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Schizophyllum commune is a fungus with applications both in medicine and foods, which produces IPS and EPS. However, there is no comparative study on the activity comparison of IPS and EPS and its mechanism of antioxidant effect. In this study, the antioxidant activities of the two polysaccharides were measured in biochemical, cellular and molecular levels, and H2O2 induced oxidative damage model of HSFs was established to explore the protective effects of EPS and IPS. We found IPS and EPS both achieved a good antioxidant effect. They can also improve the cellular levels of SOD and reduce MDA. Insights regarding the molecular mechanism were studied, we found that both EPS and IPS could increase the expression of Nrf2 in Keap1-Nrf2/ARE signaling pathway. At the same time, they could inhibit the expression of the negative feedback gene Keap1 and promote the expression of downstream gene GCLC, Gstt-1, Nqo1 and Ho-1. [ABSTRACT FROM AUTHOR]

To observe the effect of curcumin treatment on serum inflammatory factors in rats with traumatic arthritis and explores the protective effect of articular surface cartilage in rats with traumatic arthritis. A control group (group A), a model group (group B), and a curcumin group (group C) were randomly chosen. Except for the group A, the curcumin model was established by removing the medial meniscus of the right knee in the other two groups. After the model was successfully established, the group C was intraperitoneally injected with curcumin solution 50 mg/kg, while the group A and B were injected with the same volume of dimethyl sulfoxide solution for 28 d. The levels of serum vascular endothelial growth factor and tumor necrosis factoralpha and interleukin-1 beta were measured by enzyme-linked immunosorbent assay method. The arthritis index score of the two groups was calculated, the pathological morphology of articular cartilage was observed by hematoxylin and eosin staining, and the apoptosis rate of knee chondrocytes was detected by terminal deoxynucleotidyl transferase dUTP nick end labeling staining. Real-time polymerase chain reaction and Western blot methods were used to detect the expression of autophagy and apoptosis regulatory molecules Beclin-1, B-cell lymphoma 2, caspase-3, messenger ribonucleic acid and protein in knee cartilage. Curcumin can protect the articular surface cartilage of traumatic arthritis rats by reducing inflammatory factors in serum and regulating the apoptosis and autophagy of articular chondrocytes. Curcumin may be a potential drug for the treatment of traumatic arthritis. [ABSTRACT FROM AUTHOR]

Microglial activation has been recognized as being vital in the pathogenesis of several neurodegenerative disorders. Therefore, the identification of therapeutic drugs to prevent microglial activation and thus protect against inflammation-mediated neuronal injury, is required. In the present study, dextromethorphan (DM), a compound widely used in antitussive remedies that has been demonstrated to possess neuroprotective effects, was shown to reduce proinflammatory mediator production in lipopolysaccharide (LPS)-stimulated BV2 mouse microglial cells. Western blot analysis revealed that DM markedly suppressed the activation of nuclear factor-κB (NFκB), caspase-3 signaling and the expression of another inflammation-inducing factor, heat shock protein 60 (HSP60) and heat shock factor-1, induced by LPS in BV2 cells. Results from ELISA assay demonstrated that DM reduced the release of HSP60, nitric oxide (NO), inducible NO synthase, tumor necrosis factor-α, interleukin (IL)-1β and IL-6 induced by LPS in BV2 microglia. These results were confirmed by immunofluorescence, suggesting that DM may exert a neuroprotective and anti-inflammatory effect by inhibiting microglial activation through the HSP60-NFκB signaling pathway. Therefore, DM may offer substantial therapeutic benefits in the treatment of neurodegenerative diseases that are accompanied by microglial activation. [ABSTRACT FROM AUTHOR]

