No significant differences were observed in the amounts of DNA strand breaks produced by copper between male and female liver cells of long-evans cinnamon (LEC) strain rats.

The amounts of DNA single strand breaks that are oxidative damage produced by copper were examined by comet assay in the liver cells of an inbred strain of Long-Evans Cinnamon (LEC) rats that spontaneously develops fulminant hepatitis. At 4 weeks of age, copper contents in the liver of LEC rats were approximately 30-fold higher than those of WKAH rats that are control rats used in the present study. Copper accumulated in the liver of LEC rats in an age-dependent manner and no significant differences were observed between copper contents in the livers of males and females at each week of age from 4 to 15 weeks. No significant amounts of DNA strand breaks were found in the liver cells of both male and female WKAH rats from 4 to 15 weeks of age. DNA strand breaks were produced in the substantial population of LEC rat liver cells at 10 weeks of age and induced in an age-dependent manner from 10 to 15 weeks of age. The amounts of DNA strand breaks produced by copper accumulation in the liver cells of female LEC rats are not more abundant than those in the cells of male rats, although it has been reported that hepatitis in female rats is more serious than that in male rats.     

Higher sensitivity in induction of apoptosis in fibroblast cell lines derived from LEC strain rats to ultraviolet B radiation

When lung fibroblast cell lines from LEC and WKAH rats were irradiated with ultraviolet B (UVB) and assayed for colony formation, LEC rat cells showed a higher sensitivity than did WKAH rat cells. The LEC rat cells were approximately 1.5-fold more sensitive to UVB radiation than were the WKAH rat cells in terms of D37 values, which are the doses of UVB required to reduce cell survival to 37%. When the rat cells were irradiated with UVB in the presence of 0.5 M dimethyl sulfoxide (DMSO), which efficiently scavenges free radicals such as hydroxyl radicals, no significant difference was observed between the survival curves of either LEC or WKAH rat cells irradiated with UVB in the presence of 0.5 M DMSO and those irradiated with UVB in the absence of DMSO. Therefore, formation of free radicals may not be involved in cell death induced by UVB radiation. Flow cytometry showed that the percentage of apoptotic cells in the LEC rat cell population increased with post-incubation time after UVB radiation. The proportion of apoptotic cells in the UVB-irradiated LEC rat cell population increased as the dose of UVB was increased. In contrast, no significant proportion of apoptotic cells was observed in the UVB-irradiated WKAH rat cell population. These results showed a higher sensitivity in induction of apoptosis by UVB radiation in LEC rat cells than in WKAH rat cells.     

Higher sensitivity of LEC strain rat in radiation-induced acute intestinal death.

LEC strain rats (LEC rats), which have been known to develop hereditarily spontaneous fulminant hepatitis 4-5 months after birth, were highly sensitive to whole-body X-irradiation as compared to WKAH strain rats (WKAH rats). Radiation-induced acute intestinal death occurred at doses higher than 6.5 Gy in LEC rats, and at doses higher than 12.8 Gy in WKAH rats, respectively. By the probit analysis of survival data, it was shown that the LD50/7 value of LEC rats was estimated to be 7.03 Gy which was significantly lower than that (12.99 Gy) of WKAH rats. Histopathological examinations of small intestines from LEC rats 2 days after irradiation at the dose of 8.5 Gy showed severe epithelial death together with edema, whereas little or no significant changes were noted in intestinal epithelium of 8.5 Gy-irradiated WKAH rats. These results suggest that the radiosensitivity of LEC rats to ionizing radiation appears to be higher than that of other strains of rats.     

High sensitivity of thymocytes of LEC strain rats to induction of apoptosis by X-irradiation

It is known that physical disruption of cell contacts induces apoptosis of thymocytes. When thymocytes from LEC and WKAH rats were incubated in vitro at 37 degrees C for 0-6 hr and then the proportion of apoptotic cells was determined using a flow cytometer, it was found that the percentages of apoptotic thymocytes from both LEC and WKAH rats increased with incubation time and that the proportion of apoptotic cells from LEC rats was significantly higher than that from WKAH rats at each incubation time. The fact that cycloheximide, an inhibitor of protein synthesis, did not show significant inhibitory effects on induction of apoptosis of thymocytes indicates that induction of apoptosis during in vitro cultivation did not require de novo protein synthesis. When thymocytes from LEC and WKAH rats were X-irradiated in vitro at 4 and 8 Gy, the percentages of radiation-induced apoptotic cells increased with post-incubation time after X-irradiation in both LEC and WKAH rat thymocytes and the proportions of apoptotic cells from LEC rats were significantly higher than those from WKAH rat cells at 2 and 4 hr post-incubation after X-irradiation. When thymocytes from LEC and WKAH rats were X-irradiated in the presence of cycloheximide, the induction of apoptosis was substantially inhibited, indicating that radiation-induced apoptosis of thymocytes from LEC and WKAH rats required de novo protein synthesis. The present results showed high sensitivities of thymocytes of LEC rats to induction of apoptosis during in vitro cultivation and by X-irradiation.     

