Anti-aging performance improvement and enhanced combustion efficiency of boron via the coating of PDA

Boron is an ambitious fuel in energetic materials since its high heat release values,but its application is prohibited by low combustion efficiency and oxidization during storage.The polydopamine(PDA)was introduced into boron particles,investigating the impact of PDA content on the energetic behavior of boron.The results indicated that the PDA coating formed a fishing net structure on the surface of boron particles.The heat release results showed that the combustion calorific value of B@PDA was higher than that of the raw boron.Specifically,the actual combustion heat of boron powder in B@10%PDA increased by 38.08%.Meanwhile,the DSC peak temperature decreased by 100.65℃under similar oxidation rate compared to raw boron.Simultaneously,the B@PDA@AP and B@AP composites were prepared,and their combustion properties were evaluated.It was demonstrated that B@10%PDA@AP exhibited superior performance in terms of peak pressure and burning time,respectively.The peak pressure is 12.43 kPa more than B@AP and burning time is 2.22 times higher than B@AP.Therefore,the coating of PDA effectively inhibits the oxidization of boron during storage and enhances the energetic behavior of boron and corresponding composites.

Salidroside Ameliorates Lung Injury Induced by PM_(2.5) by Regulating SIRT1-PGC-1αin Mice

Objective This study aimed to clarify the intervention effect of salidroside(SAL)on lung injury caused by PM_(2.5) in mice and illuminate the function of SIRT1-PGC-1ɑaxis.Methods Specific pathogen-free(SPF)grade male C57BL/6 mice were randomly assigned to the following groups:control group,SAL group,PM_(2.5) group,SAL+PM_(2.5) group.On the first day,SAL was given by gavage,and on the second day,PM_(2.5) suspension was given by intratracheal instillation.The whole experiment consist of a total of 10 cycles,lasting 20 days.At the end of treatment,blood samples and lung tissues were collected and analyzed.Observation of pathological changes in lung tissue using inverted microscopy and transmission electron microscopy.The expression of inflammatory,antioxidants,apoptosis,and SIRT1-PGC-1ɑproteins were detected by Western blotting.Results Exposure to PM_(2.5) leads to obvious morphological and pathologica changes in the lung of mice.PM_(2.5) caused a decline in levels of antioxidant-related enzymes and protein expressions of HO-1,Nrf2,SOD2,SIRT1 and PGC-1ɑ,and an increase in the protein expressions of IL-6,IL-1β,Bax,caspase-9 and cleaved caspase-3.However,SAL reversed the aforementioned changes caused by PM_(2.5) by activating the SIRT1-PGC-1α pathway.Conclusion SAL can activate SIRT1-PGC-1ɑ to ameliorate PM2.5-induced lung injury.

In vivo anti-aging properties on fat diet-induced high fat Drosophila melanogaster of n-butanol extract from Paecilomyces hepiali

The purpose of this study was to explore the potential of the development and application of Paecilomyces hepiali,a fungus with edible and medicinal value,as a foodborne antioxidant and anti-aging agent.Its n-butanol extract(PHE)from rice cultures was selected for anti-aging experiment because of significant free radical scavenging activity in vitro.In vivo,PHE could significantly prolong the mean lifespan,50%survival days,and the maximum lifespan of Drosophila on a high-fat diet.It is amazing that the mean lifespan increased from 19.1 days to 32.9 days,50%survival days increased from 15.7 days to 34.3 days,and the maximum lifespan extended from 44.7 days to 52.7 days,when the high-fat female Drosophila model was fed with 10μg/mL PHE.Further research showed that PHE reduced the accumulation of peroxide products and increased the activity of antioxidant enzymes.Then,through antioxidant activity tracking,dimerumic acid(compound 1,the IC_(50) value of 3.4μg/mL on DPPH free radicals scavenging activity),4,5-dihydroxy-3-methoxypentanoic acid(compound 2,new compound),and thymidine(compound 3)were isolated from PHE.It is worth mentioning that dimerumic acid,the major antioxidant compound of PHE(content up to 3%),was discovered in P.hepiali for the first time.It was concluded that PHE showed excellent anti-aging activity at a very low concentration on fat diet-induced high fat Drosophila melanogaster,and dimerumic acid may be its main material basis.These results indicated that PHE had the potential to be developed as antioxidant and anti-aging agent in the healthcare industry.