Heat shock protein (HSP)60 is primarily a mitochondrial protein. Previous experiments have found that changes in the location of intracellular HSP60 have been associated with apoptosis. Extracellular HSP60 mediates apoptosis via its ligand, Toll-like receptor (TLR)-4. TLR-4 is an important factor expressed on microglia, with a central role in generating neuroimmune responses in the pathogenesis of neurodegenerative disorders. Naloxone is a highly effective nonselective opioid receptor antagonist, and has been reported to be pharmacologically beneficial for the treatment of brain diseases through inhibiting microglia activation. However, the mechanisms underlying these beneficial effects of naloxone remain poorly understood. The present study aimed to investigate the role of HSP60 in the neuroprotective effects of naloxone on the production of proinflammatory mediators in lipopolysaccharide (LPS)-stimulated BV2 murine microglial cells and the possible signaling pathways involved. The results demonstrated that naloxone significantly inhibited the expression and release of HSP60 in BV2 cells. The expression levels of heat shock factor (HSF)-1 were upregulated in LPS-activated BV2 cells, which indicated that the increased expression of HSP60 was driven by HSF-1 activation. However, increased HSF-1 levels may be downregulated by naloxone. The levels of TLR-4 were elevated in activated BV2 cells, and then inhibited by naloxone. Activation of TLR-4 is characterized by activation of nuclear factor-κB (NF-κB) followed by the production of various proinflammatory and neurotoxic factors. Data from the present study demonstrated that naloxone reduced the expression levels of NF-κB and its upstream protein caspase-3, and reduced the LPS-induced production of nitric oxide, inducible nitric oxide synthase, tumor necrosis factor α, interleukin-1β and interleukin-6 in BV2 microglia. In light of this data, it was concluded that naloxone may exert its neuroprotective and anti-inflammatory effects by inhibiting microglia activation through a HSP60-TLR-4-NF-κB signaling pathway. [ABSTRACT FROM AUTHOR]

Multiple sclerosis is an autoimmune disease with classical traits of demyelination, axonal damage, and neurodegeneration. The migration of autoimmune T cells and macrophages from blood to central nervous system as well as the destruction of blood brain barrier are thought to be the major processes in the development of this disease. Chemokines, which are small peptide mediators, can attract pathogenic cells to the sites of inflammation. Each helper T cell subset expresses different chemokine receptors so as to exert their different functions in the pathogenesis of MS. Recently published results have shown that the levels of some chemokines and chemokine receptors are increased in blood and cerebrospinal fluid of MS patients. This review describes the advanced researches on the role of chemokines and chemokine receptors in the development of MS and discusses the potential therapy of this disease targeting the chemokine network. [ABSTRACT FROM AUTHOR]

We introduce the anisotropy into the evolutions of the vortex, and discuss three different kinds of dynamics: circular shaped vortex in linear anisotropic media, elliptic shaped vortex in linear isotropic media, and elliptic shaped vortex in linear anisotropic media. The evolutionary processes dramatically depend on both the anisotropic parameter δM of the media and the initial aspect ratio ρ0 of the elliptic vortex. Under the critical condition , the elliptic vortex will not rotate, and keeps its aspect ratio invariant during the evolutions. Generally, when , the dynamics of the elliptic vortex can be divided into three stages: nonuniform process, rotational process and uniform process. In the nonuniform and the uniform processes of the vortex, the positions of the outer elliptic peaks and the inner elliptic holes do not change in spite of the nonzero energy flow. Also, the energy distributions become nonuniform in the former process, and uniform in the latter process. In the rotational process, the outer peaks and the inner holes can both rotate, but with the opposite rotational directions. [ABSTRACT FROM AUTHOR]

In this paper, we report fine tunable red-green upconversion luminescence of glass ceramic containing 5%Er3+: NaYF4 nanocrystals excited simultaneously by two near infrared femtosecond lasers. When the glass ceramic was irradiated by 800nm femtosecond laser, weak red emission centered at 670 nm was detected. Bright red light was observed when the fs laser wavelength was tuned to 1490 nm. However, when excited by the two fs lasers simultaneously, the sample emitted bright green light centered at 550 nm, while the red light kept the same intensity. The dependences of the red and the green light intensities on the two pump lasers are much different, which enables us to manipulate the color emission by adjusting the two pump laser intensities, respectively. We present a theoretical model of Er3+ ions interacting with two fs laser fields, and explain well the experimental results. [ABSTRACT FROM AUTHOR]

It has been shown that the femtosecond laser polarization modulation is a very simple and well-established method to control the multi-photon absorption process by the light–matter interaction. Previous studies mainly focused on the multi-photon absorption control in the weak field. In this paper, we further explore the polarization control behavior of multi-photon absorption process in the intermediate femtosecond laser field. In the weak femtosecond laser field, the second-order perturbation theory can well describe the non-resonant two-photon absorption process. However, the higher order nonlinear effect (e.g., four-photon absorption) can occur in the intermediate femtosecond laser field, and thus it is necessary to establish new theoretical model to describe the multi-photon absorption process, which includes the two-photon and four-photon transitions. Here, we construct a fourth-order perturbation theory to study the polarization control behavior of this multi-photon absorption under the intermediate femtosecond laser field excitation, and our theoretical results show that the two-photon and four-photon excitation pathways can induce a coherent interference, while the coherent interference is constructive or destructive that depends on the femtosecond laser center frequency. Moreover, the two-photon and four-photon transitions have the different polarization control efficiency, and the four-photon absorption can obtain the higher polarization control efficiency. Thus, the polarization control efficiency of the whole excitation process can be increased or decreased by properly designing the femtosecond laser field intensity and laser center frequency. These studies can provide a clear physical picture for understanding and controlling the multi-photon absorption process in the intermediate femtosecond laser field, and also can provide a theoretical guidance for the future experimental realization. [ABSTRACT FROM AUTHOR]

