磁疗与延缓衰老(二)

衰老的免疫学说衰老的免疫学说,是衰老机制学说的重要组成部分。免疫功能衰退是人和大多数哺乳动物老化过程的重要机制。自体免疫在导致衰老的细胞老化中起决定性作用,因而从根本上参与了整个机体老化。随着年龄的增长免疫功能逐渐下降,使人体抵抗病原微生物感染能力降低,从而更加剧各组织器官老化。老年人的免疫系统衰退的特点随着年龄的增加,机体的免疫系统,如免疫器官、免疫细胞及免疫分子都会发生一系列衰退性改变。免疫器官及免疫细胞老化的特点：根据目前研究得知,就防御功能的作用而言,较低等脊椎动物（鱼类和两栖类）免疫系…     

皮肤光老化机制及抗光老化药物

皮肤光老化是紫外线作用于皮肤细胞引发的一系列功能退化性变化,涉及染色体DNA、线粒体及细胞外基质不同程度的损伤。当前已发现多种药物在光老化各阶段发挥抑制作用,包括一些维生素、植物提取物、微量元素、信号通路调节物质等。本文综述了皮肤光老化的机制与当前已经发现的抗光老化药物,提出了该领域的研究方向及前景。     

老化红细胞膜的脂质及蛋白质变化

近年来许多学者从两个方面对机体衰老的机制进行了研究:机体的衰老过程与细胞老化过程,后者是机体衰老的基础。红细胞由于直接暴露在高氧分压下,又有铁离子催化,特别易受脂质过氧化的损伤,所以成为研究细胞老化的最好材料之一。本文仅以老化红细胞为对象,研究其膜脂、膜蛋白及脂质过氧化与老化的关系。材料与方法一.老化红细胞的分离用生理盐水将40％的葡聚糖配成五种稀释度(27％、26％、25％、24％、23％),其比重     

肺脏疾病与免疫

随着免疫学理论及技术的迅速发展与广泛应用,肺脏疾病的免疫病理学问题引起了人们的注意。近十余年来对肺脏疾病中的免疫—过敏性损伤机理及免疫缺陷与肺脏疾病的关系等问题作了广泛研究,取得了一些成就。肺脏的免疫防御机能肺脏是机体与外界直接接触的器官,空气中各种抗原性物质与非抗原性物质均可入肺;来自右心的血液几乎全部经肺过滤,因此,肺脏是易受侵袭的器官;然而它有强大的免疫与非免疫性防御机能使其免受侵害。     

免疫系统如何被激活和调节?——2011年诺贝尔医学奖的研究成果

我们生活在充满病原微生物的世界里,时时刻刻都会受到各种病原体的侵害,尤其是在消化道(包括口腔和肠道)和呼吸道,我们的机体一直在检查侵入的病原微生物并与之战斗。负责这一生理功能的就是我们机体的免疫系统,它能发现病原体的侵入并调动机体的防御和清除能力,与侵入的病原体进行战斗,就像一个国家的公检法机构和国防部,承担     

紫外线照射下小鼠T细胞CD4和CD8的表达

紫外线对机体健康的影响主要有物理性损伤 ,如引起皮肤表面的红肿 ,疼痛 ,出现水泡 ,产生皱褶 ,并出现色素沉着 ,皮肤老化等现象。严重者由于紫外线对机体的光毒性作用 ,皮肤内的各种色素集团在吸收光线的同时产生大量的氧自由基 ,进而造成ＤＮＡ分子的损伤 ,引起基因突变、癌化 ,直至细胞死亡。近年来有研究报道 ,通过紫外线照射 ,抑制机体的细胞免疫机能 ,降低接触性迟发型超敏反应 ,甚至由于抑制Ｔ细胞而出现对特异性半抗原无免疫反应状态 ,但同时也使机体对细菌、寄生虫等的侵袭易感。为进一步探讨紫外线照射对机体免疫防御机能的影响 ,…     

糖尿病病人伤口为什么不容易愈合

北京市第22中学的生物学教师陈珊问:糖尿病病人伤口为什么不容易愈合? 答:损伤修复是生命个体必备的自我防御保护功能,在各种层次和水平均具备损伤修复能力.如在分子水平上,DNA分子的损伤与修复;在亚细胞器水平上线粒体的损伤与修复;以及在细胞水平上进行的损伤与修复.损伤修复的组织学基础是,机体组织的许多类型的细胞都具有再生能力.     