Abnormal accumulation of G2/M-phase cells from LEC strain rats after X-irradiation at S phase.

The effect of X-irradiation on the progression of the cell cycle in cell lines from LEC and WKAH rats was investigated by a flow cytometer. When the cells were exposed to 5 Gy of X-rays at S phase, the proportion of S-phase cells in both cell populations decreased with incubation time and that of G2/M-phase cells was approximately 80% at 6 hr post-irradiation. At 12 hr post-irradiation, approximately 45% of the WKAH rat cells appeared in the G1 phase. However, 80-90% of LEC rat cells remained in the G2/M phase and less than 5% in the G1 phase during 6-12 hr post-irradiation. Thus, the LEC rat cells irradiated at S phase remained in the G2/M phase for at least 6 hr longer than did the WKAH rat cells.     

Inhibition of replication induces non-apoptotic cell death in fibroblast cell lines derived from LEC rats

Hydroxyurea (HU), an anticancer drug, inhibits ribonucleoside diphosphate reductase and reduces pool sizes of deoxyribonucleoside triphosphate (dNTP). The reduction of dNTP results in inhibition of DNA replication. The cytotoxic effect of HU was investigated using fibroblast cell lines from LEC rats. LEC rat cells showed significantly higher sensitivity to HU than did cell lines from control WKAH rats. No significant differences were observed between the percentages of apoptotic cells in either LEC or WKAH rat cells that had been treated with HU and those that had not been treated with HU. LEC rat cells also showed significantly higher sensitivity to aphidicolin, which blocks DNA synthesis by inhibiting DNA polymerase alpha, than did WKAH rat cells. In both LEC and WKAH rat cells, intensified bands of p53 protein were observed immediately after treatment with HU. Although the high level of p53 protein persisted in WKAH rat cells until 6 hr post-incubation time after treatment with HU, the level of p53 protein had decreased at 6 hr post-incubation time in LEC rat cells. When the cells were X-irradiated in the absence or presence of HU, the ratio of the surviving fraction without HU to that with HU only slightly increased after X-irradiation in WKAH rat cells. In contrast, the ratio in LEC rat cells significantly increased after X-irradiation in a dose-dependent manner.     

Wortmannin, a radiation sensitizer, enhances the radiosensitivity of WKAH rat cells but not that of LEC rat cells

No significant cytotoxic effect was observed in WKAH rat cells by the treatment of wortmannin, a radiation sensitizer, at concentrations lower than 30 microM for 24 hr. The relative surviving fractions of LEC rat cells were slightly, but significantly, lower than those of WKAH rat cells at each concentration of wortmannin. When the wortmannin-treated WKAH rat cells were X-irradiated, the relative surviving fractions decreased in a wortmannin concentration-dependent manner. On the contrary, no significant difference was observed between the survival curves of untreated and wortmannin-treated LEC rat cells after X-irradiation.     

Analysis of the cell cycle of fibroblasts derived from the LEC rat after X-irradiation

The LEC rat is reported to exhibit hypersensitivity to X-irradiation, deficiency in DNA double-strand break repair, and radio-resistant DNA synthesis. This character of the LEC rat has been thought to be due to abnormal G1 arrest in cells after X-irradiation. In this report, we re-investigated the effect of X-irradiation on the cell cycle in primary-cultured fibroblasts. Primary-cultured fibroblasts derived from LEC and BN rats were exposed to 4 Gy of X-ray and their cell cycle analysis was performed with a flow cytometer. Fibroblasts derived from both rats showed normal response of the cell cycle, indicating the arrest at both G1--and G2/M-phase and no difference in the cell cycle population between fibroblasts derived from both rats. In contrast, when the same analysis was performed using the cell line, L7 and W8, which had been established from the lung fibroblasts of LEC and control WKAH rats, respectively, by immortalizing with SV40 T-antigen, L7 cells but not W8 cells showed impaired G1 arrest and abnormal cell cycle. These results suggest that fibroblasts derived from LEC rats possess the normal cell cycle response after X-irradiation, if they are kept naive as not immortalized with SV40 T-antigen.     

