Blueberry treatment administered before and/or after lipopolysaccharide stimulation attenuates inflammation and oxidative stress in rat microglial cells

2022 ◽  
pp. 1-11
Author(s):  
Danielle S. Cahoon ◽  
Derek R. Fisher ◽  
Stefania Lamon-Fava ◽  
Dayong Wu ◽  
Tong Zheng ◽  
...  
2019 ◽  
Vol 126 (12) ◽  
pp. 1589-1597 ◽  
Author(s):  
Dayong Cao ◽  
Haowen Qiao ◽  
Dejiao He ◽  
Xingping Qin ◽  
Qian Zhang ◽  
...  

Antioxidants ◽  
2016 ◽  
Vol 5 (4) ◽  
pp. 33 ◽  
Author(s):  
Barbara Shukitt-Hale ◽  
Megan Kelly ◽  
Donna Bielinski ◽  
Derek Fisher

2001 ◽  
Vol 67 ◽  
pp. 141-149 ◽  
Author(s):  
Ian Anderson ◽  
Christy Adinolfi ◽  
Susan Doctrow ◽  
Karl Huffman ◽  
Ken A. Joy ◽  
...  

It is well established that inflammation and oxidative stress are key components of the pathology of Alzheimer's disease (AD), but how early in the pathological cascade these processes are involved or which specific molecular components are key, has not been fully elucidated. This paper describes the pharmacological approach to understand the molecular components of inflammation and oxidative stress on the activation of microglial cells and neuronal cell viability. We have shown that activation of microglia with the 42-amino-acid form of the ϐ-amyloid peptide (Aϐ42) activates the production of cyclooxygenase-2, the inducible form of nitric oxide synthase and tumour necrosis factor-α and there appears to be little interactive feedback between these three mediators. Moreover, we explore the effects of a series of salen-manganese complexes, EUK-8, -134 and -189, which are known to possess both superoxide and catalase activity. These compounds are able to protect cells from insults produced by hydrogen peroxide or peroxynitrite. Moreover, EUK-134 was also able to limit the output of prostaglandin E2 from activated microglial cells. The mechanisms underlying these effects are discussed. Together, these data support a pivotal role for oxidative stress and inflammation as key mediators of the pathological cascade in AD and provide some ideas about possible therapeutic targets.


2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 899-899
Author(s):  
Danielle Cahoon ◽  
Derek Fisher ◽  
Barbara Shukitt-Hale

Abstract Objectives Neuroinflammation and oxidative stress (OS) are implicated as mediators of cognitive decline and neurodegenerative diseases. Microglia, the primary immune cells of the central nervous system (CNS), are key regulators of inflammation and OS in the CNS. Blueberries (BB) are rich in anti-inflammatory and antioxidant polyphenols and reduce inflammation and OS when administered to microglia before pathogenic stimuli such as lipopolysaccharide (LPS). However, the therapeutic value of BBs administered to microglial cells after activation by LPS on inflammation and OS has not been examined. This study investigated the potential differential effects of pre-, post-, and pre-/post-BB on LPS-induced inflammation and OS in rat microglia. Methods Rat microglia were pre-treated with freeze-dried BB diluted in media (0.5 mg/mL) or control media (C) for 24 h, incubated overnight with LPS (0 or 100 ng/mL), and post-treated with BB or C for 24 h. Standard immunochemical techniques were used to measure biomarkers of inflammation and OS, including nitrite, tumor necrosis factor alpha (TNFɑ), inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2). Data were analyzed using two-way ANOVAs with treatment group (pre-/post-BB) and LPS exposure as experimental factors. Post-hoc testing was performed using Tukey's test to determine differences among groups. Results Preliminary results showed that all BB treatments (pre-, post- and pre-/post-BB) reduced LPS-induced nitrite and TNFɑ relative to no BB (P < 0.01). Pre-BB was more effective at reducing nitrite than post-BB (P < 0.01), although neither was significantly different than pre-/post-BB. In contrast, the attenuating effects of pre-BB and post-BB on TNFɑ were not different from each other, although both treatments were more beneficial than pre-/post-BB (P < 0.001). Compared to no BB, both pre-BB and post-BB, although not pre-/post-BB reduced LPS-induced iNOS expression (P < 0.05), and only pre-BB attenuated COX2 expression (P < 0.01). Conclusions Results suggest that BBs can target the downstream effects of microglial activation in addition to preventing stressor-induced neuroinflammation and OS. Therefore, although potentially more effective, BBs may not need to be present prior to microglial activation for beneficial effects. Funding Sources Supported by USDA intramural funding.


Author(s):  
Hasan Haci Yeter ◽  
Berfu Korucu ◽  
Elif Burcu Bali ◽  
Ulver Derici

Abstract. Background: The pathophysiological basis of chronic kidney disease and its complications, including cardiovascular disease, are associated with chronic inflammation and oxidative stress. We investigated the effects of active vitamin D (calcitriol) and synthetic vitamin D analog (paricalcitol) on oxidative stress in hemodialysis patients. Methods: This cross-sectional study was composed of 83 patients with a minimum hemodialysis vintage of one year. Patients with a history of any infection, malignancy, and chronic inflammatory disease were excluded. Oxidative markers (total oxidant and antioxidant status) and inflammation markers (C-reactive protein and interleukin-6) were analyzed. Results: A total of 47% (39/83) patients were using active or analog vitamin D. Total antioxidant status was significantly higher in patients with using active or analog vitamin D than those who did not use (p = 0.006). Whereas, total oxidant status and oxidative stress index were significantly higher in patients with not using vitamin D when compared with the patients who were using vitamin D preparation (p = 0.005 and p = 0.004, respectively). On the other hand, total antioxidant status, total oxidant status, and oxidative stress index were similar between patients who used active vitamin D or vitamin D analog (p = 0.6; p = 0.4 and p = 0.7, respectively). Conclusion: The use of active or selective vitamin D analog in these patients decreases total oxidant status and increases total antioxidant status. Also, paricalcitol is as effective as calcitriol in decreasing total oxidant status and increasing total antioxidant status in patients with chronic kidney disease.


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