Effect of Xiaoyu Zhixue Tablet (消瘀止血片) on Expression ofPlatelet Membrane Glycoproteins in Patients withHemorrhagic Thrombopathy

Objective: To observe the effect of Xiaoyu Zhixue tablet (消瘀止血片,XYZXT) on the expression of platelet membrane glycoproteins in patients with hemorrhagic thrombopathy, and to explore its possible mechanism. Methods: The total of 148 patients with hemorrhagic thrombopathy were randomly divided into two groups, the traditional Chinese medicicne (TCM) group (n=98) treated with XYZXT and the Western medicine (WM) group (n=50) treated with adrenosin, vitamins C, K and P, both for 6 months. The therapeutic effect and the recovery rate of platelet aggregation in the two groups were observed. And platelet membrane glycoprotein (GP) Ⅰb/Ⅸ, GPⅡb/Ⅲa complexes, GPⅠb, GPⅡb, GP Ⅲa and P-selectin were analyzed by flow cytometry in both groups before and after treatment and also in 34 normal healthy subjects. Results: The total effective rate of hemostasis was 89. 8% in TCM group and 54. 0% in the WM group (x2=45.83, P<0.01), and the recovery rate of platelet aggregation was 72.4% and 4.0% respectively (x2=62.06, P<0.01). The fluorescence intensity of GP Ⅰ b/Ⅸ, GPⅡb/Ⅲa complexes, GPⅠb, GPⅢa and P-selectin were lower in both groups before treatment than those in the healthy subjects. Expression of above-mentioned marks was elevated in TCM group after 6 months' therapy, which was insignificantly different as compared with the healthy subjects (P>0.05) and higher than those in the WM group (P<0.05). Conclusion: One of the mechanisms in treating hemorrhagic thrombopathy with XYZXT is that it could regulate the expression of GP Ⅰb/Ⅸ, GPⅡ b/Ⅲa complexes, GPⅠb, GPⅢa and P-selectin at the level of receptor protein.

Effects of Monoclonal Antibody Against Adipocyte-Specific Membrane Protein on Lipid Metabolism in Pigs

This study was to investigate the regulation of monoclonal antibodies against adipocyte membrane proteins （McAb） on lipid metabolism in pigs. Forty Landrace x Saba pigs were randomly divided into eight groups; the control group was given 10 mL saline and the treat groups were given monoclonal antibody against adipocyte-specific membrane protein with 0.1, 0.5, and 1.0 mg kg-I body weight at 15 and 60 kg body weight, respectively, by intraperitoneal injection. The results showed that McAb could increase, significantly, serum lipoprotein lipase activity and reduce serum nonesterified fatty acid （NEFA） content. Meanwhile, McAb increased content of serum lipid, triglyceride （TG）, cholesterol （CHO）, high density lipoprotein （HDL）, and low density lipoprotein （LDL） both at 15 and 60 kg body weight. However, McAb affected more significantly the lipid metabolism at 15 kg body weight than at 60 kg body weight. Moreover, this effect of McAb on lipid metabolism exhibited dose-dependent effect. These results suggested that this monoclonal antibody increased lipase activity, promoted lipolysis, and utilization of lipid so that McAb could be applied to restrain excessive fat deposition in porcine production through the regulation of fat metabolism.

Effects of Three Drugs on Membrane Metabolism Against Cysticerci cellulosae in vitro

To investigate the effects and mechanisms of the benzimidazole carbamate and benmidine drugs on Cysticerci cellulosae and choose effective drugs on Cysticerci cellulosae, the membrane metabolism of Cysticerci cellulosae in vitro was tested after three kinds of drugs which were used respectively. The indexes included the contents of lipids, the contents of SA and the changes of the membrane fluidity. The results showed that oxfendazole could inhibit the membrane metabolism of immature and mature Cysticerci cellulosae in vitro, and albendazole only inhibited the mature one, while thibendimidine neither acted on the immature nor mature one.