羰基毒害在糖尿病晚期并发症中的作用

动物机体组织的氧化紧张损伤和老化交联是糖尿病晚期并发症中神经病变、动脉粥样硬化、风湿性关节炎、肾病变、白内障等老化慢性疾病的共同特征.对氧化紧张到底是糖尿病晚期并发症的初始原因还是糖尿病组织衰变的次级诱因提出了探讨.结果表明糖尿病患者机体和血浆中的糖氧化产物及脂类过氧化物的增多表明病患者体内氧化紧张的加强;然而,它们中的某些产物与氧化紧张并不相关;此外,其它一些氧化紧张的直接指标,如氨基酸的氧化,在糖尿病患者的皮肤胶原中也并没有增多.因此,对于糖尿病患者中蛋白质化学修饰的现象,用活性羰基的毒化超过其系统解毒能力的观点来解释更合适.这种在氧化或非氧化反应中形成的不饱和羰基化合物在体内总是以相对恒定的浓度存在,因而在糖尿病中,由羰基毒害引起组织中糖类和脂类衍生物的增长可以被认为是生物化学动力学的一种必然结果.     

抗菌肽的研究现状和挑战

抗菌肽(AMPs)广泛存在于生物体内,可以协助机体抵御外源微生物的侵害,是生物体先天性防御系统中的重要组成成分。普遍认为,抗菌肽通过膜损伤机制,破坏微生物细胞膜或细胞壁的完整性,达到抑杀微生物的目的。然而,越来越多的证据表明抗菌肽还存在非膜损伤机制,作用于胞内靶位点杀伤细胞。由于其独特的作用机制及广谱抗菌活性,抗菌肽被应用于各行各业。但是,抗菌肽的推广应用也面临着诸多难题,如生物稳定性、抗菌活性的维持和微生物耐受性等。主要对抗菌肽的种类、作用机制、微生物对抗菌肽耐受性的产生机制及抗菌肽的应用和挑战进行综述。     

皮肤光老化的光学评价与治疗技术研究进展

皮肤光老化是一个极其复杂的渐进过程,不仅有临床及组织学方面变化,还有生物化学方面变化。无损、非侵入式的皮肤光老化评价技术和组织热损伤定量技术促进了光学治疗技术的发展,有助于优化选择非消融性光治疗参数。评述了基于光学方法的皮肤光老化评价和治疗技术研究进展。     

Hydroxytyrosol from olive fruits prevents blue-light-induced damage in human keratinocytes and fibroblasts

Skin aging is a complex biological process influenced by a combination of endogenous or intrinsic and exogenous or extrinsic factors due to environmental damage. The primary environmental factor that causes human skin aging is the ultraviolet irradiation from the sun. Recently, it was established that the long-term exposure to light-emitting-diode-generated blue light (LED-BL) from electronic devices seems to have a relevant implication in the molecular mechanisms of premature photoaging. BL irradiation induces changes in the synthesis of various skin structures through DNA damage and overproduction of reactive oxygen species (ROS), matrix metalloproteinase-1 and -12, which are responsible for the loss of the main components of the extracellular matrix of skin like collagen type I and elastin. In the current study, using human keratinocytes and fibroblasts exposed to specific LED-BL radiation doses (45 and 15 J/cm ²), we produced an in vitro model of skin photoaging. We verified that, compared with untreated controls, the treatment with LED-BL irradiation results in the alteration of metalloprotease-1 (collagenase), metalloprotease-12 (elastase), 8-dihydroxy-2′-deoxyguanosine, proliferating cell nuclear antigen, and collagen type I. Moreover, we showed that the photoaging prevention is possible via the use of hydroxytyrosol extracted from olive fruits, well known for antioxidant properties. Our results demonstrated that hydroxytyrosol protects keratinocytes and fibroblasts from LED-BL-induced damage. Thus, hydroxytyrosol might be proposed as an encouraging candidate for the prevention of BL-induced premature photoaging.     

Photoprotective and anti-skin-aging effects of eicosapentaenoic acid in human skin in vivo

Skin aging can be attributed to photoaging (extrinsic) and chronological (intrinsic) aging. Photoaging and intrinsic aging are induced by damage to human skin attributable to repeated exposure to ultraviolet (UV) irradiation and to the passage of time, respectively. In our previous report, eicosapentaenoic acid (EPA) was found to inhibit UV-induced matrix metalloproteinase-1 (MMP-1) expression in human dermal fibroblasts. Therefore, we investigated the effects of EPA on UV-induced skin damage and intrinsic aging by applying EPA topically to young and aged human skin, respectively. By immunohistochemical analysis and Western blotting, we found that topical application of EPA reduced UV-induced epidermal thickening and inhibited collagen decrease induced by UV light. It was also found that EPA attenuated UV-induced MMP-1 and MMP-9 expression by inhibiting UV-induced c-Jun phosphorylation, which is closely related to UV-induced activator protein-1 activation, and by inhibiting JNK and p38 activation. EPA also inhibited UV-induced cyclooxygenase-2 (COX-2) expression without altering COX-1 expression. Moreover, it was found that EPA increased collagen and elastic fibers (tropoelastin and fibrillin-1) expression by increasing transformin growth factor-beta expression in aged human skin. Together, these results demonstrate that topical EPA has potential as an anti-skin-aging agent.     

