作者机构：
College of Veterinary Medicine, Hunan Agricultural University;[YI Jin'e; JIANG Weiwei; TAN Zhuliang] 湖南农业大学
会议名称：
中国畜牧兽医学会兽医内科与临床诊疗学分会第八届代表大会暨学术研讨会
会议时间：
2015-07-22
会议地点：
大庆
会议论文集名称：
中国畜牧兽医学会兽医内科与临床诊疗学分会第八届代表大会暨学术研讨会论文集
关键词：
γ-oryzanol;oxidative damage;L02 cells
摘要：
[Backgroud]γ-oryzanol is one of the most important bioactive substances in rice bran oil that can be used for food, pharmaceutical and cosmetic fields.To investigate the proliferative and protective effects of γ-oryzanol on L02 cells.[Methods]The model of oxidative damage was set up on L02 cells induced by H2O2.The cell viability, the contents of malondialdehyde (MDA) and glutathione (GSH), the activities of superoxide dismutase (SOD) and catalase (CAT), and the level of ROS were assayed by adding different concentration of γ-oryzanol into L02 cells in vitro.[Results]The cell viability was enhanced significantly and the levels of ROS and MDA were significantly decreased, whereas the content of GSH and the activities of CAT and SOD were significantly increased by 0.1-0.4 mmol/L of γ-oryzanol pretreatment after H2O2-induced oxidative damage in a dose dependent manner.[Conclusion]γ-oryzanol can effectively attenuate H2O2-induced oxidative damage at the dose of 0.1-0.4 mmol/L and maintain the normal physiology of the cells.
摘要：
T-2 toxin is a secondary metabolite produced by Fusarium genus and is a common contaminant in food and feedstuffs of cereal origin. In porcine granulosa cells(GC), T-2 toxin has been shown to inhibit the steroidogenesis; however, the mechanism has not been well understood. Gonadotropin-stimulated steroidogenesis is regulated by the cAMP-PKA pathway. In this study, we investigated potential mechanisms for T-2 toxin-induced reproductive toxicity focusing on the critical steps of the cAMP-PKA pathway affected by T-2 toxin. We first analyzed the effects of T-2 toxin on progesterone and estrogen production in rat granulosa cells. For this purpose the granulosa cells were cultured for 48 h in 10% fetal bovine serum-containing medium followed by 24 h in serum-free medium containing FSH (10 ng/ml) and androstenedione (3 ng/ml), both are required for normal steroidogenesis. Treatment of these cells with T-2 toxin dose-dependently inhibited the growth of cells and the steroid hormone production. Cellular cyclic AMP levels were dose-dependently inhibited by T-2 toxin (0, 1, 10 and 100 nM, 24 h). Furthermore, we found that although the induction of progesterone by 8-Br-cAMP (a FSH mimetic) and 22R-HC (substrate for progesterone) could both be inhibited by T-2 toxin treatment, the T-2-imposed inhibitory effects could be reversed by increasing doses of 22R-HC, while increasing 8-Br-cAMP had no effects, suggesting that T2 toxin targeted at distinct mechanisms. cAMP-stimulated steroidogenic acute regulatory protein (StAR) is a rate limiting protein in progesterone synthesis. Exposure to T2 toxin caused significant suppression of StAR expression as determined by Western blotting and semi-quantitative RT-PCR suggesting StAR is a sensitive target for T-2 toxin. Taken together, our results strongly suggest that T2 toxin inhibits steroidogenesis by suppressing cAMP-PKA pathway and StAR is a target for T-2-toxin. The antisteroidogenesis effects were observable at low T-2 dose (1 ng/ml) suggesting T-2 toxin has an endocrine disruptive effect. (C) 2014 Elsevier Ireland Ltd. All rights reserved.
摘要：
[Backgroud]Dexamethasone (Dex), a synthetic glucocorticoid, is strictly controlled for use due to its serious side effects including immune suppression.Betulinic acid (BA), an antioxidant prepared from the white birch, exhibits properties of immunomodulation.To assess the implications and investigate the mechanisms of BA-elicited immunomodulation, we hypothesized that Dex induced lymphocyte apoptosis via oxidative stress could be lessened by BA.
作者：
LI Xiaowen;LI Rongfang;YI Jin'e;WANG Ji;LIU Biying;...
期刊：
畜牧与饲料科学,2015年(z1):353-354 ISSN：1672-5190
作者机构：
College of Veterinary Medicine, Hunan Agricultural University;[LIU Biying; LI Rongfang; HUANG Haibing; YI Jin'e; WANG Ji; LI Xiaowen; WEN Lixin] 湖南农业大学
摘要：
[Objective]The study was to investigate the effects of the complex immune stress induced by Newcastle Disease Ⅳ Series and lipopolysaccharides (LPS) on the growth performance and antioxidant capacity in broilers.[Methods] One hundred and twenty eight 1-day-old broilers were randomly divided into 4 groups.Group A was the control group,and saline was given as blank control;groups B,C,D were vaccinated with conventional dose of Neweastle Disease Ⅳ Series by putting drop in noses on the 15 d and 28 d, and also group C and group D were intraperitoneally injected with LPS 250 μg/kg body weight and 500 μg/kg body weight on 12,15,18 and 21 d for 4 times.After 7, 14, 21, 28 day of inoculation, eight chicken serum samples from each groups were collected to detect the content of malondialdehyde (MDA), and the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX).