Exploring the anti-aging effects of chlorogenic acid and the underlying mechanisms based on a Caenorhabditis elegans model

Objective:To explore the anti-aging effects of chlorogenic acid(CGA)and the underlying mechanisms based on a Caenorhabditis elegans(C.elegans)model.Methods:The anti-agingactivityofCGAwasstudied basedon thebodylength,exercisebehavior,lipofuscin content,antioxidative stress ability,swallowing frequency,body-bending frequency,and head-swinging ability of C.elegans.Through DAF-16 nuclear translocation and SOD-3-GFP fluorescence experiments,the effects of CGA on ROS levels,antioxidant enzyme activities,MDA content,mutant-strain lifespan,and anti-aging molecular signaling pathways were explored,as well as the underlying mechanisms.Results:CGA improved multiple indices of the nematode:body length was increased(all P<0.001),head-swing frequency and body-bending frequency were increased(all P<0.05),nematode longevity was prolonged(P=0.0021),lipofuscin deposition in nematodes was slowed down(all P<0.001),the chemotaxis index was improved(P=0.0012),ROS levels were reduced(all P<.001),and SOD activity and MDA content were reduced(SOD:P=0.0017 between the low-concentration group and the control group,P<.001 between the high-concentration and medium-concentration groups and the control group;MDA:P=0.0135 between the low-concentration group and the control group,and P<0.001 between the high-concentration and medium-concentration groups and the control group).In addition,CGA also activated the DAF-16 transcription factor,promoted DAF-16 nuclear translocation under oxidative stress conditions(both P<0.001 between the high-concentration and medium-concentration groups and the control group),and increased SOD-3 gene expression in nematodes(all P<0.001).Conclusion:CGA plays an anti-aging role in C.elegans.The underlying mechanisms include activation of the insulin/IGF-1 signaling pathway and enhancement of DAF-16 activity.This study lays a foundation for further research into the anti-aging effects of CGA.

Salidroside attenuates oxygen and glucose deprivation-induced neuronal injury by inhibiting ferroptosis

Objective: To evaluate the effect of salidroside on oxygen and glucose deprivation(OGD)-treated NT2 cells and its underlying mechanisms of action.Methods: Retinoic acid was used to induce the differentiation of NT2 cells into neurons. The effects of salidroside on survival, apoptosis, inflammatory response, and oxidative stress of neurons undergoing OGD were evaluated. Using precursor cells as controls, the effect of salidroside on the differentiation progression of OGDtreated cells was evaluated. In addition, the effect of erastin, a ferroptosis inducer, on NT2 cells was examined to investigate the underlying mechanisms of neuroprotective action of salidroside.Results: Salidroside alleviated the effects of OGD on neuronal survival, apoptosis, inflammation, and oxidative stress, and promoted NT2 cell differentiation. Moreover, salidroside prevented ferroptosis of OGD-treated cells, which was abolished following erastin treatment, indicating that ferroptosis mediated the regulatory pathway of salidroside.Conclusions: Salidroside attenuates OGD-induced neuronal injury by inhibiting ferroptosis and promotes neuronal differentiation.

