Influences of Fucoxanthin on Alveolar Bone Resorption in Induced Periodontitis in Rat Molars

The aim of this study was to evaluate the effects of systemic fucoxanthin treatment on alveolar bone resorption in rats with periodontitis. Thirty rats were divided into control, experimental periodontitis (EP), and experimental periodontitis-fucoxanthin (EP-FUCO) groups. Periodontitis was induced by ligature for four weeks. After removal of the ligature, the rats in the EP-FUCO group were treated with a single dose of fucoxanthin (200 mg/kg bw) per day for 28 consecutive days. At the end of the study, all of the rats were euthanized and intracardiac blood and mandible tissue samples were obtained for biochemical, immunohistochemical, and histometric analyses. Fucoxanthin treatment resulted in a slight decrease in tumor necrosis factor-α, interleukin-1β, and interleukin-6 levels and a significant decrease in oxidative stress index. It was observed that fucoxanthin caused a significant reduction in receptor activator of nuclear factor kappa-β ligand (RANKL) levels and a statistically non-significant elevation in osteoprotegerin and bone-alkaline phosphatase levels. There were no significant differences in alveolar bone loss levels between the EP and EP-FUCO groups. This experimental study revealed that fucoxanthin provides a limited reduction in alveolar bone resorption in rats with periodontitis. One of the mechanisms underlying the mentioned limited effect might be related to the ability of fucoxanthin to inhibit oxidative stress-related RANKL-mediated osteoclastogenesis.     

狭叶茶提取物对小鼠氧化应激性肝损伤的保护作用

研究狭叶茶(Camellia angustifolia Chang)提取物对拘束负荷诱发小鼠应激性肝损伤的保护作用。采用拘束负荷小鼠应激性肝损伤模型,18h拘束负荷诱发小鼠应激性肝损伤,分别用赖氏法测定小鼠血浆和肝组织丙氨酸转移酶(ALT)活性、硫代巴比妥酸法测定丙二醛(MDA)含量、HPLC法测定谷胱甘肽(GSH)水平、比色法测定黄嘌呤氧化酶(XOD)、谷胱甘肽过氧化物酶(GPX)和谷胱甘肽S转移酶(GST)活性,荧光酶标仪测定血浆、肝组织及狭叶茶提取物体外抗氧化能力指数(ORAC)。与拘束模型组相比,狭叶茶提取物可以明显提高拘束负荷小鼠血浆与肝组织匀浆的ALT活性和抗氧化能力指数,提高GSH水平,增强GPX和GST活性,有效降低肝组织中MDA含量和XOD活性,并在体外显示出较强的抗氧化能力。说明狭叶茶提取物对拘束应激引起的小鼠肝损伤具有一定的保护作用,其作用机制可能部分来自于减少拘束负荷小鼠氧化应激水平,清除自由基和抑制脂质过氧化过程。     

Protective Effects of Ulva lactuca Polysaccharide Extract on Oxidative Stress and Kidney Injury Induced by D-Galactose in Mice

Reactive oxygen species (ROS) are the key factors that cause many diseases in the human body. Polysaccharides from seaweed have been shown to have significant antioxidant activity both in vivo and in vitro. The ameliorative effect of Ulva lactuca polysaccharide extract (UPE) on renal injury induced by oxidative stress was analyzed. As shown by hematoxylin–eosin staining results, UPE can significantly improve the kidney injury induced by D-galactose (D-gal). Additionally, the protective mechanism of UPE on the kidney was explored. The results showed that UPE could decrease the levels of serum creatinine (Scr), blood urea nitrogen (BUN), serum cystatin C (Cys-C), lipid peroxidation, protein carbonylation, and DNA oxidative damage (8-OHdG) and improve kidney glutathione content. Moreover, UPE significantly increased the activities of superoxide dismutase and glutathione peroxidase and total antioxidant activity in mice. UPE also decreased the levels of inflammatory cytokines TNF-α and IL-6. Further investigation into the expression of apoptotic protein caspase-3 showed that UPE decreased the expression of apoptotic protein caspase-3. These results indicate that UPE has a potential therapeutic effect on renal injury caused by oxidative stress, providing a new theoretical basis for the treatment of oxidative damage diseases in the future.     