Expression of Platelet Membrane Glycoprotein Ib/Ⅸ/Ⅴ Complex,a Receptor of Thrombin,in Patients with Hemorrhagic Thrombopathy

To investigate the role of platelet membrane glycoprotein （GP） Ib/Ⅸ/Ⅴ complex and its subunit GP Ibα in patients with hemorrhagic thrombopathy （HT）, the expressions of GP Ib/Ⅸ/Ⅴ complex and GP Ibα,defined as mean fluorescence intensity （MFI）, were assessed by flow cytometry. The maximum aggregation of platelet was determined by turbidity method. These indicators were compared among 68 HT patients with the presenting complaint of hemorrhage, 33 well-controlled HT patients and 32 normal healthy subjects. The results showed that the MFI of GP Ib/Ⅸ /Ⅴ complex and GP Ibα was markedly lower in HT patients with current hemorrhage than that in the healthy subjects, with difference being statistically significant （P〈0.05）. There was no significant difference in the expressions of GP Ib/ Ⅸ/ Ⅴ complex and GP Ibα between well-controlled HT patients and normal healthy subjects （P〉0.05）. It was concluded that the expression of GP Ib/Ⅸ /Ⅴ complex, the receptor of thrombin and von Willebrand factor, was down-regulated in HT patients with current hemorrhage, which might result in the dysfunction of platelet aggregation and recurrence of HT.

Association of the Platelet Membrane Glycoprotein Ⅰa C807T Gene Polymorphism with Aspirin Resistance

To explore the correlation between the C807T polymorphism of platelet membrane glycoprotein Ⅰa （GP Ⅰa） gene and aspirin resistance in Chinese people, 200 patients with high-risk of atherosclerosis took aspirin （100 mg/d） for 7 days. Platelet aggregation function was detected using adenosine diphosphate （ADP） and arachidonic acid （AA） before and after the administration of aspirin. Then the subjects were divided into three groups according to the results of platelet aggregation function： an aspirin resistant （AR） group, an aspirin semi-responder （ASR） group and an aspirin-sensitive （AS） group. Platelet GP Ⅰa gene 807CT polymorphism was examined by means of polymerase chain reaction-sequence specific primers （PCR-SSP）. The results showed that T allelic frequency in AR group and ASR group were higher that of AS group （P〈0.005）, and the prevalence of genotypes （TT＋TC） of these two groups was significantly higher than that in AS group （P〈0.05）. Platelet GP Ⅰa T allele was significantly associated with aspirin resistance as revealed by multiple logistic regression （OR=3.76, 95% CI： 2.87-9.58）. The results suggest that inherited platelet GP Ⅰa variations may have an important impact on aspirin resistance and the presence of GP Ⅰa T allele may be a marker of genetic susceptibility to aspirin resistance.

Redistribution of Platelet Membrane Glycoprotein IV and Release of Intracellular α-granule Thrombospondin in Patients with Chronic Myelogenous Leukemia

The redistribution of platelet membrane glycoprotein IV (GPIV) and the release of intracellular Q-granule thrombospondin (TSP) were examined and the inhibition of 5-thromboglobulin (&TG) and platelet factor 4 (PF4) in patients with chronic myelogenous leukemia (CML) was observed and quantitation of β-TG and PF4 in sera was conducted. GPIV in inactive platelet from CML was 36080±17010 molecules/platelet as compared with 13190±4810 from the controls (P<0,01), No abnormality was found in the distribution of platelet membrane GPIb and GPIIb/III.(P>0. 05). The GPIV redistribution on active platelet membrane induced thrombin (1U/ml) from CML and healthy donors was 44320132310 and 228001 12700 molecules/platelet respectively (P<0. 01 ). The difference in the release of intracellular Q-granule TSP between CML and the control group was not found (P>0.05). There was no direct correlation between GPIV expression and TSP binding after platelet activation. The high leveIs of β-TG and PF4 in sera inhibited release of intracellular a-granule TSP in vitro. These results indicate that the abnormality of platelet membrane GPIV is a common marker in CML, therefore the specific increase of platelet GPIV in patients with CML may be a useful tool for the diagnosis and monitoring of the platelet dysfunction. The release of interna1 TSP pools is hindered by either β-TG or PF4 in sera.

