没食子酸对美国白蛾幼虫营养效应及解毒酶活性的影响

美国白蛾是我国重大外来入侵害虫,寄主范围十分广泛。酚类物质是最广泛的植物次生代谢物之一,在植物抵御昆虫取食的化学防御中具有重要作用。本研究通过人工饲料添加没食子酸的方法,探究不同浓度的没食子酸对美国白蛾幼虫的营养效应及解毒酶和乙酰胆碱酯酶活性的影响。结果表明,各浓度(1.0%、1.5%、2.0%、2.5%、3.0%)没食子酸对美国白蛾4龄幼虫的近似消化率、食物利用率、相对取食量和相对生长率均具有显著影响(P<0.05),近似消化率和相对取食量不同程度下降,食物利用率和相对生长率则不同程度上升。不同浓度的没食子酸处理对美国白蛾幼虫的乙酰胆碱酯酶、羧酸酯酶、谷胱甘肽S-转移酶和细胞色素P450的活性均具有显著影响(P<0.05)。1.0%没食子酸作用时间不同,美国白蛾4龄幼虫的乙酰胆碱酯酶、羧酸酯酶、谷胱甘肽S-转移酶和细胞色素P450的活性差异显著(P<0.05)。没食子酸能够始终诱导细胞色素P450的活性,而羧酸酯酶的活性却受到抑制。不同浓度的没食子酸对乙酰胆碱酯酶作用总体上不明显,但较低浓度时(1.0%)对乙酰胆碱酯酶活性却随处理时间延长而抑制作用加强。较低浓度(1.0%~1.5%)的没食子酸对谷胱甘肽S-转移酶的活性有一定诱导作用,但随着没食子酸浓度提高谷胱甘肽S-转移酶的活性却受到一定程度的抑制。没食子酸能抑制美国白蛾幼虫的取食,并且对解毒酶和乙酰胆碱酯酶的活性表现出一定的时间效应和剂量效应,表明美国白蛾幼虫可能通过调节食物利用和解毒代谢等多种途径降低没食子酸的毒害作用,从而对含没食子酸的寄主植物产生适应。     

Base excision repair but not DNA double‐strand break repair is impaired in aged human adipose‐derived stem cells

The decline in DNA repair capacity contributes to the age‐associated decrease in genome integrity in somatic cells of different species. However, due to the lack of clinical samples and appropriate tools for studying DNA repair, whether and how age‐associated changes in DNA repair result in a loss of genome integrity of human adult stem cells remains incompletely characterized. Here, we isolated 20 eyelid adipose‐derived stem cell (ADSC) lines from healthy individuals (young: 10 donors with ages ranging 17–25 years; old: 10 donors with ages ranging 50–59 years). Using these cell lines, we systematically compared the efficiency of base excision repair (BER) and two DNA double‐strand break (DSB) repair pathways—nonhomologous end joining (NHEJ) and homologous recombination (HR)—between the young and old groups. Surprisingly, we found that the efficiency of BER but not NHEJ or HR is impaired in aged human ADSCs, which is in contrast to previous findings that DSB repair declines with age in human fibroblasts. We also demonstrated that BER efficiency is negatively associated with tail moment, which reflects a loss of genome integrity in human ADSCs. Mechanistic studies indicated that at the protein level XRCC1, but not other BER factors, exhibited age‐associated decline. Overexpression of XRCC1 reversed the decline of BER efficiency and genome integrity, indicating that XRCC1 is a potential therapeutic target for stabilizing genomes in aged ADSCs.     

“2020年后全球生物多样性框架”进展及展望

“2020年后全球生物多样性框架”是当前《生物多样性公约》谈判的焦点议题之一。本文阐述了框架制定的背景, 介绍了“2020年后全球生物多样性框架”不限成员名额工作组(Open Ended Working Group, OEWG),的谈判过程, 综合分析了缔约方在各有关磋商进程中的观点, 以及目前缔约方对框架各个要素的共识和分歧, 评估了框架的制定进展, 并就框架的设计提出四点展望: (1)阐明转型变革的具体实施路径; (2)平衡反映公约三大目标; (3)加强与其他全球治理进程的协同; (4)强化框架对全球及缔约方履约进展的评估和审查。最后提出对我国的建议: (1)及时更新国家生物多样性战略与行动计划(National Biodiversity Strategies and Action Plans, NBSAP); (2)加强国内生物多样性工作的协调; (3)继续加强生态环境执法和责任机制。为缔约方更好参与框架制定进程, 深入了解框架及其磋商进展提供参考, 并为下一步框架制定提供参考。     

Lamin B2 promotes the progression of triple negative breast cancer via mediating cell proliferation and apoptosis