Ultraviolet radiation exposure accelerates the accumulation of the aging-dependent T414G mitochondrial DNA mutation in human skin

The accumulation of mitochondrial DNA (mtDNA) mutations has been proposed as an underlying cause of the aging process. Such mutations are thought to be generated principally through mechanisms involving oxidative stress. Skin is frequently exposed to a potent mutagen in the form of ultraviolet (UV) radiation and mtDNA deletion mutations have previously been shown to accumulate with photoaging. Here we report that the age-related T414G point mutation originally identified in skin fibroblasts from donors over 65 years also accumulates with age in skin tissue. Moreover, there is a significantly greater incidence of this mutation in skin from sun-exposed sites (chi(2)= 6.8, P < 0.01). Identification and quantification of the T414G mutation in dermal skin tissue from 108 donors ranging from 8 to 97 years demonstrated both increased occurrence with photoaging as well as an increase in the proportion of molecules affected. In addition, we have discovered frequent genetic linkage between a common photoaging-associated mtDNA deletion and the T414G mutation. This linkage indicates that mtDNA mutations such as these are unlikely to be distributed equally across the mtDNA population within the skin tissue, increasing their likelihood of exerting focal effects at the cellular level. Taken together, these data significantly contribute to our understanding of the DNA damaging effects of UV exposure and how resultant mutations may ultimately contribute towards premature aging.     

UV irradiation increases ROS production via PKCdelta signaling in primary murine fibroblasts

Ultraviolet (UV) irradiation is a major environmental factor responsible for a high incidence of premature skin aging, referred to as photoaging, as well as skin cancer and melanoma. UVA irradiation represents 90% of the solar UV light reaching the earth's surface, and yet the mechanisms by which it exerts its biological effects are not clear. UVA penetrates into the skin tissue, reaching the basal layers of the active dividing cells and, therefore, the contribution of UVA to skin damage may be significant. The majority of UVA energy is absorbed by unidentified photosensitizers in the cells which are postulated to generate reactive oxygen species (ROS). It has been believed that both chronological aging and photoaging share the same molecular features and, as such, it is very common to utilize UV irradiation for induction of skin aging. To determine the involvement of protein kinase isoforms in chronological aging and photoaging, we utilized in vitro aging model systems of primary murine fibroblasts and primary fibroblasts isolated from PKC null mice. We show for the first time distinct involvement of PKC isoforms PKCdelta and PKCalpha in photoaging versus cellular senescence. While chronological aging is accompanied by overexpression and activation of PKCalpha, UV irradiation and ROS production are associated with photoaging accompanied by PKCdelta downregulation and nuclear translocation.     

Aging‐like skin changes in metabolic syndrome model mice are mediated by mineralocorticoid receptor signaling

Aging is accelerated, at least in part, by pathological condition such as metabolic syndrome (MetS), and various molecular pathways such as oxidative stress are common mediators of aging and MetS. We previously developed the aging‐like skin model by single ultraviolet (UV) irradiation on the MetS model mice. Recent studies revealed that mineralocorticoid receptor (MR) signaling plays a pivotal role for various tissue inflammation and damages in MetS. Although previous studies reported that MR is expressed in the skin and that overexpression of MR in the skin resulted in the skin atrophy, the physiological or pathological functions of MR in the skin are not fully elucidated. Here, we show the involvement of MR signaling in the aging‐like skin changes in our own model. Elevations of oxidative stress and inflammation markers were observed in the MetS mice, and the UV‐evoked aging‐like skin damages were attenuated by topical antioxidant. MR expression was higher in the MetS mouse skin, and notably, expression of its effecter gene Sgk1 was significantly upregulated in the aging‐like skin in the UV‐irradiated MetS mice. Furthermore, topical application of MR antagonist spironolactone suppressed Sgk1 expression, oxidative stress, inflammation, and the aging‐like changes in the skin. The 2‐week UV onto the non‐MetS mice, the more usual photoaging model, resulted in the skin damages mostly equivalent to the MetS mice with single UV, but they were not associated with upregulation of MR signaling. Our studies suggested an unexpected role of MR signaling in the skin aging in MetS status.     