Plasma membrane calcium pump regulation by metabolic stress

The plasma membrane Ca2+-ATPase(PMCA)is an ATPdriven pump that is critical for the maintenance of low resting[Ca2+]i in all eukaryotic cells.Metabolic stress, either due to inhibition of mitochondrial or glycolytic metabolism,has the capacity to cause ATP depletion and thus inhibit PMCA activity.This has potentially fatal consequences,particularly for non-excitable cells in which the PMCA is the major Ca2+efflux pathway.This is because inhibition of the PMCA inevitably leads to cytosolic Ca2+ overload and the consequent cell death.However,the relationship between metabolic stress,ATP depletion and inhibition of the PMCA is not as simple as one would have originally predicted.There is increasing evidence that metabolic stress can lead to the inhibition of PMCA activity independent of ATP or prior to substantial ATP depletion.In particular,there is evidence that the PMCA has its own glycolytic ATP supply that can fuel the PMCA in the face of impaired mitochondrial function.Moreover, membrane phospholipids,mitochondrial membrane potential,caspase/calpain cleavage and oxidative stress have all been implicated in metabolic stress-induced inhibition of the PMCA.The major focus of this review is to challenge the conventional view of ATP-dependent regulation of the PMCA and bring together some of the alternative or additional mechanisms by which metabolic stress impairs PMCA activity resulting in cytosolic Ca2+ overload and cytotoxicity.

Membrane glycoprotein M6A promotes μ-opioid receptor endocytosis and facilitates receptor sorting into the recycling pathway

The interaction of p-opioid receptor （MOPr） with the neuronal membrane glycoprotein M6a is known to facilitate MOPr endocytosis in human embryonic kidney 293 （HEK293） cells. To further study the role of M6a in the post-endocytotic sorting of MOPr, we investigated the agonist-induced co-internalization of MOPr and M6a and protein targeting after internalization in HEK293 cells that co-expressed HA-tagged MOPr and Myc-tagged M6a. ,We found that M6a, MOPr, and Rab 11, a marker for recycling endosomes, co-localized in endocytotic vesicles, indicating that MOPr and M6a are primarily targeted to recycling endosomes after endocytosis. Furthermore, co-expression of M6a augmented the post-endocytotic sorting of 6-opioid receptors into the recycling pathway, indicating that M6a might have a more general role in opioid receptor post-endocytotic sorting. The enhanced post-endocytotic sorting of MOPr into the recycling pathway was accompanied by a decrease in agonist-induced receptor down-regulation of M6a in co-expressing cells. We tested the physiological relevance of these findings in primary cultures of cortical neurons and found that co-expression of M6a markedly increased the translocation of MOPrsfrom the plasma membrane to intracellular vesicles at steady state and significantly enhanced both constitutive and agonist-induced receptor endocytosis. In conclusion, our results strongly indicate that M6a modulates MOPr endocytosis and post-endocytotic sorting and has an important role in receptor regulation.

In situ tumor vaccination with adenovirus vectors encoding measles virus fusogenic membrane proteins and cytokines