Triple negative breast cancer (TNBC) is a more common type of breast cancer with high distant metastasis and poor prognosis. The potential role of lamins in cancer progression has been widely revealed. However, the function of lamin B2 (LMNB2) in TNBC progression is still unclear. The present study aimed to investigate the role of LMNB2 in TNBC. The cancer genome atlas (TCGA) database analysis and immunohistochemistry (IHC) were performed to examine LMNB2 expression levels. LMNB2 short hairpin RNA plasmid or lentivirus was used to deplete the expression of LMNB2 in human TNBC cell lines including MDA-MB-468 and MDA-MB-231. Alterations in cell proliferation and apoptosis in vitro and the nude mouse tumorigenicity assay in vivo were subsequently analyzed. The human TNBC tissues shown high expression of LMNB2 according to the bioinformation analysis and IHC assays. LMNB2 expression was correlated with the clinical pathological features of TNBC patients, including pTNM stage and lymph node metastasis. Through in vitro and in vivo assays, we confirmed LMNB2 depletion suppressed the proliferation and induced the apoptosis of TNBC cells, and inhibited tumor growth of TNBC cells in mice, with the decrease in Ki67 expression or the increase in caspase-3 expression. In conclusion, LMNB2 may promote TNBC progression and could serve as a potential therapeutic target for TNBC treatment.     

Sirt3 Protects Against Ischemic Stroke Injury by Regulating HIF-1α/VEGF Signaling and Blood–Brain Barrier Integrity

Sirtuin 3 (Sirt3) is a member of the Sirtuin family proteins and known to regulate multiple physiological processes such as metabolism and aging. As stroke is an aging-related disease, in this work, we attempt to examine the role and potential mechanism of Sirt3 in regulating ischemic stroke by using a permanent middle cerebral artery occlusion (pMCAO) model in wild type (WT) and Sirt3 knockout (KO) mice, coupled with oxygen glucose deprivation (OGD) experiments in cultured primary astrocytes. Sirt3 deficiency aggravated neuronal cell apoptosis and neurological deficits after brain ischemia. In addition, Sirt3 KO mice showed more severe blood–brain barrier (BBB) disruption and inflammatory responses compared with WT group in the acute phase. Furthermore, specific overexpression of Sirt3 in astrocytes by injecting glial fibrillary acidic protein (GFAP)::Sirt3 virus in ischemic region showed protective effect against stroke-induced damage. Mechanistically, Sirt3 could regulate vascular endothelial growth factor (VEGF) expression by inhibiting hypoxia inducible factor-1α (HIF-1α) signaling after ischemia (OGD). Our results have shown that Sirt3 plays a protective role in ischemic stroke via regulating HIF-1α/VEGF signaling in astrocytes, and reversal of the Sirt3 expression at the acute phase could be a worthy direction for stroke therapy.

     

The optimum dietary methionine requirement of juvenile humpback grouper (Cromileptes altivelis): effects on growth,micromorphology, protein and lipid metabolism

An 8-week feeding trial was conducted to evaluate optimum dietary methionine (Met) requirement of juvenile humpback grouper (Cromileptes altivelis) and the influence of dietary methionine (Met) supplementations on growth, gut micromorphology, protein and lipid metabolism. Seven isoproteic (48.91%) and isolipidic diets (10%) were made to contain 0.70, 0.88, 1.04, 1.27 1.46, 1.61 and 1.76% of dry matter Met levels. Results showed that lower survival, weight gain (WG%), protein efficiency ratio (PER), protein productive value (PPV) but higher daily feed intake (DFI) and feed conversion ratio (FCR) were observed in the Met deficient groups (0.70 and 0.88%). Optimum dietary Met requirement for humpback grouper was found to be 1.07% through the straight-broken line analysis of WG% against Met. Fish fed Met deficient diets (0.70, 0.88%) exhibited lower mRNA levels of growth hormone (GH), growth hormone receptor (GHR), insulin-like growth factor-I (IGF-1), target of rapamycin (TOR) as well as S6 kinase 1 (S6K1) than other dietary groups. Whereas, expression of genes related to general control nonderepressible (GCN2) kinase i.e., GCN2 and C/EBPβ enhancer-binding protein β was upregulated in fish fed low Met diets (P < 0.05). The mRNA expression of hepatic fatty acid synthase (FAS) and sterol regulatory element-binding protein-1 (SREBP-1) were higher in fish fed 0.70 and 0.88% dietary Met group and the lipolytic genes, hepatic peroxisome proliferator-activated receptor α (PPARα) and carnitine palmitoyl transferase-1 (CPT-1) showed an opposite variation tendency as FAS or SREBP1. Generally, the optimum Met requirement for humpback grouper was predicted to be 1.07% of dry matter.