Toxicity of dietary monensin in quail

Quail were fed monensin to determine liver damage, as measured by changes in activities of serum enzymes and liver microsomal enzymes. Monensin fed at a therapeutic level of 110 ppm for 2 weeks produced an increase in cytochrome P-450 and cytochrome b5 and induction of the activities of benzphetamine N-demethylase, aminopyrine N-demethylase, and aniline hydroxylase, with no changes in the activities of serum sorbitol dehydrogenase (SDH), alanine aminotransferase (ALT), and aspartate aminotransferase (AST). On the other hand, quail fed 110 ppm, 220 ppm, and 330 ppm monensin in feed for 6 weeks showed a significant rise in SDH and AST activities at 330 ppm but not at 110 ppm and 220 ppm. The manifestations of liver toxicity observed at 330 ppm were accompanied by a significant decrease in all the aforementioned hepatic microsomal mixed-function oxidases. In contrast, quail fed monensin at 110 ppm and 220 ppm for 6 weeks produced no change in these parameters except for benzphetamine N-demethylase, aminopyrine N-demethylase, and aniline hydroxylase, which were significantly increased in birds fed 220 ppm of monensin.     

土庄绣线菊水浸液对小鼠急性酒精肝损伤保护作用的研究

本试验旨在研究土庄绣线菊水浸液对小鼠急性酒精肝损伤的保护作用。将试验小鼠随机分为低剂量组、中剂量组、高剂量组、模型组和空白组5组。采用一次酒精灌胃法建立急性酒精性肝损伤小鼠模型。建模后,测定各小鼠肝组织谷胱甘肽(GSH)与丙二醛(MDA)含量及血清中冬氨酸氨基转移酶(AST)和丙氨酸转移酶(ALT)的活性,并进行肝组织病理切片观察。结果显示,土庄绣线菊水浸液能够明显降低酒精性肝损伤引起的AST和ALT活性的升高,能有效保持肝脏中GSH含量和明显降低MDA含量,说明土庄绣线菊水浸液对乙醇所致肝损伤具有保护作用,能明显改善酒精引起的肝脏损害。     

活血疏肝健脾汤对犬实验性肝损伤血清学和组织学影响

观察活血疏肝健脾汤对 CCl4诱导的犬肝纤维化的血清学指标和病理组织学变化影响 ,以探讨中药复方防治犬肝纤维化的机制。采用皮下多点注射和口服 CCl4菜籽油的方法制作动物实验性肝损伤模型。对照组仅给予 CCl4,中药组在给予 CCl4的同时口服中药复方煎剂 ;西药组在给予 CCl4的同时口服秋水仙碱。每周采集血样测定犬血清中 AL B、AST、AL T与羟脯氨酸 ( HYP)含量 ;8周后处死动物 ,观察肝脏组织的病理学变化 :1从试验开始到第 8周结束 ,对照组犬血清中的 AL B降低 ,AL T、AST升高 ,而中药组犬在试验的前 5周 ,血清白蛋白含量明显降低 ,自第 6周开始回升 ,第 7周时升至试验前的水平 ,血清 ALT和 AST活性无明显变化 ;2中药组犬的血清 HYP含量从第 5周开始显著高于对照组 ( P <0 .0 5 ) ,试验结束时其肝脏胶原含量显著低于对照组 ( P <0 .0 1) ;3对照组犬肝细胞变性、坏死 ,胶原纤维大量增生 ,中药组犬胶原纤维数量明显少于对照组。活血疏肝健脾汤具有减轻 CCl4对肝脏的损伤 ,保护肝细胞的功能和抗肝纤维化的作用     