AIM： To evaluate whether intratumoral expression of measles virus fusogenic membrane glycoproteins H and F （MV-FMG）, encoded by an adenovirus vector Ad.MV-HI F, alone or in combination with local coexpression of cytokines （IL-2, IL-12, IL-18, IL-21 or GM-CSF）, can serve as a platform for inducing tumor-specific immune responses in colon cancer.METHODS： We used confocal laser scanning microscopy and flow cytometry to analyze cell-cell fusion after expression of MV-FMG by dye colocalization. In a syngeneic bilateral subcutaneous MC38 and Colon26 colon cancer model in C57BL/6 and BALB/c mice, we assessed the effect on both the directly vector-treated tumor as well as the contralateral, not directly vector- treated tumor. We assessed the induction of a tumorspecific cytotoxic T lymphocyte （CTL） response with a lactate dehydrogenase （LDH） release assay.RESULTS： We demonstrated in vitro that transduction of MC38 and Colon26 cells with Ad.MV-H/F resulted in dye colocalization, indicative of cell-cell fusion, in addition, in the syngeneic bilateral tumor model we demonstrated a significant regression of the directly vector-inoculated tumor upon intratumoral expression of MV-FMG alone or in combination with the tested cytokines. We observed the highest anti-neoplastic efficacy with MV-FMG and lL-21 coexpression. The degree of tumor regression of the not directly vector-treated tumor correlated with the anti-neoplastic response of the directly vector-treated tumor. This regression was mediated by a tumor-specific CTL response.CONCLUSION： Our data indicate that intratumoral expression of measles virus fusogenic membrane glycoproteins is a promising tool both for direct tumor treatment as well as for tumor vaccination approaches that can be further enhanced by cytokine coexpression.

Apolipoprotein E elicits targetdirected miRNA degradation to maintain neuronal integrity

Apolipoprotein E has diverse functions in neurons:Apolipoprotein E(ApoE)is a glycoprotein that primarily regulates lipid metabolism and transport in the central nervous system.There are three predominant human ApoE protein isoforms with cysteine and arginine substitutions at amino acid positions 112 and 158 that impact their lipidation and related functions(Flowers and Rebeck,2020).ApoE2 is characterized by Cys112 and Cys158,ApoE3 by Cys112 and Arg158,whereas ApoE4 contains Arg112 and Arg158.

The membrane lipid metabolism in horticultural products suffering chilling injury

Horticultural commodities suffer chilling injury following exposure to extremely low temperatures,which results in visible symptoms and considerable quality loss.Therefore,it is of significance to understand the mechanism of this physiological disorder and to develop effective strategies to control it.Chilling stress causes alteration in structure and function of the plasma membrane,which is assumed to be the primary event in response to cold stress.During this process,the membrane lipid metabolism plays a pivotal role in membrane fluidity and stability.In this review,we summarized the possible roles of membrane lipid metabolism in the development of chilling injury,having the potential for developing effective strategies to alleviate chilling injury in horticultural products under refrigerated storage in practice.

Apelin-12 improves metabolic and functional recovery of rat heart after global ischemia

This work was designed to explore efficacy of apelin-12 (A-12) as a cardioprotective agent when given before ischemia or at reperfusion using the isolated working heart model. Hearts of male Wistar rats were subjected to 30-min stabilization period followed by 35-min global ischemia and 30-min reperfusion. A short-term infusion of Krebs-Henseleit buffer (KHB) con-taining A-12 (35, 70, 140, 280 or 560 ?M) was ap-plied prior to ischemia (A-12-I) or at onset of reperfusion (A-12-R). KHB infusion was used as control. A-12 infusions induced a dose-dependent increase in recovery of coronary flow, contractile and pump function during reperfu-sion, with the largest augmentation of these indices in the A-12-I group. Both A-12 groups exhibited a significant reduction of LV diastolic pressure rise during reperfusion compared with control. Enhanced functional recovery in the A-12-I group was combined with a decrease in LDH leakage in perfusate on early reperfusion (by 36% vs. control, p < 0.05). Preischemic infusion of 140 ?M A-12 markedly increased myocardial ATP content, enhanced preservation of the total adenine nucleotide pool and improved recovery of the energy charge in reperfused hearts. There was a trend towards increase in myocardial phosphocreatine by the end of re- perfusion in the A-12-I group;however this benefit did not reach statistical significance. At the end of reperfusion, myocardial lactate and lactate/pyruvate ratio were on average 5-fold lower in A-12-I treated hearts compared with control ones and did not differ significantly from the initial values. Therefore, improved cardiac dysfunction after I/R injury and less cell mem-brane damage induced by A-12 are associated with maintaining high energy phosphates, particularly ATP, in reperfused myocardium. Changes in energy metabolism may play a role in mechanisms of cardioprotection afforded by A-12 during I/R stress.