茯砖茶提取物对葡聚糖硫酸钠诱导小鼠炎症性肠病的保护作用研究

茯砖茶是我国特有的一种黑茶。本文以茯砖茶为原料,分别制备了茯砖茶水提物（FWE）、经95%乙醇沉后得到的醇溶物（FES）和醇沉物（FEP）,并探究了3种提取物对葡聚糖硫酸钠诱导小鼠炎症性肠病的保护作用。研究表明,3种茯砖茶提取物都能够减轻炎症性肠病的肠道结构损伤,其中FWE组效果最好;同时茯砖茶提取物可以显著提升小鼠血清和肠道组织上清液中超氧化物岐化酶（SOD）、过氧化氢酶（CAT）和谷胱甘肽（GSH）水平以及降低白细胞介素-6（IL-6）、白细胞介素-1β（IL-1β）和肿瘤坏死因子-α（TNF-α）水平,且作用效果均为FWE组>FES组>FEP组;在蛋白水平上,FWE组小鼠肠道组织的NF-κB p65蛋白水平有所降低;IκBα的蛋白水平在FWE组和FES组中有所增加;核因子E2相关因子2（Nrf2）和血红素氧化酶-1（HO-1）的相关蛋白水平在FWE组和FES组也有所增加。综上所述,茯砖茶提取物可以通过抗氧化和抗炎途径对葡聚糖硫酸钠诱导小鼠炎症性肠病发挥预防保护作用。     

大豆异黄酮对过氧化氢诱导的肝细胞损伤的保护作用

为探索大豆异黄酮对过氧化氢(H_2O_2)致肝细胞损伤的保护作用,以H_2O_2损伤Chang Liver细胞建立肝细胞氧化应激损伤模型,并以10,20和40 mg·L~(-1)大豆异黄酮进行干预。采用四甲基偶氮唑盐比色(MTT)法检测肝细胞存活率;以微板法检测细胞培养液中乳酸脱氢酶(LDH)、谷丙转氨酶(ALT)、谷草转氨酶(AST)活性和肝细胞超氧化物歧化酶(SOD)活性,以及肝细胞还原型谷胱甘肽(GSH)和丙二醛(MDA)含量;采用蛋白印迹技术检测肝细胞核因子-E2相关因子2(Nrf2)蛋白含量。在10~40 mg·L~(-1)范围内,大豆异黄酮对Chang Liver细胞不显示细胞毒作用。300μmol·L~(-1)H_2O_2刺激后,模型组肝细胞存活率与正常组比较下降,细胞外液中ALT、AST、LDH水平上升,说明Chang Liver细胞损伤显著;而模型组肝细胞中SOD和GSH水平与正常组比较下降,丙二醛水平上升,说明模型组Chang Liver细胞氧化应激增强。大豆异黄酮可剂量依赖性地提高Chang Liver细胞存活率,降低ALT、AST、LDH向细胞外液的释放;降低细胞MDA水平,升高细胞SOD和GSH水平,增高核中Nrf2蛋白水平。研究结果显示大豆异黄酮对H_2O_2致肝细胞氧化应激损伤具有保护作用。     

油酸在黄曲霉毒素诱导肝细胞损伤中的保护作用

为了解油酸在黄曲霉毒素B1（aflatoxin B1,AFB1）诱发的肝损伤中所起的保护作用,以体外培养的肝细胞（L-02）作为靶细胞,研究油酸的保护机制。设置3组实验：对照组（无处理）、AFB1组（只有AFB1）、油酸组（AFB1和油酸共同处理）,药物处理24h后显微镜观察细胞形态,细胞增殖-毒性检测试剂盒（Cell Counting Kit-8, CCK-8）检测细胞活力,荧光法检测活性氧（reactive oxygen species,ROS）水平,Annexin V-FITC/PI检测细胞凋亡率,蛋白质免疫印迹检测血红素加氧酶-1（heme oxygenase 1,HO-1）、Caspase-3以及Survivin蛋白的表达。采用t检验或单因素方差分析进行统计分析。结果发现：与对照组相比,AFB1暴露能够明显抑制细胞活力（P<0.05）,促进细胞凋亡（P<0.001）,升高ROS水平（P<0.001）;与AFB1组相比,油酸作用后细胞活力显著增加（P<0.01）,细胞凋亡减少（P<0.01）,ROS水平降低（P<0.001）。与AFB1组相比,油酸作用后可显著提高 HO-1（P<0.05）和抑凋亡蛋白Survivin的表达（P<0.05）,降低凋亡蛋白Caspase-3（P<0.01）表达。因此认为油酸对AFB1引发的肝细胞损伤具有保护作用,其机制可能与其通过促进抗氧化酶蛋白HO-1的表达,从而降低氧化应激水平,降低细胞凋亡有关。     