Genetic Cell Therapy in Anti-Aging Regenerative Cosmetology

As post-WWII baby boomer approaching age 80, Anti-Aging Regenerative Cosmetology (AARC) has been developed and patented for beautifying and strengthening the human body using live cells;to enhance the appearance and function of various bodily parts to provide health and aestheticism of human being throughout life. It is a combined cosmetic and preventive medicine to intervene with and to correct the undesirable phenotypic expression of aging. The intrinsic properties of myoblasts and foreskin fibroblasts in development and regeneration are harnessed to formulate a genetic cell therapy program which is safe and efficacious as previously been tested in FDA Phase III clinical trials. Myoblasts are selected for strength development and foreskin fibroblasts for tenacity and smooth-to-the-touch. Both cell types are highly mitotic and non-carcinogenic. In additional to providing large quantities of nuclei as regenerative gene medicine, and of mitochondria as energy generators, myoblasts secret tumor necrosis factor alpha (TNF-α) for skin whitening and melanoma prevention. Myoblasts, because of their small size, spindle shape, and resilience, grow readily on collagen and laminin within wrinkles of skin surfaces, thus enhancing the color, luster, and texture of the skin “plated” with them. Alternatively, they can be injected subcutaneously as cell filler to reduce wrinkles. Intramuscular injection of myoblasts can augment the size, shape, consistency, tone, and strength of muscle groups, improving the lines, contours, and vitality to sculpt a youthful appearance. By improving cell genetics and organ functions, the program holds promise to sustain the human subject in good health and appearance, with a good quality of life and life prolongation.

Protective Role of Salidroside against Aging in A Mouse Model Induced by D-galactose

Objective To investigate the protective effects of putative AGEs （advanced glycation endproducts） inhibitor salidroside against aging in an accelerated mouse aging model induced by D-galactose. Methods A group of 5-month-old C57BL/6J mice were treated daily with D-galactose, D-galactose combined with salidroside, salidroside alone, and control buffer for 8 weeks. At the end of the treatment, serum AGEs levels, neurological activities, expression of glial fibrillary acidic protein （GFAP） and neurotrophin-3 （NT-3） in the cerebral cortex, as well as lymphocyte proliferation and IL-2 production were determined. Results D-galactose induced mouse aging model was developed as described before. As expected, salidroside blocked D-galactose induced increase of serum AGEs levels. It also reversed D-galactose induced aging effects in neural and immune system, as evidenced by improving motor activity, increasing memory latency time, and enhancing lymphocyte mitogenesis and interleukin-2 （IL-2） production. Furthermore, elevated expression of GFAP and NT-3 in the aged model mice was also reduced upon salidroside treatment. Conclusion Salidroside inhibits AGEs formation in vivo, which at least partially contributes to its anti-aging effect in D-galactose induced aging model.

Effects of salidroside on glioma formation and growth inhibition together with improvement of tumor microenvironment

Objective：To test the effects of salidroside on formation and growth of glioma together with tumor microenvironment.Methods：Salidroside extracted from Rhodiola rosea was purified and treated on human glioma cells U251 at the concentration of 20 μg/mL.3-（4,5-dimethylthiazol-2-yl）-2,5-dephenyltetrazolium bromide （MTT） assay for cytotoxicity and flow cytometry （FCM） for cell cycle analysis were performed.Then for in vivo study,xenotransplantation tumor model in nude mice was generated and treated with salidroside at the concentration of 50 mg/kg.d for totally 20 d.Body weight and tumor size were detected every 2 d after the treatment.The levels of 8-isoprostane,superoxide dismutase （SOD） and malondialdehyde （MDA）,special markers for oxidative stress,were detected while immunofluoresence staining was performed for astrocyte detection.Results：For in vitro study,salidroside could decrease the viability of human glioma cells U251 and the growth of U251 cells at G0/G1 checkpoint during the cell cycle.For in vivo study,salidroside could also inhibit the growth of human glioma tissue in nude mice.The body weight of these nude mice treated with salidroside did not decrease as quickly as control group.In the tumor xenotransplantation nude mice model,mice were found of inhibition of oxidative stress by detection of biomarkers.Furthermore,overgrowth of astrocytes due to the stimulation of oxidative stress in the cortex of brain was inhibited after the treatment of salidroside.Conclusions：Salidroside could inhibit the formation and growth of glioma both in vivo and in vitro and improve the tumor microenvironment via inhibition of oxidative stress and astrocytes.