Zinc-α2-glycoprotein 1 attenuates non-alcoholic fatty liver disease by negatively regulating tumour necrosis factor-α

BACKGROUND Zinc-α2-glycoprotein 1 (AZGP1) plays important roles in metabolism-related diseases. The underlying molecular mechanisms and therapeutic effects of AZGP1 remain unknown in non-alcoholic fatty liver disease (NAFLD). AIM To explore the effects and potential mechanism of AZGP1 on NAFLD in vivo and in vitro. METHODS The expression of AZGP1 and its effects on hepatocytes were examined in NAFLD patients, CCl4-treated mice fed a high fat diet (HFD), and human LO2 cells. RESULTS AZGP1 levels were significantly decreased in liver tissues of NAFLD patients and mice. AZGP1 knockdown was found to activate inflammation;enhance steatogenesis, including promoting lipogenesis [sterol regulatory elementbinding protein (SREBP)-1c, liver X receptor (LXR), fatty acid synthase (FAS), acetyl-CoA carboxylase (ACC), and stearoyl CoA desaturase 1 (SCD)-1], increasing lipid transport and accumulation [fatty acid transport protein (FATP), carnitine palmitoyl transferase (CPT)-1A, and adiponectin], and reducing fatty acid β-oxidation [farnesoid X receptor (FXR) and peroxisome proliferator-activated receptor (PPAR)-α];accelerate proliferation;and reverse apoptosis in LO2 cells. AZGP1 overexpression (OV-AZGP1) had the opposite effects. Furthermore, AZGP1 alleviated NAFLD by blocking TNF-α-mediated inflammation and intracellular lipid deposition, promoting proliferation, and inhibiting apoptosis in LO2 cells. Finally, treatment with OV-AZGP1 plasmid dramatically improved liver injury and eliminated liver fat in NAFLD mice. CONCLUSION AZGP1 attenuates NAFLD with regard to ameliorating inflammation, accelerating lipolysis, promoting proliferation, and reducing apoptosis by negatively regulating TNF-α. AZGP1 is suggested to be a novel promising therapeutic target for NAFLD.

Association between Metabolic Syndrome and Erythrocyte Fatty Acid Profile in Mexican Adolescents: A Trans Fatty Acid Approach

The type of fat consumed in the Mexican diet could predispose to the development of Metabolic Syndrome (MS) which has been associated with an increased risk to develop cardiovascular disease and type 2 diabetes mellitus. Our study included adolescents between 12 and 16 years of age, divided in two groups: Control Group (n = 31) and MS Group (n = 44). Waist circumference, blood pressure, fasting glucose, triglycerides, and HDL-cholesterol were determined. Erythrocytes’ fatty acids methyl esthers were quantified using gas chromatography with ionized flame detector. We identified 16 fatty acids (FA) with chain lengths from C12 to C24, with emphasis in four trans FA (TFA) isomers: vaccenic (C18:1n7t), elaidic (C18:1n9t), linoelaidic (C18:2n6t), and conjugated linoelaidic acids (C18:2n7t). MS Group had a less proportion of: myristic (C14), palmitoleic (C16:1), C18:1n7t, and linoleic acids (C18:2);and a higher one of C18:1n9t, C18:2n7t, and nervonic acids (C24:1) when compared to the control group. C24:1 and C18:1n9t had a significant positive association with MS (OR = 14.17 and OR = 12.94, respectively);whereas C14 (OR = 0.14), C18:1n7t (OR = 0.14), and C18:2 (OR = 0.22) appear to have a protective effect against the disease. The proportion of specific FAs in erythrocytes’ membranes differs between adolescents with MS and healthy controls;these FA not only showed a strong association with MS, but also correlated with most of its individual components. Interestingly, TFA displayed an antagonic behavior;while C18:1n9t had a strong association with MS, apparently C18:1n7t confers a protective effect;these results suggest that analyzing each TFA separately will constitute a more accurate approach to determine the role of TFAs in the pathogenesis of MS or other related metabolic disorders.