Background: Lycopene is an important carotenoid pigment in red fruits and vegetables, especially in tomato. Although lycopene biosynthesis and catabolism have been found to be regulated by multiple factors including phytohormones, little is known about their regulatory mechanism. Cytokinins are crucial to various aspects of plant growth. Isopentenyltransferases (IPTs) catalyze the initial rate-limiting step of cytokinins biosynthesis, however, their roles in fruit ripening remain unclear. Results: Here, the functions of SlIPT4, encoding an isopentenyltransferase, were characterized via RNAi-mediated gene silencing in tomato. As we expected, silencing of SlIPT4 expression resulted in accelerated leaf senescence. However, down-expression of SlIPT4 generated never-red orange fruits, corresponding with a dramatic reduction of lycopene. Among lycopene biosynthesis-related genes, the fact of remarkable decrease of ZISO transcript and upregulation of other genes, revealed that SlIPT4 regulates positively lycopene biosynthesis via directly affecting ZISO expression, and also supported the existence of regulatory loops in lycopene biosynthesis pathway. Meanwhile, the accumulation of abscisic acid (ABA) was reduced and the transcripts PSY1 were increased in SlIPT4-RNAi fruits, supporting the feedback regulation between ABA and lycopene biosynthesis. Conclusion: The study revealed the crucial roles of SlIPT4 in leaf senescence and the regulatory network of lycopene biosynthesis in tomato, providing a new light on the lycopene biosynthesis and fruit ripening. [ABSTRACT FROM AUTHOR]

Background: Neuroinflammation plays hypertensive roles in the uninjured autonomic nuclei of the central nervous system, while its mechanisms remain unclear. The present study is to investigate the effect of neuroinflammation on autophagy in the neurons of the rostral ventrolateral medulla (RVLM), where sympathetic premotor neurons for the maintenance of vasomotor tone reside.Methods: Stress-induced hypertension (SIH) was induced by electric foot-shock stressors with noise interventions in rats. Systolic blood pressure (SBP) and the power density of the low frequency (LF) component of the SAP spectrum were measured to reflect sympathetic vasomotor activity. Microglia activation and pro-inflammatory cytokines (PICs (IL-1β, TNF-α)) expression in the RVLM were measured by immunoblotting and immunostaining. Autophagy and autophagic vacuoles (AVs) were examined by autophagic marker (LC3 and p62) expression and transmission electron microscopy (TEM) image, respectively. Autophagy flux was evaluated by RFP-GFP-tandem fluorescent LC3 (tf-LC3) vectors transfected into the RVLM. Tissue levels of glutamate, gamma aminobutyric acid (GABA), and plasma levels of norepinephrine (NE) were measured by using high-performance liquid chromatography (HPLC) with electrochemical detection. The effects of the cisterna magna infused minocycline, a microglia activation inhibitor, on the abovementioned parameters were analyzed.Results: SIH rats showed increased SBP, plasma NE accompanied by an increase in LF component of the SBP spectrum. Microglia activation and PICs expression was increased in SIH rats. TEM demonstrated that stress led to the accumulation of AVs in the RVLM of SIH rats. In addition to the Tf-LC3 assay, the concurrent increased level of LC3-II and p62 suggested the impairment of autophagic flux in SIH rats. To the contrary, minocycline facilitated autophagic flux and induced a hypotensive effect with attenuated microglia activation and decreased PICs in the RVLM of SIH rats. Furthermore, SIH rats showed higher levels of glutamate and lower level of GABA in the RVLM, while minocycline attenuated the decrease in GABA and the increase in glutamate of SIH rats.Conclusions: Collectively, we concluded that the neuroinflammation might impair autophagic flux and induced neural excitotoxicity in the RVLM neurons following SIH, which is involved in the development of SIH. [ABSTRACT FROM AUTHOR]