Salidroside Attenuates LPS-stimulated Activation of THP-1 Cell-derived Macrophages through Down-regulation of MAPK/NF-kB Signaling Pathways

Summary： Excessive activation of macrophages is implicated in various inflammatory injuries. Salidroside （Sal）, one of the main bioactive components ofRhodiola Sachalinensis, has been reported to possess anti-inflammatory activities. This study aimed to examine the effect of Sal on the activa- tion of macrophages and the possible mechanism. The lipopolysaccharide （LPS）-stimulated phrobol 12-myristate 13-acetate （PMA）-differentiated THP-1 macrophage models were established. The changes in the inflammatory profiles of THP-l-derived macrophages were determined. The results showed that Sal significantly decreased the expression of inducible nitric oxide synthase （iNOS）, cyclooxygenase-2 （COX2）, interleukin-lbeta （IL-1β）, interleukin-6 （IL-6） and tumor necrosis fac- tor-or （TNF-a） at both mRNA and protein levels in THP-l-derived macrophages, and the effect was dose-depedent. Moreover, NF-B activation was significantly suppressed and the phosphorylation of ERK, p38 and JNK was substantially down-regulated after Sal treatment. The findings suggested that Sal can suppress the activation of LPS-stimulated PMA-differetiated THP-1 cells, as evidenced by the decreased expression of iNOS, COX2, IL-1β, IL-6 and TNF-a, and the mechanism involves the inhibition of NF-r,B activation and the phosphorylation of the MAPK signal pathway.

LC-MS determination and pharmacokinetic study of salidroside in rat plasma after oral administration of suspensions of traditional Chinese medicine Erzhi Wan and Fructus Ligustri lucidi

A simple,rapid and sensitive liquid chromatography-mass spectrometry（LC-MS）method was developed for the determination of salidroside in rat plasma and study of its pharmacokinetics after oral administration of suspension of Erzhi Wan and Fructus Ligustri lucidi into Wistar rats.Plasma sample of 200 μL was extracted with acetic ether-isopropanol（2∶1）and the extraction was performed on a Kromasil C18 column（150 mm×4.6 mm,5 μm）with the mobile phase of methanol-water（41∶59,v/v）within a run time of 6.0 min.The analyte was monitored with positive electrospray ionization（ESI）by selected ion monitoring（SIM）mode.The target ions were m/z 323.05 for salidroside and m/z 411.05 for internal standard（IS）geniposide.A good linear relationship was obtained over the range of 5.0-500.0 ng/mL and the lower limit of quantification was 5.0 ng/mL.The validated method was successfully applied to the pharmacokinetic study of salidroside in rat plasma after oral administration of suspension of Erzhi Wan and Fructus Ligustri lucidi.

Neuroprotective effects of salidroside on focal cerebral ischemia/reperfusion injury involve the nuclear erythroid 2-related factor 2 pathway

Salidroside,the main active ingredient extracted from Rhodiola crenulata,has been shown to be neuroprotective in ischemic cerebral injury,but the underlying mechanism for this neuroprotection is poorly understood.In the current study,the neuroprotective effect of salidroside on cerebral ischemia-induced oxidative stress and the role of the nuclear factor erythroid 2-related factor 2（Nrf2）pathway was investigated in a rat model of middle cerebral artery occlusion.Salidroside（30 mg/kg）reduced infarct size,improved neurological function and histological changes,increased activity of superoxide dismutase and glutathione-S-transferase,and reduced malon-dialdehyde levels after cerebral ischemia and reperfusion.Furthermore,salidroside apparently increased Nrf2 and heme oxygenase-1 expression.These results suggest that salidroside exerts its neuroprotective effect against cerebral ischemia through anti-oxidant mechanisms and that activation of the Nrf2 pathway is involved.The Nrf2/antioxidant response element pathway may become a new therapeutic target for the treatment of ischemic stroke.

Current Perspective in the Discovery of Anti-aging Agents from Natural Products

Aging is a process characterized by accumulating degenerative damages,resulting in the death of an organism ultimately.The main goal of aging research is to develop therapies that delay age-related diseases in human.Since signaling pathways in aging of Caenorhabditis elegans(C.elegans),fruit flies and mice are evolutionarily conserved,compounds extending lifespan of them by intervening pathways of aging may be useful in treating age-related diseases in human.Natural products have special resource advantage and with few side effect.Recently,many compounds or extracts from natural products slowing aging and extending lifespan have been reported.Here we summarized these compounds or extracts and their mechanisms in increasing longevity of C.elegans or other species,and the prospect in developing antiaging medicine from natural products.