黑豆根尖边缘细胞对盐胁迫的防护效应

采用振荡培养(移除根尖边缘细胞)和静置培养(保持边缘细胞附着在根尖)方法,对比研究盐胁迫对黑豆根系生长和根尖边缘细胞发育、根系Na+、K+含量的影响以及根系生理特性的变化。结果显示:100和200 mmol.L-1NaCl处理抑制边缘细胞发育,引起根系相对电导率和MDA含量增加。振荡培养去除根尖边缘细胞处理36 h,黑豆根相对伸长率、根尖K+含量明显低于对应NaCl浓度的静置培养处理,同时根尖Na+含量、相对电导率和MDA含量在去除边缘细胞后显著增加。说明包裹于根尖的边缘细胞通过调节Na+和K+的吸收和维持较高的细胞膜完整性,以适应盐害环境。     

The Protect Effects of Chitosan Oligosaccharides on Intestinal Integrity by Regulating Oxidative Status and Inflammation under Oxidative Stress

The aim of this study was to evaluate the effects of the dietary supplementation of chitosan oligosaccharides (COS) on intestinal integrity, oxidative status, and the inflammation response with hydrogen peroxide (H₂O₂) challenge. In total, 30 rats were randomly assigned to three groups with 10 replications: CON group, basal diet; AS group, basal diet + 0.1% H₂O₂ in drinking water; ASC group, basal diet + 200 mg/kg COS + 0.1% H₂O₂ in drinking water. The results indicated that COS upregulated (p < 0.05) villus height (VH) of the small intestine, duodenum, and ileum; mucosal glutathione peroxidase activity; jejunum and ileum mucosal total antioxidant capacity; duodenum and ileum mucosal interleukin (IL)-6 level; jejunum mucosal tumor necrosis factor (TNF)-α level; duodenum and ileum mucosal IL-10 level; the mRNA expression level of zonula occludens (ZO)-1 in the jejunum and ileum, claudin in the duodenum, nuclear factor-erythroid 2-like 2 in the jejunum, and heme oxygenase-1 in the duodenum and ileum; and the protein expression of ZO-1 and claudin in jejunum; however, it downregulated (p < 0.05) serum diamine oxidase activity and D-lactate level; small intestine mucosal malondialdehyde content; duodenum and ileum mucosal IL-6 level; jejunum mucosal TNF-α level; and the mRNA expression of IL-6 in the duodenum and jejunum, and TNF-α in the jejunum and ileum. These results suggested COS could maintain intestinal integrity under oxidative stress by modulating the intestinal oxidative status and release of inflammatory cytokines.     

H2S对盐碱混合胁迫下裸燕麦叶片脂肪酸组成的影响

脂肪酸是细胞膜脂的重要组成成分,信号分子硫化氢(H₂S)在植物响应盐碱胁迫中发挥着重要作用。为探讨H₂S对盐碱混合胁迫下裸燕麦脂肪酸组成的效应,采用盆栽砂培试验,研究了外施H₂S供体硫氢化钠(NaHS)和H₂S生成抑制剂羟胺(HA)对50 mmol·L^-1盐碱混合胁迫下裸燕麦品种定莜9号植株生长、叶片细胞膜脂氧化和脂肪酸组成的影响。结果表明：(1)喷施50μmol·L^-1 NaHS可显著缓解盐碱混合胁迫下定莜9号植株干重的下降和叶片超氧阴离子、过氧化氢和丙二醛含量的提高;增添HA后逆转了喷施NaHS缓解盐碱混合胁迫抑制定莜9号植株生长和叶片膜脂氧化损伤的作用。(2)盐碱混合胁迫导致定莜9号叶片50种脂肪酸中的部分组分含量发生显著改变,使总脂肪酸含量和脂肪酸不饱和程度显著降低。喷施50μmol·L^-1 NaHS使盐碱混合胁迫下定莜9号叶片5种脂肪酸组分棕榈酸(C16∶0)、岩芹酸(C18∶1N12)、异油酸(C18∶1N7)、亚油酸(C...     