骆驼乳清蛋白对热应激所致大鼠肝氧化损伤的保护作用

本试验旨在研究骆驼乳清蛋白（CWP）对热应激（HS）大鼠肝损伤、氧化应激及肝功能的保护作用。选取6周龄SD大鼠36只,适应性饲养2周后随机分为6组：正常对照组饲喂基础日粮;CWP对照组添加400 mg·kg^-1的CWP;HS组除饲喂基础日粮外,每天进行2 h HS处理,连续8 d;3个CWP干预组分别于每次HS前灌服100、200和400 mg·kg^-1的CWP。试验结束后,取大鼠肝组织,HE染色观察肝组织病理学变化,同时检测肝功能生物标志物、氧化应激标志物水平及抗氧化酶活性。结果表明：CWP降低了HS大鼠血清谷草转氨酶（AST）和谷丙转氨酶（ALT）活性,400 mg·kg^-1的CWP干预效果最好（P<0.01）;400 mg·kg^-1CWP干预组有效降低了HS诱导的大鼠肝组织病理学改变; CWP降低了大鼠肝活性氧（ROS）及丙二醛（MDA）水平,增加了超氧化物歧化酶（SOD）、过氧化氢酶（CAT）、谷胱甘肽过氧化物酶（GSH-Px）活性及谷胱甘肽（GSH）水平,400 mg·kg^-1的CWP干预效果最好（P<0.01）。结果提示,CWP干预能够以剂量依赖性方式降低大鼠肝氧化应激,增加抗氧化系统防御能力,从而缓解HS所致大鼠肝损伤。     

决明子水煎液对CCl4所致急性肝损伤大鼠血液生化指标的影响

目的:研究决明子水煎液对CCl4所致急性肝损伤大鼠血清各项生化指标的影响及对肝损伤的保护作用。方法:32只体重180～240 g的SD大鼠,随机分为正常对照组、模型对照组、决明子Ⅰ组和决明子Ⅱ组,每组8只。正常对照组和模型对照组大鼠饮用蒸馏水,决明子Ⅰ组和决明子Ⅱ组分别饮用浓度为40 g/L和80 g/L决明子水煎液,连用2周后,模型对照组、决明子Ⅰ组和决明子Ⅱ组腹腔注射CCl4(2.0 mL/kg体重),正常对照组注射等体积生理盐水,24 h后采血低速离心,取血清分别测AST、ALT、ALP、镁、磷、钾、钠、钙、胆固醇、葡萄糖、总蛋白等血液生化指标。结果:决明子水煎液(40 g/L)能极显著降低CCl4所致急性肝损伤大鼠血清中ALT、AST、血清总蛋白含量的升高(P<0.01);极显著升高CCl4所致急性肝损伤大鼠血清中胆固醇、葡萄糖、ALP和镁含量的降低(P<0.01);同时还能显著升高CCl4所致急性肝损伤大鼠血钠含量的降低(P<0.05)。结论:决明子水煎液对CCl4所致大鼠的急性肝损伤有一定保护作用,增强机体对应激的耐受力,从决明子组对各血清指标的作用来看,决明子Ⅰ组的保肝作用更优于决明子Ⅱ组。     

Effects of long-term phenobarbital treatment on the liver in dogs

Long-term administration of phenobarbital has been reported to cause hepatic injury in dogs. Phenobarbital induces hepatic enzymes, and it may be difficult to distinguish the effect of enzyme induction on serum liver enzyme activities from actual hepatic damage. The hepatotoxicity of phenobarbital and the impact of enzyme induction on serum liver enzyme activity were investigated prospectively in 12 normal dogs. Phenobarbital was administered for 29 weeks at 5 mg per kilogram of body weight (range, 4.8— 6.6 mg/kg) PO q12h, resulting in therapeutic serum phenobarbital concentrations (20–40 μg/mL). Serum alkaline phosphatase (ALP), alanine transaminase (ALT), aspartate transaminase (AST), γ-glutamyltransferase (GGT), fasted bile acids (fBA), total bilirubin, and albumin were determined before and during treatment. Lateral abdominal radiographs, abdominal ultrasounds, and histopathologic examinations of liver tissue obtained by ultrasound-guided biopsy were performed before and during treatment. Radiographs revealed a moderate increase in liver size in most dogs. Ultrasonographic examination revealed no change in liver echogenicity or architecture. No evidence of morphologic liver damage was observed histopathologically. ALP and ALT increased significantly ( P < .05), GGT increased transiently, and albumin decreased transiently during the study. There were no significant changes in AST, bilirubin, and fBA. These results suggest that increases in serum ALP, ALT, and GGT may reflect enzyme induction rather than hepatic injury during phenobarbital treatment in dogs. Serum AST, fBA, and bilirubin, and ultrasonographic evaluation of the liver are not affected by the enzyme-inducing effect of phenobarbital and can therefore be helpful to assess liver disease in dogs treated with the drug.     

MR imaging of hepatic injury in the LEC rat under a high magnetic field (7.05 T).

