Velasquezroach3228
FSTL1 upregulated expression of nuclear factor (erythroid-derived 2)-like 2 (Nrf2) in DOX-treated hearts. FSTL1 was not capable of protecting against these toxic effects in Nrf2-deficient mice. In conclusion, FSTL1 protected against DOX-induced cardiotoxicity via upregulation of Nrf2 expression.In the present study, the replicative lifespan assay of yeast was used to guide the isolation of antiaging substance from Gentiana rigescens Franch, a traditional Chinese medicine. A compound with antiaging effect was isolated, and the chemical structure of this molecule as amarogentin was identified by spectral analysis and compared with the reported data. It significantly extended the replicative lifespan of K6001 yeast at doses of 1, 3, and 10 μM. Furthermore, amarogentin improved the survival rate of yeast under oxidative stress by increasing the activities of catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx), and these enzymes' gene expression. selleck products In addition, this compound did not extend the replicative lifespan of sod1, sod2, uth1, and skn7 mutants with K6001 background. These results suggested that amarogentin exhibited antiaging effect on yeast via increase of SOD2, CAT, GPx gene expression, enzyme activity, and antioxidative stress. Moreover, we evaluated antioxidant activity of this natural products using PC12 cell system, a useful model for studying the nervous system at the cellular level. Amarogentin significantly improved the survival rate of PC12 cells under H2O2-induced oxidative stress and increased the activities of SOD and SOD2, and gene expression of SOD2, CAT, GPx, Nrf2, and Bcl-x1. Meanwhile, the levels of reactive oxygen species (ROS) and malondialdehyde (MDA) of PC12 cells were significantly reduced after treatment of the amarogentin. These results indicated that antioxidative stress play an important role for antiaging and neuroprotection of amarogentin. Interestingly, amarogentin exhibited neuritogenic activity in PC12 cells. Therefore, the natural products, amarogentin from G. rigescens with antioxidant activity could be a good candidate molecule to develop drug for treating neurodegenerative diseases.Age-related macular degeneration (AMD) is a leading cause of severe visual loss and irreversible blindness in the elderly population worldwide. Retinal pigment epithelial (RPE) cells are the major site of pathological alterations in AMD. They are responsible for the phagocytosis of shed photoreceptor outer segments (POSs) and clearance of cellular waste under physiological conditions. Age-related, cumulative oxidative stimuli contribute to the pathogenesis of AMD. Excessive oxidative stress induces RPE cell degeneration and incomplete digestion of POSs, leading to the continuous accumulation of cellular waste (such as lipofuscin). Autophagy is a major system of degradation of damaged or unnecessary proteins. However, degenerative RPE cells in AMD patients cannot perform autophagy sufficiently to resist oxidative damage. Increasing evidence supports the idea that enhancing the autophagic process can properly alleviate oxidative injury in AMD and protect RPE and photoreceptor cells from degeneration and death, although overactivated autophagy may lead to cell death at early stages of retinal degenerative diseases. The crosstalk among the NFE2L2, PGC-1, p62, AMPK, and PI3K/Akt/mTOR pathways may play a crucial role in improving disturbed autophagy and mitigating the progression of AMD. In this review, we discuss how autophagy prevents oxidative damage in AMD, summarize potential neuroprotective strategies for therapeutic interventions, and provide an overview of these neuroprotective mechanisms.
To investigate the serum changes of oxidative stress markers and the relationship between these factors and visual field (VF) progression in patients with primary angle closure glaucoma (PACG).
A case-control and a prospective cohort study. A total of 94 patients with PACG and 89 normal controls were enrolled. Furthermore, 94 PACG subjects were followed up for at least two years (once every six months). All participants were evaluated for serum levels of superoxide dismutase (SOD), total antioxidant status (TAS), hydrogen peroxide (H
O
), malondialdehyde (MDA), glutathione peroxidase, glutathione reductase, and detailed eye and systematic examination. Binary logistic regression analysis and Cox regression analysis were performed.
The serum levels of SOD and TAS in the PACG group were significantly lower than those in the control group (
< 0.001). Meanwhile, PACG subjects had significantly higher levels of MDA and H
O
than the normal control subjects (
< 0.001). Serum levels of TAS (OR = 0tients with PACG. These findings suggest that oxidative stress was involved in the onset and development of PACG.The storage and preparation of corn for animal feed inevitably lead to lipid and protein peroxidation. Granulosa cells play an important role in follicular development in the ovaries, and hen laying productivity is likely to be dependent on follicle health and number. We hypothesized that oxidized oil and protein induce apoptosis via oxidative stress in laying hen granulosa cells. A sample of 360 38-week-old Lohmann commercial laying hens was used in a 2 × 2 factorial design for 8 weeks. Dietary treatments included dietary oil (fresh corn oil (FO) or oxidized corn oil (OO)) and corn gluten meal (fresh corn gluten meal (FP) or oxidized corn gluten meal (OP)). Productivity, ovarian histology, granulosa cell apoptosis, and indicators of oxidative stress were evaluated in all groups. Both dietary OO and OP decreased egg production and the average daily feed intake (ADFI) of laying hens. Flow cytometry, TUNEL, and real-time PCR revealed that both dietary OO and OP induced granulosa cell apoptosis in prehierarchical and hierarchical follicles. Furthermore, dietary OO and OP caused oxidative stress in prehierarchical and hierarchical follicles, as indicated by the downregulation of antioxidant-related-gene expression. Moreover, forkhead box O1 (FoxO1), extracellular regulated protein kinase (ERK), and c-Jun NH2 kinase (JNK) are involved in potential apoptosis regulation pathways in the granulosa cells of laying hens fed OO and OP, as indicated by the upregulation of FoxO1 expression and downregulation of ERK/JNK expression. These results indicate that OO and OP induce granulosa cell apoptosis via oxidative stress, and the combined use of OO and OP aggravates the adverse effects of oxidative stress in laying hens.