Approaches to biosynthesis of salidroside and its key metabolic enzymes

As a main component of efficiency in Rhodiola plants, salidroside is a promising environmental acclamation medicine and possesses specific medical properties against symptoms of fatigue, old age, microwave radiation, viral infections and tumors. Salidroside plays important roles, especially in military, aerospace, sport and healthcare medicine and has, therefore, recently, drawn more and closer attention. This article probes mainly into the probable biosynthetic pathway of salidroside following a brief introduction of the exploitation and utilization values of Rhodiola plants and the current condition of its natural resources. We have come to the conclusion that tyrosol, the aglycon of salidroside, is biosynthesized through the well-characterized shikimic acid pathway. A molecule of glucose is transferred by the UDP-glucosyltransferase （or possibly by the β-D-glucosidase too） to the tyrosol to form salidroside. On the other hand, salidroside may be degraded into tyrosol and glucose by β-D-glucosidase. Progress in research of these two key-enzymes, involved in the metabolism of salidroside, is finally elaborated.

Salidroside Inhibits Lipopolysaccharide-ethanol-induced Activation of Proinflammatory Macrophages via Notch Signaling Pathway

Activation of macrophages is a key event for the pathogenesis of various inflammatory diseases.Notch signaling pathway recently has been found to be a critical pathway in the activation of proinflammatory macrophages.Salidroside (Sal),one of main bioactive components in Rhodiola crenulata (Hook.F.et Thoms) H.ohba,reportedly possesses anti-inflammatory activity and ameliorates inflammation in alcohol-induced hepatic injury.However,whether Sal regulates the activation of proinflammatory macrophages through Notch signaling pathway remains unknown.The present study investigated the effects of Sal on macrophage activation and its possible mechanisms by using both alcohol and lipopolysaccharide (LPS) to mimic the microenvironment of alcoholic liver.Detection of THP-1-derived macrophages exhibited that Sal could significantly decrease the expression of tumor necrosis factor-α(TNF-α),interleukinbeta (IL-1β)and IL-6 in the macrophages at both mRNA and protein levels.Furthermore,Sal significantly suppressed NF-kB activation via Notch-Hes signaling pathway in a dose-dependent manner.Moreover,in the microenvironment of alcoholic liver,the expression of Notch-dependent pyruvate dehydrogenase phosphatase 1 (PDP1) was elevated,and that of Ml gene expression [inducible NO synthase (NOS2)] was up-regulated.These changes could all be effectively ameliorated by Sal.The aforementioned findings demonstrated that Sal could inhibit LPS-ethanol-induced activation of proinflammatory macrophages via Notch signaling pathway.

Anti-fatigue effects of salidroside in mice

目的将在老鼠学习 salidroside 的反疲劳效果。完全， 120 个正常男 Kunming 鼠标基于身体重量被使随机化进 5 个组(4 个 salidroside 干预组和控制组) 的方法。控制组被给提取的水和组们被给 salidroside 的各种各样的剂量的 4 干预(60， 180， 360， 720 mg/kg ) 为 15 连续的天分别地。层次喂奶，浆液脲氮，肌肉和肝肝糖，最长的游泳时间和血红素在游泳前后被决定测试。结果 salidroside 的不同剂量显著地变长游泳时间并且当减少的时，增加了血红素和肌肉和肝肝糖的内容与控制组相比显著地在血喂奶，特别在 180 mg/kg salidroside 组。结论 Salidroside 在老鼠上有显著反疲劳效果。这些效果是剂量依赖者，并且大多数 biomarkers 上的最强壮的效果与中间的剂量被看见。

Salidroside improves endothelial function and alleviates atherosclerosis by activating a mitochondria-related AMPK/PI3K/Akt/eNOS pathway

