＥＴ含量     

心内直视术中患者血浆PGE2水平变化及其负性免疫调节作用

为了探讨心内直视术体外循环（ＣＰＢ）对患者血浆前列腺素Ｅ２（ＰＧＥ２）含量影响及ＰＧＥ２与ＣＰＢ后免疫功能关系，选择了３０例心内直视术患者，分别监测术前、ＣＰＢ６０分钟、１２０分、术毕、术后第１、７、１４天外周静脉血血浆ＰＧＥ２水平和外周血淋巴细胞白介素－２受体（ＩＬ－２Ｒ）表达及诱生白介素－２能力变化。结果显示ＣＰＢ中ＰＧＥ２急剧升高，是基础值的１０倍，术毕及术后第７天仍高于基础值（Ｐ〈０．０５     

急性胰腺炎大鼠氧自由基,血栓素和前列环素的变化及维生素E…

本实验对氧自由基，血栓素和前列环素在急性胰腺炎发病过程中的作用及维生素Ｅ治疗进行了研究。结果显示：治疗鼠血浆和胰腺组织丙二醛含量，血浆ＴＸＡ２及ＴＸＡ２／ＰＧＩ２比值较ＡＰ大鼠明显降低，病理改变减轻；胰腺组织ＭＤＡ含量变化与血浆ＴＸＡ２及ＴＸＡ２／ＰＧＩ２比值变化均呈显著正相关。     

急性胰腺炎大鼠氧自由基、血栓素和前列环素的变化及维生素E治疗的研究

本实验对氧自由基、血栓素（ＴＸＡ２）和前列环素（ＰＧＩ２）在急性胰腺炎（ＡＰ）发病过程中的作用及维生素Ｅ（ＶｉｔＥ）治疗进行了研究。结果显示：治疗鼠血浆和胰腺组织丙二醛（ＭＤＡ）含量、血浆ＴＸＡ，及ＴＸＡ２／ＰＧＩ２比值较ＡＰ大鼠明显降低，病理改变减轻；胰腺组织ＭＤＡ含量变化与血浆ＴＸＡ，及ＴＸＡ２／ＰＧＩ２比值变化均呈显著正相关。提示氧自由基在ＡＰ发病中作用不仅表现在其对胰腺腺泡细胞有直接损害作用，还表现在其通过促进花生四烯酸代谢紊乱加剧ＡＰ病程的发展。抗氧化剂ＶｉｔＥ对ＡＰ具有良好的治疗作用。     

异丙酚诱导插管对血浆降钙素基因相关肽及内皮素水平的影响

目的 探讨异丙酚诱导插管对血浆ＣＧＲＰ含量的影响。方法 择期手术病人３６例,ＡＳＡⅠ～Ⅱ级,随机分为异丙酚（ＰＰ组,２０例）硫喷妥钠（ＳＰ组,１６例）两组,分别于麻醉前、用药后、插管后２ｍｉｎ、７ｍｉｎ、１５ｍｉｎ测定血浆中ＣＧＲＰ、ＥＴ的含理及血液动力学变化。结果 两组给药后血压均下降,插管后硫喷妥钠组血压迅速上升,异丙酚组插管后ＣＧＲＰ、ＥＴ含量略有下降,但无统计学意义（Ｐ〉０．０５）。硫喷妥     

再灌注损伤胃粘膜组织前列腺素含量的变化及丹参提取物F的作用

研究失血性休克再灌注大鼠胃粘膜损伤指数，组织 ＰＧＥ２、 ＰＧＩ２（ ６－ｋｅｔｏ－ＰＧＦ１ａ示） ＴＸＡ２（ＴＸＢ２示）含量，６－ｋｅｔｏ－ＰＧＦ１ａ／ＴＸＢ２比值及丹参提取物 Ｆ对上述各值的影响。结果显示，再灌注后胃粘膜有明显的出血性损伤，组织ＰＧＥ２、６－ｋｅｔｏ－ＰＧＦ１ａ含量明显下降，ＴＸＢ２含量明显增加，６－ｋｅｔｏ－ＰＧＦ１ａ／ＴＸＢ２比值明显降低，单纯失血性休克组未见上述损伤；丹参提取物Ｆ能明显降低胃粘膜损伤指数，且与组织ＰＧＥ２含量６－ｋｅｔｏ－ＰＧ１ａ／ＴＸＢ２比值的增加呈负相关。     

