Hyperbaric oxygen preconditioning improves postoperative cognitive dysfunction by reducing oxidant stress and inflammation

Postoperative cognitive dysfunction is a crucial public health issue that has been increasingly studied in efforts to reduce symptoms or prevent its occurrence. However, effective advances remain lacking. Hyperbaric oxygen preconditioning has proved to protect vital organs, such as the heart, liver, and brain. Recently, it has been introduced and widely studied in the prevention of postoperative cognitive dysfunction, with promising results. However, the neuroprotective mechanisms underlying this phenomenon remain controversial. This review summarizes and highlights the definition and application of hyperbaric oxygen preconditioning, the perniciousness and pathogenetic mechanism underlying postoperative cognitive dysfunction, and the effects that hyperbaric oxygen preconditioning has on postoperative cognitive dysfunction. Finally, we conclude that hyperbaric oxygen preconditioning is an effective and feasible method to prevent, alleviate, and improve postoperative cognitive dysfunction, and that its mechanism of action is very complex, involving the stimulation of endogenous antioxidant and anti-inflammation defense systems.

Edaravone protects against oxygen-glucose-serum deprivation/restoration-induced apoptosis in spinal cord astrocytes by inhibiting integrated stress response

We previously found that oxygen-glucose-serum deprivation/restoration（OGSD/R） induces apoptosis of spinal cord astrocytes, possibly via caspase-12 and the integrated stress response, which involves protein kinase R-like endoplasmic reticulum kinase（PERK）, eukaryotic initiation factor 2-alpha（eIF2α） and activating transcription factor 4（ATF4）. We hypothesized that edaravone, a low molecular weight, lipophilic free radical scavenger, would reduce OGSD/R-induced apoptosis of spinal cord astrocytes. To test this, we established primary cultures of rat astrocytes, and exposed them to 8 hours/6 hours of OGSD/R with or without edaravone（0.1, 1, 10, 100 μM） treatment. We found that 100 μM of edaravone significantly suppressed astrocyte apoptosis and inhibited the release of reactive oxygen species. It also inhibited the activation of caspase-12 and caspase-3, and reduced the expression of homologous CCAAT/enhancer binding protein, phosphorylated（p）-PERK, p-eIF2α, and ATF4. These results point to a new use of an established drug in the prevention of OGSD/R-mediated spinal cord astrocyte apoptosis via the integrated stress response.

Sodium fluoride induces apoptosis through reactive oxygen species-mediated endoplasmic reticulum stress pathway in Sertoli cells

Excessive fluoride exposure is known to contribute to reproductive system dysfunction,ultimately leading to pathological damage and apoptosis in cells. Although both oxidative and endoplasmic reticulum（ER） stresses have been implicated in fluorosis, the signaling pathways and their roles in sodium fluoride（Na F）-induced apoptosis of Sertoli cells have been sparsely described. In this study, oxidative damage, ER stress, and apoptosis were analyzed after Sertoli cells were treated with varying doses of Na F for 24 hr. Moreover, the antioxidant N-acetylcysteine（NAC） and pro-apoptotic transcription factor CHOP knockdown were used to clarify the precise interplay between reactive oxygen species（ROS）, ER stress and their roles in NaF-induced apoptosis in Sertoli cells. The present study indicated that NaF significantly decreased cell viability and induced apoptosis in Sertoli cells. In addition, NaF exposure facilitated the accumulation of ROS and increased nuclear translocation of nuclear factor erythroid 2-related factor 2（Nrf2） in Sertoli cells. Treatment with NAC caused remarkable recovery from these NaF-induced responses. Meanwhile, excessive NaF triggered ER stress as evidenced by up-regulated glucose-regulated protein 78 k Da（GRP78）, PKR-like ER kinase（PERK）, phosphorylation of eukaryotic translation initiation factor 2α（p-eI F2α） and CCAAT/enhancer-binding protein-homologous protein（CHOP）, without affecting total eukaryotic translation initiation factor 2α（e IF2α）. NAC effectively blocked the activation of ER stress, suggesting that Na F-induced ROS is an early event that triggers ER stress. Taken together, the results demonstrate that the ROS-mediated ER stress pathway is the crucial mechanistic event involved in NaF-induced apoptosis of Sertoli cells.

Reactive oxygen species signaling and stomatal movement in plant responses to drought stress and pathogen attack

Stomata, the pores formed by a pair of guard cells, are the main gateways for water transpiration and photosynthetic CO2 exchange, as well as pathogen invasion in land plants. Guard cell movement is regulated by a combination of environmental factors, including water status, light, CO2 levels and pathogen attack, as well as endogenous signals, such as abscisic acid and apoplastic reactive oxygen species （ROS）. Under abiotic and biotic stress conditions, extracellular ROS are mainly produced by plasma membrane-localized NADPH oxidases, whereas intracellular ROS are produced in multiple organelles. These ROS form a sophisticated cellular signaling network, with the accumulation of apoplastic ROS an early hallmark of stomatal movement. Here, we review recent progress in understanding the molecular mechanisms of the ROS signaling network, primarily during drought stress and pathogen attack. We summarize the roles of apoplastic ROS in regulating stomatal movement, ABA and CO2 signaling, and immunity responses. Finally, we discuss ROS accumulation and communication between organelles and cells. This information provides a conceptual framework for understanding how ROS signaling is integrated with various signaling pathways during plant responses to abiotic and biotic stress stimuli.