Visualization of copper-induced hepatitis (CuH) in LEC rats was performed by using an MRI apparatus equipped with a magnet producing a high magnetic field of 7.05 T. When three groups of LEC rats (6-16 [pre-hepatitis], 15-26 [acute hepatitis] and 40-77 [chronic hepatitis] weeks old) were examined by MRI under T2-weighted imaging conditions which are suitable for the diagnosis of human hepatitis, hypointense MR images of the livers were, as a whole, obtained in all groups, suggesting that these conditions were not adequate for imaging of CuH of LEC rats. The shortening of the T1 and T2 relaxation times of livers due to an excess amount of paramagnetic irons under the high magnetic field was responsible for the lowering of MR signal intensities of the livers, especially those of 15 to 26-week old rats showing acute hepatitis. However, theoretical calculation of the MR signal intensities using the T1 and T2 relaxation times of the livers indicated that their imaging might be possible under proton density-weighted conditions even with a high magnetic field. Experimental results showed that hepatic injury was visualized as hyperintense regions in the MR image of the liver in the acute-phase rat.     

黄芪复方剂提取物总黄酮对四氯化碳致大鼠肝损伤保护作用研究

目的:探讨黄芪复方剂提取物总黄酮(EFA)对CCl4致大鼠肝氧化损伤的保护作用及机制。方法:将雄性SD大鼠60只随机分成4组,即灌胃灭菌生理盐水空白对照组和模型组、联苯双酯(100 mg/kg)溶液阳性药物对照组、黄芪复方剂提取物总黄酮(200 mg/kg)组。除空白对照组腹腔注射等量生理盐水外,其余各组腹腔注射四氯化碳玉米油(2 mL/kg)造成大鼠肝氧化损伤模型,后分别于12、24 h将相应大鼠处死,检测血清中ALT、AST、ALB含量与肝组织中MDA、SOD、GSH-PX活性。结果:与模型组比较,经黄酮药物组预防性治疗后,AST、ALT转氨酶明显降低(P<0.05),而ALB含量增加不明显;同时肝脏中MDA含量明显降低(P<0.05),SOD、GSH-PX活性接近空白组,且明显高于模型组(P<0.01)。结论:EFA对四氯化碳造成的大鼠肝氧化损伤具有保护作用。     

Effect of Luteolin on Blood Indexes,Liver and Kidney in Mice with Acute Mercury Poisoning

To study the effect of luteolin on blood indexes,liver and kidney in mice with acute mercury poisoning,28 mice were randomly divided into four groups:Control group (intraperitoneal injection 0.9% saline),luteolin group (lavage 100 mg/kg luteolin),mercuric chloride group (intraperitoneal injection 4 mg/kg mercury chloride) and mercury chloride+luteolin group (intraperitoneal injection 4 mg/kg mercuric chloride,lavage 100 mg/kg luteolin).The activities of ALT in serum,AST,CREA and BUN contents,blood WBC,RBC,HGB content and GSH and MDA contents of liver tissue were detected.Morphological changes of liver and kidney tissues were observed.The results showed that compared with the control group,the activities of ALT and AST of mercuric chloride group were extremely significantly increased (P < 0.01),serum CREA,BUN,blood WBC and liver tissue MDA contents were significantly increased (P < 0.05) while blood RBC,HGB and liver tissue GSH contents were significantly decreased (P < 0.05).Liver,kidney pathological changes were obviously.Compared with mercuric chloride group,the activities of ALT,AST in serum,CREA,BUN,blood WBC and liver tissue MDA contents of mercuric chloride+luteolin group were significantly decreased (P < 0.05),while blood RBC,HGB and liver tissue GSH contents were significantly elevated (P < 0.05).Liver,kidney pathological changes were attenuated obviously.The poisoning were characterized by inflammation and the occurrence of anemia when acute mercury poisoning occurred,liver and kidney showed different degrees of injury in mice.Luteolin could reduce the toxic effects of acute mercury poisoning on blood,liver and kidney.     