早期肠内营养对烧伤后高代谢反应调节作用的研究

目的 观察早期肠内营养对烧伤高代谢反应的调节作用。方法 通过３０例烧伤患者用间接测热法监测静息能量消耗（ＲＥＥ）,监测血浆激素、脂类调节因子、细胞因子水平,并结合临床疗效和氮平衡变化来评价早期肠内营养的作用。结果 早期肠内营养（ＥＥＮ）组较延迟肠内营养（ＤＥＮ）组ＲＥＥ显著下降（Ｐ＜０.０５－０.０１）,升高的时间缩短（Ｐ＜０.０５）;ＥＥＮ组非蛋白呼吸商（ＮＰＲＱ）较ＤＥＮ组更接近生理状态,负氮平衡时间缩短。伤后第４天ＥＥＮ组血浆去甲肾上腺素（ＮＥ）、胰高糖素（ＧＬＵＣＡＧＯＮ）、前列腺素Ｅ２（ＰＧＥ２）、血栓素Ｂ２（ＴＸＢ２）、低于ＤＥＮ组（Ｐ＜０.０５）;伤后８－１２d肿瘤坏死因子α（ＴＮＦ－α）、白细胞介素－６（ＩＬ－６）显著低于ＤＥＮ组（Ｐ＜０.０５－０.０１）,胰岛素水平呈相反变化。结论 严重烧伤后尽早开始肠内营养对高代谢反应有重要的调节作用。     

补肾中药对骨质疏松大鼠性激素影响的实验研究

目的　探讨补肾中药骨康对去势所造成骨质疏松大鼠性激素及骨密度的影响及性激素水平在骨质疏松发病中的作用。方法　通过切除大鼠睾丸和卵巢造成骨质疏松模型,观察中药骨康不同剂量对骨质疏松大鼠血睾酮（Ｔ）、血清雌二醇（Ｅ２）、ＢＭＤ 和ＢＭＣ的影响,并与特乐定、尼尔雌醇作阳性对照。结果　中药骨康高、中剂量防治的去势大鼠Ｔ 含量高于模型组（Ｐ＜ ０．０５ 和０．０１）,高、中、低剂量组的Ｅ２、全身及左、右股骨ＢＭＤ、ＢＭＣ高于模型组（Ｐ＜ ０．０５）。结论　骨康能提高去势大鼠血性激素含量、骨的骨矿含量及骨密度,其提高骨矿含量及骨密度的作用可能与其提高性激素水平有关。     

葛根汤对大鼠退变颈椎间盘组织前列腺素E2及环氧合酶的影响

目的：观察葛根汤对模型大鼠退变颈椎间盘组织PGE2及COX活性的影响。以探讨葛根汤治疗颈椎病的抗炎作用机理。方法：选用动力失衡性颈椎病动物模型,造模后6个月,取出颈椎间盘组织,采用放免法,催化活性测定法分别测定PGE2含量及COX活性。结果：模型组PGE2含量及COX活性明显升高,葛根汤可下调PGE2的含量及抑制COX的活性。结论：葛根汤下调退变颈椎间透组织中PGE2的含量,与抑制COX活性密切相关,这可能是其治疗颈椎病的作用机制之一。     

Effect of Prostaglandin E1 Injected Into Donors in a Heterotopic Heart Transplant Model of Sprague Dawley Rats