The Potential Protective Effect and Possible Mechanism of Peptides from Oyster (Crassostrea hongkongensis) Hydrolysate on Triptolide-Induced Testis Injury in Male Mice

Peptides from oyster hydrolysate (OPs) have a variety of biological activities. However, its protective effect and exact mechanism on testicular injury remain poorly understood. This study aimed to evaluate the protective effect of OPs on triptolide (TP)-induced testis damage and spermatogenesis dysfunction and investigate its underlying mechanism. In this work, the TP-induced testis injury model was created while OPs were gavaged in mice for 4 weeks. The results showed that OPs significantly improved the sperm count and motility of mice, and alleviated the seminiferous tubule injury. Further study showed that OPs decreased malonaldehyde (MDA) level and increased antioxidant enzyme (SOD and GPH-Px) activities, attenuating oxidative stress and thereby reducing the number of apoptotic cells in the testis. In addition, OPs improved the activities of enzymes (LDH, ALP and ACP) related to energy metabolism in the testis and restored the serum hormone level of mice to normal. Furthermore, OPs promoted the expression of Nrf2 protein, and then increased the expression of antioxidant enzyme regulatory protein (HO-1 and NQO1) in the testis. OPs inhibited JNK phosphorylation and Bcl-2/Bax-mediated apoptosis. In conclusion, OPs have a protective effect on testicular injury and spermatogenesis disorders caused by TP, suggesting the potential protection of OPs on male reproduction.     

茯砖茶对H2O2诱发LLC-PK1细胞损伤的保护作用

探讨茯砖茶乙醇提取物(FTE)对H2O2诱发猪肾近曲小管LLC-PK1上皮细胞氧化损伤的保护作用.以不同质量浓度(10～200 μg/mL)的FTE预培养LLC-PK1细胞24 h后,换用含500 μmol/L H2O2的DMEM细胞培养液继续培养4h建立细胞氧化损伤模型.MTT法检测细胞生存率,硫代巴比妥酸比色法测定细胞内丙二醛(malondialdehyde,MDA)含量,比色法测定细胞内过氧化氢酶(catalase,CAT),超氧化物歧化酶(superoxide dismutase,SOD)和谷胱甘肽过氧化物酶(glutathione peroxidase,GSH-px)含量.经不同浓度     

Effects of High Temperature Stress on Microscopic and Ultrastructural Characteristics of Mesophyll Cells in Flag Leaves of Rice

The microscopic and ultrastructural characteristics of mesophyll cells in flag leaves of two rice lines (a thermo-sensitive line 4628 and a thermo-resistant line 996) under high temperature stress (37°C during 8:00-17:00 and 30°C during 17:00-8:00) were investigated using an optical and a transmission electron microscopy. The membrane permeability and malondialdehyde content increased under the high temperature stress, and the increase of both variables was greater in the line 4628 than in the line 996. Und...     

达玛树脂提取物对人参细胞中皂苷单体含量的影响

用硅胶柱层析分离达玛树脂石油醚-丙酮提取物,选分离得到的2种提取物组分分别饲喂悬浮培养的人参细胞,考察细胞生长、人参皂苷积累的变化情况。试验结果表明：提取物II可以最大提高人参细胞人参皂苷Rb1含量42.3 %±2.6 %,Rg1含量33.2 %±1.4 %,Re含量35.6 %±1.6 %;而提取物I对人参细胞的生长和皂苷的合成有抑制作用。     

绿茶多酚对被动吸烟引起小鼠肺氧化应激的干预研究

研究了绿茶多酚（Green tea polyphenol,GTP）对被动吸烟致小鼠肺部氧化应激损伤的干预作用,并探讨其可能机制。将40只KM雌性小鼠随机分成正常对照C组、被动吸烟模型M组、100βmg·kg^-1 GTP1组、200βmg·kg^-1 GTP2组,每组10只。实验12周结束后处死小鼠,测定其肺质量及血清氧化应激炎症水平;采用荧光定量PCR测定白细胞介素6（IL-6）、白细胞介素33（IL-33）、肿瘤坏死因子-α（TNF-α）和白细胞介素1β（IL-1β）基因表达水平。研究结果表明,与M组相比,灌喂GTP后使得小鼠生存质量、肺形态有明显改观,显著提高小鼠血清T-SOD及GSH-Px活力,显著降低MDA、IL-6、TNF-α表达水平,显著抑制IL-6、IL-33、TNF-α及IL-1β炎性相关基因的表达,灌胃200βmg·kg^-1 GTP比100βmg·kg^-1的GTP作用更加显著。研究发现,GTP可能通过抑制炎性细胞因子表达水平、提高抗氧化能力来保护肺部组织形态与结构的完整,保护被动吸烟对肺部的损害。     