Effects of dehydration speed on the metabolism of membrane lipids and its relation to the browning of the Thompson seedless grape

Xinjiang is the main producing area of raisins and the largest green raisins production base in China.The browning of Thompson seedless grape raisin is extremely serious during the drying process,and has become the key issue in the development of Xinjiang raisin industry.Previous studies have shown that dehydration speed has a great impact on the browning of Thompson seedless grape,but few relevant mechanisms have been studied.Here,we demonstrate the effect of dehydration speed on lipid metabolism and its relation to the browning of the Thompson seedless grape during drying.Compared to slow dehydration treatment,rapid dehydration treatment of the Thompson seedless grape exhibited a lower degree of browning and activities of lipoxygenase(LOX),a higher index of unsaturated fatty acids and degree of unsaturated fatty acid.Moreover,the Thompson seedless grape treated with rapid dehydration resulted in a lower rate of superoxide anion production,hydrogen peroxide content,membrane permeability,and malondialdehyde content.These findings demonstrate that rapid dehydration inhibiting the browning of Thompson seedless grapes might be due to the inhibiting activities of LOX and the lower accumulation of reactive oxygen species.These activities can inhibit lipid peroxidation and slow the decomposition of unsaturated fatty acid in the membrane in Thompson seedless grapes,protecting the cellular membrane structural integrity,which may result in less contact of polyphenol oxidase with phenolic substrates and less enzymatic browning during drying.The results provide a theoretical basis for the application of rapid dehydration in drying Thompson seedless grapes.

原发与继发免疫性血小板减少症患者血小板膜糖蛋白特异性抗体及其与出血评分关系的研究

目的探讨原发与继发免疫性血小板减少症(ITP)患者抗GPⅡb/Ⅲa及GPΙb/Ⅸ抗体的表达、抗体阳性表达与出血评分的关系,以及不同抗体类型出血评分的差异,为原发与继发ITP患者的诊治和出血严重程度提供临床依据。方法选取2013年10月—2020年8月在新疆医科大学第一附属医院诊断为原发ITP患者(42例)及继发ITP患者(42例)为研究对象,所有患者入院时采用ITP出血评分量表行出血评分。应用改良MAIPA法检测患者抗GPⅡb/Ⅲa和抗GPΙb/Ⅸ抗体。结果原发与继发组患者抗GPⅡb/Ⅲa抗体、抗GPΙb/Ⅸ抗体阳性率比较,差异无统计学意义(P>0.05),原发组患者抗体表达以抗GPⅡb/Ⅲa抗体为主,继发组抗体表达以抗GPΙb/Ⅸ抗体为主,两者抗体阳性构成比较,差异有统计学意义(P<0.05)。继发组患者整体出血程度较原发组重(P<0.05)。抗体阳性表达与出血程度的关系:(1)抗GPⅡb/Ⅲa抗体阳性患者出血程度较抗体阴性患者重(P<0.05)。(2)抗GPΙb/Ⅸ抗体阳性患者出血程度较抗体阴性患者重(P<0.05),双抗体阳性患者出血程度较抗体阴性患者重(P<0.05)。结论抗GPⅡb/Ⅲa抗体、抗GPΙb/Ⅸ抗体阳性表达对原发与继发ITP无鉴别意义,但原发ITP患者抗体表达以抗GPⅡb/Ⅲa抗体为主,继发ITP患者抗体表达以抗GPΙb/Ⅸ抗体为主。继发ITP患者临床出血程度较原发ITP患者重。抗GPⅡb/Ⅲa抗体、抗GPΙb/Ⅸ抗体及抗体双阳性患者出血程度较抗体阴性患者重。