IntroductionProstaglandin E₁ (PGE₁) administered to patients in the immediate post-transplant period has been known to reduce ischemic reperfusion injuries (IRIs), but the effect on IRI of PGE₁ administered to the donor is unknown. The purpose of this study was to determine the effect on IRI of PGE₁ injected into donor rats during heterotopic heart transplantation.MethodsGenetically identical male Sprague Dawley rats with a body weight of 300–320 g at 8–9 weeks of age were used for the study. Experimental methods were the same in the control (G₀, n = 6) and experimental groups (G₁, n = 6), but only the donor rats in the experimental group received an intramuscular injection of PGE₁ (5 μg/kg) prior to the donor surgery. On day 1 the animals were sacrificed with the removal of the transplanted heart. Histologic analysis was performed in the hematoxylin-eosin-stained slides to assess interstitial edema and neutrophil infiltration by a pathologist.ResultsMedian times of the donor organ procurement, cold ischemia, and warm ischemia were 37, 69, and 35 minutes, respectively, in the G₀ group and 38, 76.5, and 33 minutes respectively in G₁ group; there were no statistical differences. Heartbeats were observed in the transplanted graft in 2 of the G₀ group and 2 of G₁ group immediately after heart transplantation, but in all transplanted grafts on day 1 after surgery. Histologic scores for neutrophil infiltration showed significantly lower in the G₁ group than in the G₀ group.ConclusionPGE₁ administration to donors in a rat heart transplantation model may significantly reduce IRI.     

Comparative study on the cardio-respiratory change during prostaglandin E1-induced hypotension in the patients in the supine and prone position

Prostaglandin E₁-induced hypotension (25% reduction from the preadministration level in mean arterial pressure) was applied to thirteen patients. Eight patients among them were operated in the supine position (group I) and other five in the prone position (group II). The maintenance dose of PGE₁ was considerably lower in group II than in group I (0.067µg·kg^–1·min^–1 vs. 0.119µg·kg^–1·min^–1). In group I, there was a significant increase in CI, with a significant decrease in SVRI and PVRI during PGE₁-induced hypotension. Such a high dose of PGE₁ (0.119µg·kg^–1·min^–1) was considered to have a direct dilating action on the systemic resistance bed as well as on the pulmonary vasculature. It was considered that the suppression of hypoxic pulmonary vasoconstriction could be a mechanism to increase venous admixture during PGE₁-induced hypotension. In group II, there was no significant increase in CI, and no significant decrease in SVRI and PVRI. PGE₁-induced hypotension can be safely applied to the anesthetized patients, but we should be careful to apply it to the patients in the prone position, because lower dose of PGE₁ can induce severe hypotension, which is not accompanied by the increase in CI as occures in the patients in the supine position.(Hirose M, Yoda K, Sakai K, et al.: Comparative Study on the cardio-respiratory change during prostaglandin E₁-induced hypotention in the patients in the supine and prone position. J Anesth 5: 30–35, 1991)     

Dietary lipids,prostaglandin E2 levels,and tooth movement in alveolar bone of rats

Summary A previous study showed that certain dietary lipids can alter arachidonic acid concentrations in alveolar bone. Because arachidonic acid is a precursor of prostaglandin (PG) E₂, which is known to play an important role in orthodontic tooth movement, the purpose of the present study was to determine the effect of dietary lipids on PGE₂ levels and tooth movement. Two groups of male Sprague-Dawley rats (20/group) were fed nutritionally adequate purified diets containing 10% corn oil (group I, rich in n-6 fatty acids) or 9% ethyl ester concentrate of n-3 fatty acids + 1% corn oil (group II rich in n-3 fatty acids). After 5 weeks of feeding the diets, orthodontic force of 56 g was applied to the maxillary incisors to tip them distally. Prior to killing the rats at day 4 and 8 of orthodontic force application, tooth movement was measured by computerized image analysis. Premaxillae were dissected out free of soft tissue and incisors. The alveolar bone was frozen in liquid nitrogen, pulverized, and lipids were extracted. The concentrations of arachidonic acid and fatty acid composition of total phospholipids were measured by gas chromatography. PGE₂ levels were measured by enzyme immunoassay. Arachidonic acid and PGE₂ concentration were significantly lower (P < 0.001) in alveolar bone of rats in group II than in group I. The tooth movement was also significantly lower (P < 0.02) in group II than in group I at both 4 and 8 days. The results suggest that PGE₂ levels in alveolar bone and orthodontic tooth movement can be affected by the type of dietary fat.Presented in part for the Hatton Award Competition at the International Association for Dental Research Meeting, Chicago, Illinois, March 10–14, 1993.     