Aim Salidroside （SAL） is a phenylpropanoid glycoside isolated from the medicinal plant Rhodiola rosea. A recent study has reported that SAL can efficiently decrease atherosclerotic plaque formation in low-density lipoprotein receptor - deficient mice. This study was to investigate the molecular mechanism of antiatherogenic effects of SAL. Method Six-week old apoE-/- male mice were fed a high-fat diet for 8 weeks and then were ad- ministered with SAL for another 8 weeks. Atherosclerotic lesion and vascular function were analyzed. Primary cul- tured human umbilical vein endothelial cells （HUVECs） were prepared. Superoxide anion （O2^-）, NO produc- tion, mitochondrial membrane potential （△ψm） and intracellular ATP and AMP levels were measured. Expression of eNOS and AMPK were analyzed by Western blot. Result SAL significantly improved endothelial function asso- ciated with increasing eNOS activation thus reduced the atherosclerotic lesion area. SAL increased eNOS-Serl177 phosphorylation and decreased eNOS-Thr495 phosphorylation. SAL significantly activated AMP-activated protein ki- nase （AMPK）. Both AMPK inhibitor and AMPK small interfering RNA （siRNA） abolished SAL-induced Akt- Ser473 and eNOS-Serl177 phosphorylation. In contrast, LY294002, the PI3k/Akt pathway inhibitor, abolished SAL-induced phosphorylation and expression of eNOS. SAL decreased cellular ATP content and increased the cel- lular AMP/ATP ratio, which was associated with the activation of AMPK. SAL was found to decrease A^m, which is likely consequence of reduced ATP production. Conclusion The action of SAL to reduce atherosclerotic lesion formation may at least be attributed to its effect on improving endothelial function by promoting nitric oxide （NO） production, which was associated with mitochondria depolarization and subsequent activation of the AMPK/PI3 IC/ Akt/eNOS pathway. Taken together, our data described the effects of SAL on mitochondria, which played critical roles in improving endothelial function in atherosclerosis.

Separation of salidroside from the fermentation broth of engineered Escherichia coli using macroporous adsorbent resins

Salidroside(8-O-β-D-glucoside of tyrosol),a plant-derived natural product,is used for treatment of hypoxia,fatigue and aging diseases.The availability of salidroside is restricted since it is extracted from3-5 years old Rhodiola roots,which grow very slowly in the cold region of northern hemisphere of Earth.Our laboratory has constructed an engineered Escherichia coli and established a fermentation process to produce salidroside from glucose.In this article,nine macroporous resins from polarity to non-polarity,including NKA-9,S-8,AB-8,SP825,D101,LSA-8,LX-12,LX-18 and LX-68 resins,were tested to separate salidroside from fermentation broth.After static and dynamic experiments,the weakly polar SP825 resin had a better separation efficiency among nine resins.The adsorption kinetic and isotherm of salidroside on the SP825 resin were determined,and the pseudo-second-order kinetic model and Langmuir model could be fitted well.The effects of the pH on adsorption and ethanol concentration on desorption were investigated,and an optimal separation process was established.The adsorption for salidroside in the SP825 resin column was conducted with loading 150 ml at pH 7,and desorpted by washing 50 ml of80%ethanol solution.Under the best process conditions,the purity and yield of salidroside in the final product were 91.6%and 74.0%,respectively.The results showed that the macroporous SP825 resin would be feasible and effective to prepare salidroside and has promising application in the downstream process of microbial fermentation.