与肌少症发病相关的线粒体自噬靶点基因筛选及其在骨骼肌组织中表达观察

目的基于GEO数据库数据筛选与肌少症发病相关的线粒体自噬靶点基因,并观察其在肌少症患者骨骼肌组织中的表达变化。方法从GEO数据库检索肌少症的基因图谱数据,筛选肌少症发病的差异表达基因。从GeneCard数据库中检索并收集线粒体自噬相关基因。使用“VennDiagram”包将肌少症发病的差异表达基因与线粒体自噬相关基因取交集,得到与肌少症发病相关的线粒体自噬差异表达基因。运用基因本体论(GO)和京都基因与基因百科全书(KEGG)通路富集分析与肌少症发病相关的线粒体自噬差异表达基因的生物学功能,通过Cytoscape软件筛选与肌少症发病相关的线粒体自噬靶点基因,观察GSE136344基因表达图谱中肌少症、健康对照者骨骼肌与肌少症发病相关的线粒体自噬靶点基因表达情况。结果得到与肌少症发病相关的线粒体自噬差异表达基因99个。与肌少症发病相关的线粒体自噬差异表达基因主要涉及神经变性途径-多种疾病信号通路、帕金森疾病信号通路、朊毒体病信号通路等;主要调控能量代谢、细胞呼吸、氧化磷酸化调节等生物学过程,主要定位于线粒体内膜、线粒体内部的大分子蛋白质复合物等,参与调节跨膜转运活性等分子功能。与肌少症发病相关的线粒体自噬靶点基因有线粒体内膜蛋白基因(IMMT)、动态蛋白1样蛋白基因(DNM1L)及ATP合酶F1亚基α基因(ATP5A1)等;与正常骨骼肌组织相比,肌少症患者骨骼肌组织中IMMT、DNM1L表达低(P均<0.05)。结论与肌少症发病相关的线粒体自噬靶点基因为IMMT、DNM1L。与肌少症发病相关的线粒体自噬靶点基因可通过影响神经变性途径-多种疾病信号通路、帕金森疾病信号通路及朊毒体病信号通路等,参与调控能量代谢、细胞呼吸、氧化磷酸化调节等生物学过程,参与肌少症的发病。肌少症患者骨骼肌组织中IMMT、DNM1L低表达。

1-甲基环丙烯结合气调处理对‘帕拉英达’和‘吉禄’芒果保鲜效果的影响

为探究1-甲基环丙烯(1-Methylcyclopropene,1-MCP)结合气调处理对采后‘帕拉英达’和‘吉禄’芒果贮藏品质的影响,以元江晚熟芒果品种‘帕拉英达’和‘吉禄’为试材,分别用0.5μL/L 1-MCP、微孔膜、PBI气调保鲜袋、1-MCP+微孔膜及1-MCP+PBI气调保鲜袋对芒果进行处理,对其外观指标、失重率、硬度、可溶性固形物(TSS)含量、VC含量、可滴定酸(TA)含量、呼吸强度、商品率以及呼吸代谢相关酶活性变化进行检测分析。结果表明:在(13±1)℃贮藏过程中,与未作任何处理的对照组相比,5种处理在一定时间内均能延缓‘帕拉英达’和‘吉禄’果实黄化指数、病情指数、腐烂指数、色差、失重率、可溶性固形物含量和呼吸强度的上升,抑制果实硬度、VC含量、可滴定酸含量及商品率的下降,显著抑制果实呼吸代谢相关酶活性变化。综合分析,在(13±1)℃贮藏环境中,1-MCP+PBI气调保鲜袋处理对‘帕拉英达’和‘吉禄’芒果的保鲜效果最优,更有利于果实的贮藏。研究结果可为低纬度、高海拔地区晚熟芒果采后保鲜提供技术参考和科学依据。