The immunosuppressive effects of a leukotriene B4 receptor antagonist on liver allotransplantation in rats

The immunosuppressive effects of a leukotriene B₄ (LTB₄) receptor antagonist, ONO4057, on liver allotransplantation in rats were evaluated, and the levels of prostaglandin E₂ (PGE₂) in the liver tissue during rejection of the allografts examined. The rats were divided into four groups: group 1: Lewis rats (LEW) given a sham operation with dimethyl sulfoxide (DMSO); group 2: LEW given syngenic orthotopic liver transplantation (OLT) from LEW, with DMSO; group 3: LEW given allogenic OLT from ACI rats (ACI), with DMSO; and group 4: LEW given allogenic OLT from ACI, with ONO4057 as 10, 30, or 100 mg/kg per day dissolved in DMSO to subgroups 4a, 4b, and 4c, respectively. Histological examinations were performed, survival times monitored, and liver tissue PGE₂ levels 3, 5, 7, and 14 days after transplantation measured. The mean graft survival times in groups 4a, b, and c, at 37.5±10.4, 52.2±24.4, and 34.0±4.9 days (mean±SEM), respectively, were significantly longer than that in group 3 (at 13.0±3.2 days). Moreover, the levels of tissue PGE₂ in the liver allografts in group 4a were significantly higher than those in group 3 on days 5 and 7. These results suggest that ONO4057 has an immunosuppressive effect on liver allotransplantation since it reduces the activities of LTB₄ which augments immune responses, and also because it indirectly increases the PGE₂ level.     

Anabolic Effect of Prostaglandin E2 in Bone Is not Dependent on Pituitary Hormones in Rats

Prostaglandin E₂ (PGE₂) is an anabolic agent of bone in vivo but the mechanism of its action still remains unclear. The aim of this study was to determine whether the effect of PGE₂ on skeleton is mediated by pituitary hormones. Forty female, Sprague-Dawley rats were divided into four groups: baseline control (basal), age-matched intact control (CON), hypophysectomy (HX), and HX + PGE₂ (2 mg/kg/day) with 10 animals in each group. The basal group was sacrified at 2 months of age, and the remaining groups after 6 weeks of treatment. Cancellous and cortical bone histomorphometry was performed on double fluorescent-labeled 40 μm-thick sections of the proximal tibia and tibial shaft. Our results show that HX resulted in a cessation of bone growth, a decrease in cancellous bone volume, and cortical bone gain compared with the age-matched, intact CON rats. Compared with the HX group, the HX + PGE₂ group had a significantly greater tibial bone density (mean ± SE, HX + PGE₂:1.595 ± 0.007 versus HX:1.545 ± 0.013), percent cancellous bone volume (21.4 ± 2.0 versus 8.41 ± 1.70), percent cortical bone area (87.2 ± 0.85 versus 81.7 ± 0.7), and ratio of cortical area to marrow area (7.14 ± 0.56 versus 4.52 ± 0.21). Increased bone masses by PGE₂ in the HX animals were accompanied by an increase in the trabecular and endosteal-labeled surface and bone formation rate. The trabecular number and width were increased whereas trabecular separation was decreased in the HX + PGE₂ group compared with the HX group (P < 0.05). PGE₂ treatment also caused a decrease in the tibial endosteal eroded surface and medullar cavity of the HX animals. In conclusion, this study clearly demonstrates that PGE₂ (2 mg/kg/day) in the HX rats increases both cortical and cancellous bones and improves trabecular architecture in the tibia after 6 weeks of treatment. These skeletal alterations are due to a stimulation of bone formation and a suppression of bone resorption activity. These findings suggest that the anabolic effect of PGE₂ in bone is independent of pituitary hormones.     