木犀草素对急性汞中毒小鼠血液生化指标、肝脏及肾脏的影响

试验旨在研究小鼠急性汞中毒后血液、肝脏及肾脏的中毒表现及木犀草素对急性汞中毒小鼠血液指标、肝脏及肾脏的影响。将28只小鼠随机分成4组,分别为对照组(腹腔注射0.9%生理盐水)、木犀草素组(灌胃100 mg/kg木犀草素)、氯化汞组(腹腔注射4 mg/kg氯化汞)和氯化汞+木犀草素组(腹腔注射4 mg/kg氯化汞,灌胃100 mg/kg木犀草素)。检测血清谷丙转氨酶(ALT)和谷草转氨酶(AST)活性,肌酐(CREA)和尿素氮(BUN)水平,血液白细胞(WBC)、红细胞(RBC)和血红蛋白(HGB)水平及肝脏组织谷胱甘肽(GSH)和丙二醛(MDA)水平,并观察肝脏、肾脏组织形态学改变。结果显示,与对照组相比,氯化汞组的血清ALT、AST活性极显著升高(P < 0.01),血清CREA、BUN,血液WBC及肝脏组织MDA含量均显著增加(P < 0.05),血液RBC、HGB及肝脏组织GSH水平均显著降低(P < 0.05),肝脏、肾脏病理变化明显。与氯化汞组相比,氯化汞+木犀草素组的血清ALT、AST活性,CREA和BUN,血液WBC及肝脏组织MDA含量均显著降低(P < 0.05);血液RBC、HGB及肝脏组织GSH含量均显著升高(P < 0.05),肝脏、肾脏病理变化减轻。小鼠急性汞中毒后,其中毒表现为炎症和贫血的发生及肝脏、肾脏不同程度的损伤,木犀草素可减弱急性汞中毒小鼠血液、肝脏和肾脏的毒性作用。     

Hepatic effects of halothane and isoflurane anesthesia in goats

OBJECTIVE: To determine hepatic effects of halothane and isoflurane anesthesia in young healthy goats. DESIGN: Randomized prospective clinical trial. ANIMALS: 24 healthy 9-month-old female goats. PROCEDURE: Goats were sedated with xylazine hydrochloride and ketamine hydrochloride and anesthetized with halothane (n = 12) or isoflurane (12) while undergoing tendon surgery. End-tidal halothane and isoflurane concentrations were maintained at 0.9 and 1.2 times the minimal alveolar concentrations, respectively, and ventilation was controlled. Venous blood samples were collected approximately 15 minutes after xylazine was administered and 24 and 48 hours after anesthesia, and serum aspartate aminotransferase (AST), sorbitol dehydrogenase (SDH), alkaline phosphatase (ALP), and gamma-glutamyltransferase (GGT) activities and bilirubin concentration were measured. Goats were euthanatized 25 or 62 days after anesthesia, and postmortem liver specimens were submitted for histologic examination. RESULTS: All goats recovered from anesthesia and survived until euthanasia. Serum SDH, GGT, and ALP activities and bilirubin concentration did not increase after anesthesia, but serum AST activity was significantly increased. However, serum hepatic enzyme activities were within reference limits at all times in all except 1 goat in which serum AST activity was high 24 and 48 hours after anesthesia. This goat had been anesthetized with halothane and had the longest duration of anesthesia. No clinically important abnormalities were seen on histologic examination of liver specimens. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that use of halothane or isoflurane for anesthesia in young healthy goats is unlikely to cause hepatic injury.     

地顶孢霉培养物对大鼠生长性能、血清与肝脏抗氧化及免疫指标的影响

本试验旨在研究地顶孢霉培养物对大鼠生长性能、血清与肝脏抗氧化以及免疫指标的影响。选用体重相近的SD大鼠40只,随机分成5组,每组8个重复,每个重复1只大鼠。5组分别是对照组和4个不同地顶孢霉培养物剂量组(10、50、250和1 250 mg/kg BW组),连续灌胃21 d。结果表明:地顶孢霉培养物极显著提高大鼠的平均日增重(P0.01);提高了大鼠肝脏指数、胸腺指数;提高了大鼠血清中总蛋白(TP)、白蛋白(ALB)、球蛋白(GLB)和葡萄糖(GLU)含量,降低了谷丙转氨酶(ALT)、谷草转氨酶(AST)活力和低密度脂蛋白(LDL)含量;提高了血清和肝脏中谷胱甘肽过氧化物酶(GSH-Px)活力和总抗氧化能力(T-AOC),降低丙二醛(MDA)含量,同时提高了肝脏中的总超氧化物歧化酶(T-SOD)含量;提高了血清免疫球蛋白A、免疫球蛋白G和免疫球蛋白M含量,同时提高血清和肝脏中白介素-4(IL-4)含量,降低白介素-1β(IL-1β)和白介素-17(IL-17)含量。综合各项指标,地顶孢霉培养物能够提高SD大鼠平均日增重,改善血清生化指标,提高大鼠机体抗氧化能力和免疫能力,其中以250 mg/kg BW的添加量为最佳。