Redox Report最新文献

Background: As a chronic autoimmune disease, rheumatoid arthritis (RA) is related to oxidative stress, which may lead to the occurrence and persistence of inflammation in RA. The purpose of this study is to evaluate the potential antioxidant effect of triptolide in collagen-induced arthritis (CIA) rat model.

Methods: We examined the severity of arthritis, levels of local and systemic oxidative stress, periarticular bone erosion and weight of organs in CIA rats treated with triptolide.

Results: We found that triptolide decreased the paw thickness and clinical arthritis score, significantly. The mRNA expression and activity of myeloperoxidase and inducible nitric oxide synthase were remarkably decreased in the paws of the CIA rats after triptolide treatment. Triptolide significantly inhibited the levels of nitrite and nitrate in serum, as well as the urinary level of dityrosine. Triptolide treatment also markedly increased bone volume of tibia, but suppressed epiphyseal plate thickness of both femur and tibia. In addition, there was no significant difference in the weight of organs after the therapy, except decreased spleen weight.

Conclusions: These results suggested that the local and systemic oxidative stress was enhanced in the CIA rats and the therapeutic dose of triptolide had a definite antioxidant effect.

Background: Progression of Benign Prostate hyperplasia (BPH) is vulnerable to oxidative stress (OS) and prostatic enlargement among the aging males through apoptosis deregulation. Our present study aimed to investigate the effect of neferine (NF) in the regulation of oxidative stress and apoptosis in human BPH-1 cells.

Methods: BPH epithelial cell line BPH-1 was treated with NF for 24 and 48 h. To measure oxidative stress (OS) we investigated MDA, SOD, and GST expression along with Nrf2 and its downstream gene and protein expression. Cell proliferation and apoptosis regulation was assayed with respective methods.

Results: Investigation revealed NF remarkably activate Nrf2 and its downstream proteins HO-1 and NQO1 at 48 h more substantially. Nrf2/Keap1 relative gene and protein expression indicated that NF might trigger Nrf2 upregulation by decreasing Keap1 expression. Both NF concentrations (3 µM and 9 µM) were able to deplete ROS and lipid peroxidation, concurrently, up-regulated SOD and GST. NF reduced cell proliferation significantly along with the regulation of apoptotic proteins Bax, Bcl2, Cyt-C, Caspase 9, and Caspase 3 at the same time (48 h).

Conclusion: This study is the first to manifest that NF may potentially regulate BPH by counterbalancing between OS and apoptosis through the activation of Nrf2-ARE pathway.

Objectives: In obesity, there is a shift in the pro-oxidative-antioxidant balance towards the oxidationreactions. However, it has been shown that in people with normal body composition, after a series of whole-body cryotherapy (WBC), the balance shifts in the opposite direction. Design: The aim of the study was to assess the impact of 20 WBC treatments on blood pro-oxidative-antioxidant balance. Interventions: Study included 14 obese (BMI > 35) and 10 non-obese volunteers. Methods: The total antioxidative (TAS/TAC) and pro-oxidative status (TOS/TOC) in serum and activity of antioxidant enzymes in erythrocytes were determined before the first and 2 hours after the last cryostimulation. Results: In the obese group, a significantly higher level of TOS/TOC, and its significant decrease after the WBC series, was observed. Cryotherapy had no influence on TAS/TAC level which was similar in both groups. Changes in activity of antioxidant enzymes were multidirectional. An increase in CAT activity in the obese group was observed. OSI, both before and after a series of treatments, was significantly higher in obese subjects. Conclusions: A beneficial effect on the level of TOS/TOC and CAT activity was indicated, but the proposed number of treatments for patients with class II obesity turned out to be insufficient. Trial registration: Australian New Zealand Clinical Trials Registry identifier: ACTRN12619000524190.

Background: The extent of the damage following surgery has been subject of study for several years. Numerous surgical complications can impact postoperative quality of life of patients and even can cause mortality. Although these complications are generally due to multifactorial mechanisms, oxidative stress plays a key pathophysiological role. Moreover, oxidative stress could be an unavoidable effect derived even from the surgical procedure itself.

Methods: A systematic review was performed following an electronic search of Pubmed and ScienceDirect databases. Keywords such as sepsis, oxidative stress, organ dysfunction, antioxidants, outcomes in postoperative complications, among others, were used. Review articles were preferably used between the years 2015 onwards, not excluding older ones.

Results: The vast majority point to the role of oxidative stress in generating greater damage and worse prognosis in postoperative patients without the necessary care and precautions, taking importance on the use of antioxidants to prevent this problem.

Discussions: Oxidative stress represents a common final pathway related to pathological processes such as inflammation or ischemia-reperfusion, among others. The expression of greater severity of these complications can result in multiple organ dysfunction or sepsis. The aim of this study was to present an update of the role of oxidative stress on surgical postoperative complications.

Objective: The aim of this study was to investigate how modifications at the periphery of the porphyrin ring affect the anticancer activity of Mn porphyrins (MnPs)-based SOD mimics.

Methods: Six compounds: MnTE-2-PyP with a short ethyl chain on the pyridyl ring; MnTnHexOE-2-PyP and MnTnOct-2-PyP with linear 8-atom alkyl chains, but the former with an oxygen atom within the alkyl chain; MnTE-2-PyPhP and MnTPhE-2-PyP with pyridyl and phenyl substituents, were investigated. Cytotoxicity was studied using pII and MDA-MB-231 cancer cell lines. Viability was assessed by the MTT (3-[4,5-dimethylthiazol-2-yl)]-2,5-diphenyltetrazolium bromide) assay and cell proliferation was determined by the sulforhodamine B assay.

Results: Cellular uptake was increased with the increase of the lipophilicity of the compounds, whereas reduction potential (E_½) of the Mn(III)/Mn(II) redox couple shifted away from the optimal value for efficient redox cycling with ascorbate, necessary for ROS production. Amphiphilic MnPs, however, exerted anticancer activity by a mechanism not involving ROS.

Conclusion: Two different processes account for MnPs cytotoxicity. MnPs with appropriate E_½ act via a ROS-dependent mechanism. Amphiphilic MnPs with suitable structure damage sensitive cellular constituents, leading to the suppression of proliferation and loss of viability. Design of compounds interacting directly with sensitive cellular targets is highly promising in the development of anticancer drugs with high selectivity and specificity.