Prostaglandin E<Subscript>2</Subscript> Suppresses NK Activity In Vivo and Promotes Postoperative Tumor Metastasis in Rats

Background: Prostaglandins (PGs) were shown in vitro to suppress several functions of cellular immunity. It is unclear, however, whether physiological levels of PGs can suppress cellular immunity in vivo and whether such suppression would compromise postoperative host resistance to metastasis.Methods: Fischer 344 rats were administered PGE₂ in doses (18 to 300 g/kg subcutaneously) that increased the serum levels approximately 2- to 4-fold. We then assessed the number and activity of circulating natural killer (NK) cells, as well as rats resistance to experimental metastasis of a syngeneic NK-sensitive tumor (MADB106). To study whether endogenously released PGs after surgery compromise these indices, we tested whether laparotomy adversely affects them and whether a cyclooxygenase-synthesis inhibitor, indomethacin (4 mg/kg), attenuates these effects.Results: PGE₂ dose-dependently suppressed NK activity per NK cell and dose-dependently increased 4- and 24-hour MADB106 lung tumor retention (LTR); 240 g/kg of PGE₂ quadrupled the number of lung metastases counted 3 weeks later. Selective depletion of NK cells abrogated the promotion of LTR by PGE₂. Surgery significantly suppressed NK activity and increased MADB106 LTR, and indomethacin halved these effects without affecting nonoperated rats.Conclusions:PGE₂ is a potent in vivo suppressor of NK activity, and its postoperative release may promote tumor recurrence.     

The effects of prolonged peritendinous administration of PGE1 to the rat Achilles tendon: a possible animal model of chronic Achilles tendinopathy

We studied the effects of peritendinous Achilles tendon injections of prostaglandin E₁ (PGE₁) on the Achilles tendon of rats. Five groups of Sprague-Dawley rats (n = 24 each) were studied. Groups 1 to 4 received weekly peritendinous injections. In group 1, one side was injected with 800 ng of PGE₁ in 0.5 ml of 0.9% NaCl and the contralateral side was injected with 0.5 ml of 0.9% NaCl. In group 2, one side was injected with 800 ng of PGE₁. In group 3, one side was injected with 0.5 ml of 0.9% NaCl. In group 4, a syringe needle was inserted in the peritenon unilaterally, but no substances were administered. In groups 2, 3, and 4, the contralateral tendon was used as the control. In group 5, treatment was not administered. Eight rats in each group were killed at each time point, after 7, 21, and 35 days of treatment. On day 7, values for average water content and average wet weight of the tendons treated with PGE₁ were significantly higher than those in the control tendons (analysis of variance [ANOVA]; P = 0.02), with a histological picture of acute inflammation. On day 21, approximately half of the PGE₁-treated tendons showed fibrosis of the paratenon, with adhesions and intra-tendinous degeneration, with the other half still showing a picture of acute inflammation. On day 35, all of the PGE₁-treated tendons showed fibrosis of the paratenon, with adhesions and intra-tendinous degeneration. At all time points, there was no evidence of pathology in the tendons that had not received PGE₁. Sham peritendinous injections and injections of normal saline did not produce inflammation in the Achilles tendons. Initially, local administration of PGE₁ produced acute inflammation of the tendon and its surrounding tissues. Prolonged PGE₁ administration produced peri- and intra-tendinous degeneration, providing a cheap, reproducible model of Achilles tendinopathy, which would allow studies of the effects of conservative and surgical management of the condition. Received: September 11, 2000 / Accepted: March 24, 2001     

Effects of prostaglandin E2 and F2α on the skeleton of osteopenic ovariectomized rats