摘要：
Betulinic acid (BA) is a bioactive pentacyclic triterpene that exhibits a variety of biological activities including antioxidative and immunomodulative properties. The objective of this study was to investigate the potential splenocytes protective effect and underlying mechanism of BA using dexamethasone (Dex)-induced mice as a model system. Pretreatment with BA (0.25, 0.5, and 1.0 mg/kg) dose-dependently ameliorated Dex-induced oxidative damage and apoptosis after 14 days of feeding. In addition to reactive oxygen species scavenging activity in Dex-induced splenocytes, BA administration up-regulated antioxidant enzymes, decreased lipid peroxidation, restored mitochondrial function, decreased the expression of pro-apoptotic protein Bax, prevented the decline of anti-apoptotic protein Bcl-2, inhibited caspase-9 and caspase-3 activation, and improved cell survival. These findings reveal that BA was able to mitigate Dex-induced oxidative stress and might play an important role in repairs of oxidative damage in immunological system.
摘要：
Betulinic acid (BA), a pentacyclic lupane-type triterpene, has a wide range of bioactivities. The main objective of this work was to evaluate the hepatoprotective activity of BA and the potential mechanism underlying the ability of this compound to prevent liver damage induced by alcohol in vivo. Mice were given oral doses of BA (0.25, 0.5, and 1.0 mg/kg) daily for 14 days, and induced liver injury by feeding 50% alcohol orally at the dosage of 10 ml/kg after 1 h last administration of BA. BA pretreatment significantly reduced the serum levels of alanine transaminase, aspartate transaminase, total cholesterol, and triacylglycerides in a dose-dependent manner in the mice administered alcohol. Hepatic levels of glutathione, superoxide dismutase, glutathione peroxidase, and catalase were remarkably increased, while malondialdehyde contents and microvesicular steatosis in the liver were decreased by BA in a dose-dependent manner after alcohol-induced liver injury. These findings suggest that the mechanism underlying the hepatoprotective effects of BA might be due to increased antioxidant capacity, mainly through improvement of the tissue redox system, maintenance of the antioxidant system, and decreased lipid peroxidation in the liver.
摘要：
Objective: To investigate the effect of gossypol acetic acid (GA) on proliferation and apoptosis of macrophage cell line RAW264.7 and further understand the possible underlying mechanism responsible for GA-induced cell apoptosis. Methods: RAW264.7 cells were treated with GA (25-35μmol/L) for 24h. Concomitantly, the cytotoxicity was determined by using MTT assay, and apoptotic cells were identified by TUNEL assay, AO/EB staining and flow cytometry. Meanwhile, mitochondrial membrane potential (ΔΨm) with Rhodamine 123 and reactive oxygen species (ROS) with DCFH-DA were analyzed by fluorescence spectrofluorimeter, respectively. In addition, the expressions of caspase-3 and caspase-9 were assessed by Western Blot assay. Finally, the GA-induced cell apoptosis was evaluated by flow cytometry in the present of caspase inhibitors Z-VAD-FMK and Ac-LEHD-FMK , respectively. Results: GA significantly inhibited the proliferation of RAW264.7 cells in a dose-dependent manner, caused an obvious cell apoptosis and a loss of ΔΨm in RAW264.7 cells. Moreover, the ROS production in cells was elevated, and the levels of activated caspase-3 and caspase-9 were up-regulated in a dose-dependent manner. Notably, GA-induced cell apoptosis can be markedly inhibited by caspase inhibitors, respectively.Conclusion: These results suggest that GA-induced RAW264.7 cell apoptosis may be mediated via a caspase-dependent mitochondrial signaling pathway.
通讯机构：
[Yuan, Hui] H;Hunan Agr Univ, Coll Vet Med, Changsha 410128, Hunan, Peoples R China.
关键词：
DNA damage;Gossypol;Oxidase;Sertoli cells
摘要：
The study was designated to explore the toxic effects of gossypol on piglet sertoli cells. Sertoli cellswere isolated from piglet testes using a two-step enzyme digestion and followed by differential plating.Piglet sertoli cells were cultured and classified into five groups, that is, group A, the control withoutgossypol, group B with 2.5 μg/ml gossypol, group C with 5 μg/ml gossypol, group D with 10 μg/mlgossypol and group E with 20 μg/ml gossypol. We found that sertoli cells’ growth was inhibited bygossypol at dose 2.5 μg/ml when compared with the control group. The oxidase activity of sertoli cellalso decreased at 2.5 μg/m gossypol. Moreover, DNA damage of sertoli cells was observed at 5 μg/mlgossypol. Putting this into consideration, our study suggests that exposure of gossypol to sertoli cellsleads to an inhibition of sertoli cell growth and oxidase activity of sertoli cells at a low concentration,whereas gossypol results in DNA damage of sertoli cells at a higher concentration.Keywords: Gossypol, sertoli cells, oxidase, DNA damage
摘要：
The objective of this study was to explore the immunomodulatory effects of betulinic acid (BA) extracted from the bark of white birch on mice. Female mice were orally administered BA for 14 days in doses of 0, 0.25, 0.5, and 1 mg/kg body weight. We found that BA significantly enhanced the thymus and spleen indices, and stimulated lymphocyte proliferation induced by Concanavalin A and lipopolysaccharide as shown by MTT assay. Flow cytometry revealed that BA increased the percentage of CD4(+) cells in thymus as well as the percentage of CD19(+) and the ratios of CD4(+)/CD8(+) in spleen. BA increased the number of plaque-forming cell and macrophage phagocytic activity as indicated by a neutral red dye uptake assay, and the peritoneal macrophages levels of TNF-alpha were also increased. In contrast, serum levels of IgG and IgM and serum concentrations of IL-2 and IL-6 were significantly decreased in BA-treated mice compared to the control as assayed by haemagglutination tests and ELISA, respectively. Taken together, these results suggest that BA enhances mouse cellular immunity, humoral immunity, and activity of macrophages. Thus, BA is a potential immune stimulator and may strengthen the immune response of its host.