功能性益生乳酸菌的研究进展

益生菌的效果已被认识和探究了超过一个世纪,有关益生菌的功效以及它们与宿主之间的相互关系已逐渐为世人所知,越来越多的益生机制得到了验证。虽然现在有足够的临床证据支持益生菌的某些健康宣称,然而,我们还需要进行大量的工作来证实其功能性作用,如提供必需营养因子,保护肠道和心血管健康,甚至预防神经系统退行性衰老。本文综述了几种典型的益生菌功能特性,为更好的将益生菌应用于人体提供理论参考。     

益生菌-水凝胶递送系统的研究进展及应用潜力

益生菌是能够改善人体胃肠道、皮肤、阴道和口腔四大微生态系统的微生物群,常借由递送系统到达靶点以用于预防和治疗目的.水凝胶是最常见的递送系统载体,最近的研究针对水凝胶材料的改良主要可分为基质结构、填充物和外部涂层3个方面,新型水凝胶能够更好地帮助益生菌适应加工、储存环境及人体内微环境.人体不同微环境下益生菌对递送载体具有...     

Protective effects of silkworm hemolymph extract and its fractions on UV-induced photoaging

Ultraviolet (UV) irradiation induces skin photoaging by generating reactive oxygen species (ROS). ROS caused by UV-irradiation results in loss of skin cells and degradation of extracellular matrix. A number of antioxidants have been chemically synthesized or naturally extracted to prevent ROS-mediated skin photoaging. In our previous work, silkworm hemolymph extract (SHEX) was prepared, and its antioxidant activity was tested by free radical-scavenging assay. This study assessed the protective effects of SHEX on UV-induced photoaging of human immortalized keratinocytes (HaCaT). UVA (365 nm)-induced ROS generation was inhibited by supplementation of silkworm hemolymph (SH). Treatment with SHEX prepared by boiling SH inhibited death of HaCaT cells caused by UVB (315 nm) and UVA irradiation in a dose-dependent manner. Seven fractions were obtained by separating SHEX by gel permeation chromatography and the antioxidant activity of the fractions was examined. The fraction showing the highest protective efficacy on UV-induced cell damage corresponded to the lutein-containing fraction isolated in our previous study. Moreover, the SHEX fraction suppressed the expression of MMP-1 (matrix metalloproteinase-1), a matrix-degrading enzyme, suggesting that the active constituent of SHEX has the potential to inhibit skin photoaging. These results suggest that SHEX can be developed as a dietary and cosmetic supplement for prevention of skin photoaging.     

Orally administered collagen peptide protects against UVB-induced skin aging through the absorption of dipeptide forms,Gly-Pro and Pro-Hyp

Collagen hydrolysate is a well-known nutritional supplement for the improvement of healthy skin. Here, collagen peptide NS (CPNS) from fish scale was prepared, and its physicochemical properties were investigated. Gly-Pro was revealed as a representative low molecular weight peptide of CPNS, by performing prep-HPLC and LC-MS/MS. CPNS treatment attenuated matrix metalloproteinase-1 production and increased the synthesis of type 1 procollagen in HDF cells. After orally administering CPNS to rats, the plasma concentrations of Gly-Pro and Pro-Hyp increased dramatically. To examine the protective effects of CPNS against ultraviolet B (UVB)-induced photoaging in vivo, the dorsal skins of hairless mice were exposed to UVB and supplemented with CPNS for 12 weeks. The CPNS consumption significantly attenuated UVB-induced wrinkle formation, transepidermal water loss, and epidermis thickness, and increased skin hydration. Collectively, these results suggest that bioactive peptides of CPNS, Gly-Pro and Pro-Hyp, exert beneficial effects on skin health.     

Mexoryl: a review of an ultraviolet a filter

It is widely known that ultraviolet light causes skin damage and melanoma. Different wavelengths of ultraviolet light penetrate the skin at different depths, causing varying levels of damage. Higher wavelengths tend to penetrate deeper and, consequently, are thought to induce a myriad of skin conditions, thereby playing a significant role in the photoaging process. Sunscreens containing the ultraviolet A blocker Mexoryl are important in impeding ultraviolet A light, potentially reducing many of the characteristics of skin aging and preventing biochemical changes that can lead to nonmelanoma carcinoma. Until now, sunscreen products sold in the United States focused on blocking ultraviolet B light. Those that did provide ultraviolet A filtering contained physical blocks (zinc oxide or titanium dioxide) or the chemical block Parsol 1789 (avobenzone). These broad-spectrum sunscreens have limitations, such as degradation under ultraviolet exposure, that resulted in decreased effectiveness. Mexoryl, a novel ultraviolet A filter, provides efficient ultraviolet A coverage, better photostability, and enhanced water resistance. Sunscreens containing Mexoryl are widely used in Europe and Canada. It was not until July 24, 2006, that the U.S. Food and Drug Association approved the compound.