This article contains the histomorphometric evaluation of the effects of prostaglandin F_2α (PGF_2α on cancellous bone from the lumbar vertebra and cortical bone from the tibial shaft of ovariectomized, osteopenic rats. These effects were then compared with those of prostaglandin E₂ (PGE₂). Three-month-old rats were either ovariectomized (ovx) or shamovx. Then, either PGF_2α or PGE₂ in doses of 1 and 3 mg/kg/day was given subcutaneously for 21 days at 150 days post ovx. Histomorphometric analysis was performed separately on both the primary and secondary spongiosae of the fourth lumbar vertebral bodies (LVB) and on tibial shafts. The ovx rats exhibited osteopenia in both primary (−23% to −37%) and secondary (−20%) spongiosae of the LVB, but not in the tibial shafts at 150 and 171 days post ovx. In the LVB, PGE₂ in doses of 1 or 3 mg/kg/day for 21 days restored trabecular bone volume to the levels of sham-ovx controls in the primary spongiosa. However, in the secondary spongiosa, the treatments only thickened the trabeculae. The effects of the PGF_2α treatment were similar to those of the PGE₂ in both the primary and the secondary spongiosae. While both PGF_2α and PGE₂ treatments stimulated bone formation in the LVB as indicated by the increases in labeled perimeter, tissue and bone area-based bone formation rates, PGE₂ is about 10 times more potent than PGF_2α in these effects. The PGE₂ treatment also elevated activation frequency in the LVB, while the PGF_2α treatment did not. The treatments differed in that PGE₂ at these dose levels did not alter the eroded surface in the LVB while PGF_2α decreased it significantly. Thus, the increase of the ratio of labeled to eroded perimeter in the LVB in PGF_2α treated animals was much more than that in PGE₂-treated animals. In the tibial shafts, PGE₂ in doses of I and 3 mg/kg/day produced new marrow trabeculae in 2 of 6 and 3 of 6 of the ovx rats. However, no new trabecula was found in PGF_2α treated tibial shafts. Higher doses of PGE₂ also increased periosteal labeled perimeter, MAR, and BFR/BS, while PGF_2α did not produce any significant change in these parameters. Both PGE₂ and PGF_2α in doses of 1 and 3 mg/kg/day increased the labeled perimeter, MAR and BFR/BS and decreased the eroded perimeter in the endocortical surface. We concluded that both PGF_2α and PGEE₂ in doses of 1 and 3 mg/kg/day for 21 days exhibited anabolic bone effects. The effects were mostly confined to an increase in trabecular volume in the primary spongiosa of the LVB and in the endocortical surface of tibial shafts. The tissue level mechanism behind this appears to be that PGEE₂ and PGF_2α can both stimulate osteoblast recruitment and activity. Overall, we found PGE₂ to be more potent than PGF_2α at the same dose level at the endocortical surface. Furthermore, new marrow trabecular bone formed only after PGE₂ treatment. PGF_2α differed from PGE₂ by significantly reducing the trabecular eroded surface in ovx rats.     

大剂量甲基强的松龙对大鼠急性脊髓损伤后神经细胞Bcl-2表达及细胞凋亡的影响

目的：观察大剂量甲基强的松龙（MP）治疗对大鼠急性脊髓损伤（ASCI）后神经细胞凋亡及凋亡基因Bcl-2的影响。方法：选取48只雌性SD大鼠随机等分为2组,对照组与治疗组,按Nystrom法制备大鼠急性脊髓损伤模型。治疗组伤后30min经腹膜腔注入MP30mg／kg,以后每小时腹膜腔注入MP5．4mg／kg,维持24h;对照组应用生理盐水替代MP,处理方法同治疗组。两组分别于伤后4、8h及1、3、7、14d灌注固定后取材。免疫组织化学检测损伤段脊髓内Bcl-2蛋白表达,TUNEL检测细胞凋亡,染色结果应用图像分析仪进行半定量分析。结果：大鼠ASCI后4h即可见脊髓内TUNEL阳性细胞,8h表达达高峰,此后表达量逐渐下降,14d时仍可见少量阳性细胞。凋亡相关蛋白Bcl-2在伤后4h即可见表达,伤后1d达高峰,伤后14d仍有表达,与对照组相比,治疗组伤后8h、1d和3d时凋亡细胞数减少有统计学意义,伤后8h和1d Bcl-2蛋白表达增高有统计学意义。结论：大剂量甲基强的松龙治疗可抑制大鼠ASCI后神经细胞凋亡,并增加凋亡相关蛋白Bcl-2的表达：