Effects of bistheonellide A,an Actin-polymerization Inhibitor,on Chinese Hamster V79 Cells and on IL-8 Production in PMA-stimulated HL-60 Cells

Bioassay-guided isolation from the ethanol extract of a marine sponge Theonella sp. collected in Palau yielded bistheonellide A, which strongly inhibited the colony formation of Chinese hamster V79 cells (EC₅₀ = 6.8 nM). Bistheonellide A is an actin-polymerization inhibitor and was suggested to control cytokine production. Therefore, we attempted to detect an effect of this compound on IL-8 production in PMA-stimulated HL-60 cells. Interestingly, bistheonellide A did not modulate the production of IL-8 under cytotoxic concentrations as determined by LDH analysis. Although the correlation between the inhibition of microtubule assembly and the stimulation of IL-8 production has been observed for several compounds, the polymerization of actin was not related to an IL-8 production in the case of bistheonellide A. It will be suggested that the actin polymerization is not involved in the IL-8 production system.     

水分胁迫对香蕉幼苗保护酶活性的影响

采用水培试验方法研究香蕉幼苗叶片在不同水分胁迫下,超氧化物歧化酶(SOD)、过氧化氢酶(CAT)和过氧化物酶(POD)3种保护酶的活性变化。结果表明,胁迫后,香蕉幼苗叶片的SOD、CAT和POD活性都呈现先升高后下降的趋势。复水后3种保护酶活性均可恢复到与对照相当的水平。因此认为,水分胁迫影响香蕉幼苗保护酶活性,降低幼苗的抗旱能力。     

Simultaneous Inhibitory Effects of All-Trans Astaxanthin on Acetylcholinesterase and Oxidative Stress

Alzheimer´s disease is a global neurodegenerative health concern. To prevent the disease, the simultaneous inhibition of acetylcholinesterase and oxidative stress is an efficient approach. In this study, the inhibition effect of all-trans astaxanthin mainly from marine organisms on acetylcholinesterase and oxidative stress was evaluated by a chemical-based method in vitro and cell assay model. The results show that all-trans astaxanthin was a reversible competitive inhibitor and exhibited a strong inhibition effect with half inhibitory concentration (IC₅₀ value) of 8.64 μmol/L. Furthermore, all-trans astaxanthin inhibited oxidative stress through reducing malondialdehyde content and increasing the activity of superoxide dismutase as well as catalase. All-trans astaxanthin could induce the changes of the secondary structure to reduce acetylcholinesterase activity. Molecular-docking analysis reveals that all-trans astaxanthin prevented substrate from binding to acetylcholinesterase by occupying the space of the active pocket to cause the inhibition. Our finding suggests that all-trans astaxanthin might be a nutraceutical supplement for Alzheimer´s disease prevention.     

Ameliorative Effects of Oyster Protein Hydrolysates on Cadmium-Induced Hepatic Injury in Mice

Cadmium (Cd) is a widespread environmental toxicant that can cause severe hepatic injury. Oyster protein hydrolysates (OPs) have potential effects on preventing liver disease. In this study, thirty mice were randomly divided into five groups: the control, Cd, Cd + ethylenediaminetetraacetic acid (EDTA, 100 mg/kg), and low/high dose of OPs-treatment groups (100 mg/kg or 300 mg/kg). After continuous administration for 7 days, the ameliorative effect of OPs on Cd-induced acute hepatic injury in Cd-exposed mice was assessed. The results showed that OPs significantly improved the liver function profiles (serum ALT, AST, LDH, and ALP) in Cd-exposed mice. Histopathological analysis showed that OPs decreased apoptotic bodies, hemorrhage, lymphocyte accumulation, and inflammatory cell infiltration around central veins. OPs significantly retained the activities of SOD, CAT, and GSH-Px, and decreased the elevated hepatic MDA content in Cd-exposed mice. In addition, OPs exhibited a reductive effect on the inflammatory responses (IL-1β, IL-6, and TNF-α) and inhibitory effects on the expression of inflammation-related proteins (MIP-2 and COX-2) and the ERK/NF-κB signaling pathway. OPs suppressed the development of hepatocyte apoptosis (Bax, caspase-3, and Blc-2) and the activation of the PI3K/AKT signaling pathway in Cd-exposed mice. In conclusion, OPs ameliorated the Cd-induced hepatic injury by inhibiting oxidative damage and inflammatory responses, as well as the development of hepatocyte apoptosis via regulating the ERK/NF-κB and PI3K/AKT-related signaling pathways.