Protective Effect of Salidroside on Mitochondrial Disturbances via Reducing Mitophagy and Preserving Mitochondrial Morphology in OGD-induced Neuronal Injury

Salidroside is the active ingredient extracted from Rhodiola rosea,and has been reported to show protective effects in cerebral ischemia,but the exact mechanisms of neuronal protective effects are still unrevealed.In this study,the protective effects of salidroside(1 jimol/L)in ameliorating neuronal injuries induced by oxygen-glucose deprivation(OGD),which is a classical model of cerebral ischemia,were clarified.The results showed that after 8 h of OGD,the mouse hippocampal neuronal cell line HT22 cells showed increased cell death,accompanied with mitochondrial fragmentation and augmented mitophagy.However,the cell viability of HT22 cells showed significant restoration after salidroside treatment.Mitochondrial morphology and mitochondrial function were effectively preserved by salidroside treatment.The protective effects of salidroside were further related to the prevention of mitochondrial over-fission.The results showed that mTOR could be recruited to the mitochondria after salidroside treatment,which might be responsible for inhibiting excessive mitophagy caused by OGD.Thus,salidroside was shown to play a protective role in reducing neuronal death under OGD by safeguarding mitochondrial function,which may provide evidence for further translational studies of salidroside in ischemic diseases.

Determining the in vitro Anti-Aging Effect of the Characteristic Components from Eucommia ulmoides

To evaluate the potential anti-aging ability of Eucommia ulmoides,four characteristic components(chlorogenic acid,geniposidic acid,aucubin,quercetin)were selected to assess their effects on H_(2)O_(2)-induced oxidative damage model of human umbilical vein endothelial cell(HUVEC).Oxidative damage indexes,inflammatory factors,cell cycle,cell apoptosis,cell senescence,and their related proteins were analyzed by methyl thiazolyl tetrazolium(MTT)assay,enzyme-linked immunosorbent assay(ELISA),propidium iodide(PI)staining,annexin V-FITC/PI double staining,SAβ-galactosidase staining,and western blotting(WB).The results showed that H_(2)O_(2)-induced cell growth inhibition rate decreased as supplementation with characteristic components when compared to H_(2)O_(2) group.Meanwhile,the contents of antioxidant indexes(reactive oxygen species,lactate dehydrogenase,molondialdehyde,superoxide dismutase,glutathione),inflammatory factors(nuclear factor kappa-B,intercellular cell adhesion molecule-1,vascular cell adhesion protein 1),and functional factors(NO,Endothelin-1)in characteristic components treated groups improved if comparison with H_(2)O_(2) group,suggesting the characteristic components of E.ulmoides could alleviate H_(2)O_(2)-induced oxidative damage.Moreover,cell cycle,cell apoptosis,cell senescence,and their related proteins under characteristic components treatment exhibited a better effect than under H_(2)O_(2) treatment,implying the characteristic components could participate in anti-aging via multiple pathways.These results manifested that the characteristic components of E.ulmoides posses the capacity of anti-aging,which provided a basis for investigating the anti-aging ability of E.ulmoides itself.

Anti-Aging Genes Improve Appetite Regulation and Reverse Cell Senescence and Apoptosis in Global Populations

Appetite regulation by nutritional intervention is required early in life that involves the anti-aging gene Sirtuin 1 (Sirt 1) with Sirt 1 maintenance of other cellular anti-aging genes involved in cell circadian rhythm, senescence and apoptosis. Interests in anti-aging therapy with appetite regulation improve an individual’s survival to metabolic disease induced by gene-environment interactions by maintenance of the anti-aging genes connected to the metabolism of bacterial lipopolysaccharides, drugs and xenobiotics. Interventions to the aging process involve early calorie restriction with appetite regulation connected to appropriate genetic mechanisms that involve mitochondrial biogenesis and DNA repair in neurons. In the aging process as the anti-aging genes are suppressed as a result of transcriptional dysregulation chronic disease accelerations and connected to insulin resistance, non-alcoholic fatty liver disease (NAFLD) and neurodegenerative diseases such as Parkinson’s disease and Alzheimer’s disease. Interests in the gene-environment interaction indicate that the anti-aging gene Sirt 1that regulates food intake has been repressed early in the aging process in various global populations. The connections between Sirt 1 and other anti-aging genes such as Klotho, p66Shc (longevity protein) and Forkhead box proteins (FOXO1/ FOXO3a) have been associated with programmed cell death and alterations in these anti-aging genesregulate glucose, lipid and amyloid beta metabolism that are important to various chronic diseases.