茉莉酸甲酯对猕猴桃果实抗葡萄座腔菌过程中能量代谢和膜脂代谢的影响

【背景】由葡萄座腔菌(Botryosphaeria dothidea)引起的软腐病是猕猴桃果实贮藏期的重要病害,对猕猴桃产业造成了严重的经济损失。茉莉酸甲酯(MeJA)是一类广泛存在于植物体内的生物信号分子,前期研究发现MeJA能够有效诱导猕猴桃果实抵御B.dothidea的侵染。【目的】分析MeJA对果实能量代谢和膜脂代谢的影响,深入解析MeJA介导的猕猴桃果实抗病机理。【方法】以‘红阳’猕猴桃(Actinidia chinensis cv.Hongyang)为试验材料,分3组进行试验:接种组(Inoculation),果实不经过MeJA处理,但接种B.dothidea;MeJA+接种组(MeJA+inoculation),果实经过0.1 mmol·L^(-1)MeJA熏蒸处理24 h并接种B.dothidea;对照组(Control),不作任何处理,即未经MeJA处理且不接种B.dothidea。所有果实于培养箱((20±1)℃、相对湿度90%—95%)中贮藏8 d。利用2,7-二氯二氢荧光素乙酰乙酸(H2DCFDA)染色分析果实活性氧(ROS)积累情况,测定丙二醛(MDA)含量和相对电导率,分析磷脂酶D(PLD)、脂肪酶(LPS)、脂氧合酶(LOX)、琥珀酸脱氢酶(SDH)、苹果酸脱氢酶(MDH)、H^(+)-ATP酶(H+-ATPase)、Ca^(2+)-ATP酶(Ca^(2+)-ATPase)和细胞色素C氧化酶(CCO)活性及其相应基因的表达,利用高效液相色谱仪(HPLC)检测三磷酸腺苷(ATP)、二磷酸腺苷(ADP)、单磷酸腺苷(AMP)、草酰乙酸和延胡索酸的含量,并对接种组和MeJA+接种组猕猴桃果实膜脂代谢和能量代谢指标进行相关性分析。【结果】与接种组相比,MeJA处理抑制了接种B.dothidea果实中活性氧(ROS)的过量累积,减缓了膜脂过氧化程度,并有效降低了PLD、LPS和LOX活性及AcLOXs、AcPLD和AcLPS的表达,但提高了SDH、MDH、H^(+)-ATPase、Ca^(2+)-ATPase和CCO的活性及AcSDH、AcMDH、AcH^(+)-ATPase、AcCa^(2+)-ATPase和AcCCO转录水平,促进了ATP、ADP、草酰乙酸和延胡索酸的产生,延缓了果实能荷的下降,保障了果实抵御病原菌所需的能量。相关性分析表明,猕猴桃果实膜脂代谢与ROS的积累呈正相关,而与能荷呈负相关。【结论】MeJA诱导猕猴桃果实对B.dothidea的抗性与其调控果实能量水平和减缓ROS参与的膜脂代谢进程有关。

O⁃连接⁃N⁃乙酰葡糖胺糖基化蛋白质的富集方法

O-连接-N-乙酰葡糖胺(O-GlcNAc)糖基化修饰是将N-乙酰葡萄糖胺添加到细胞核和细胞质蛋白质的丝氨酸和苏氨酸残基上的一种丰富的、独特的翻译后修饰,与癌症、神经退行性病变和糖尿病等疾病密切相关。明确O-GlcNAc修饰位点是探究其在相关疾病中调控机制的前提,同时也是临床诊断和靶向干预的关键。本文介绍了近年来O-GlcNAc糖基化修饰与疾病之间的关系以及相关修饰位点的富集方法,包括抗体和凝集素、化学酶法、亲水作用液相色谱法和非天然糖代谢标记等;此外,“凹凸理论”、“定点活化”等靶向标记特定组织内蛋白质的糖基化修饰策略已成为当前研究热点,同时基于“一石多鸟”的多功能酶法标记,以及“一锅法”分析多种糖链结构等方法也将极大促进糖蛋白组学的快速发展。总之,开发更加高效、特异的糖蛋白富集策略,将对阐明包括O-GlcNAc在内的异常糖基化修饰在相关疾病中的调控机制具有重要的研究意义。