Toxicity of superparamagnetic iron oxide nanoparticles: Research strategies and implications for nanomedicine

Superparamagnetic iron oxide nanoparticles （SPIONs） are one of the most versatile and safe nanoparticles in a wide variety of biomedical applications. In the past decades, considerable efforts have been made to investigate the potential adverse biological effects and safety issues associated with SPIONs, which is essential for the development of next-generation SPIONs and for continued progress in translational research. In this mini review, we summarize recent developments in toxicity studies on SPIONs, focusing on the relationship between the physicochemical properties of SPIONs and their induced toxic biological responses for a better toxicological understanding of SPIONs.

Extracts of passion fruit peel and seed of Passiflora edulis(Passifloraceae) attenuate oxidative stress in diabetic rats

This study was aimed at evaluating the anti-diabetic potential of passion fruit Passiflora edulis(EPE) extracts in diabetic rats, following Streptozotocin(STZ) induced oxidative stress. Thirty adult Wistar rats were divided into five groups, with six rats in each group. The control rats were injected intraperitoneally with citrate buffer(pH 4.5). The remaining groups of rats were administered single dose of 45 mg·kg-1 of STZ by intraperitoneal route to induce diabetes. The diabetic animals were treated with 250 and 500 mg·kg-1 of EPE and glibenclamide 0.6 mg·kg-1 for fifteen days by oral route. Blood glucose, end organ oxidative stress marker, and anti-oxidants were assayed. Further, histopathological investigation of pancreas was studied at the end of the experimentation. The results revealed that subacute administration of EPE significantly(P < 0.001) controlled the blood glucose level in the diabetic rats. In addition, EPE extract protected the end organs by restoring the anti-oxidants enzyme, significantly increasing super oxide dismutase level(SOD) and decreasing catalase(CAT) and TBARS level in visceral organs. In conclusion, that EPE extracts showed anti-diabetic and anti-oxidant potential against streptozotocin-induced diabetes.

Protection of Salidroside on Primary Astrocytes from Cell Death by Attenuating Oxidative Stress

Objective To investigate whether salidroside（SAL） has protective and anti-oxidative effects on astrocytes. Methods Firstly, SAL was extracted from the roots of Rhodiola rosea with 70% ethanol and butanol to obtain crude phenylethyl alcohol glycosides which have been known as bioactive part of R. rosea; Secondly, WST-1 assay was carried out to assess the cell viability of astrocytes and cortical neurons under the treatment of the purified（〉 95%） SAL. Moreover, WST-1 assay was also used to evaluate the cytoprotective effects of SAL preventing astrocytes from staurosporine-induced cell death; Thirdly, we examined the spontaneous reactive oxygen species（ROS） and staurosporine-induced ROS generation in astrocytes in the absence or presence of SAL.Results SAL was observed to improve the astrocytes viability but not cortical neurons. In addition, SAL was able to ameliorate staurosporine-induced cell death. Moreover, SAL was able to attenuate the spontaneous ROS and staurosporine-induced ROS generation. Conclusion We here confirm that the anti-oxidative effect of SAL on primary astrocytes might be an important mechanism accounting for the cytoprotective effects from SAL.

A comparative study to evaluate the effect of limited access dressing on diabetic ulcers

Aim:Emerging evidence favors the important role of antioxidants,matrix metalloproteinases(MMPs),and nitric oxide(NO)in the healing of diabetic wounds.There is a lack of substantial evidence regarding the effects of negative pressure on antioxidants,MMPs and NO in chronic wounds associated with diabetes.Methods:A total of 55 type 2 diabetic patients with leg ulcers were divided into 2 groups:a limited access dressing(LAD)group(n=27)and a conventional dressing group(n=28).Levels of hydroxyproline,total protein,MMP-2 and MMP-9,NO and antioxidants including reduced glutathione(GSH)and the oxidative biomarker malondialdehyde(MDA)were measured in the granulation tissue at days 0 and 10.Changes in levels between the LAD and conventional groups were determined by the Student’s t-test.Results:After 10 days of treatment,the LAD vs.conventional dressing group showed increase in the levels of hydroxyproline(mean±standard deviation=55.2±25.1 vs.29.2±1,P<0.05),total protein(12.8±6.5 vs.8.34±3.2,P<0.05),NO(1.13±0.52 vs.0.66±0.43,P<0.05),GSH(7.0±2.4 vs.6.6±2.2,P<0.05)and decrease in MMP-2(0.47±0.33 vs.0.62±0.30,P<0.05),MMP-9(0.32±0.20 vs.0.53±0.39,P<0.05)and MDA(6.8±2.3 vs.10.4±3.4,P<0.05).Conclusion:When compared to conventional dressings,LAD induces biochemical changes by significantly increasing the levels of hydroxyproline,total protein,NO and antioxidants levels,and significantly reducing MMPs(MMP-2 and MMP-9)and an oxidative biomarker in diabetic wounds.These biochemical changes are thought to favor diabetic wound healing.