The role of cyclooxygenase inhibition in the effect of α-melanocyte-stimulating hormone on reactive oxygen species production by rat peritoneal neutrophils

2004 ◽  
Vol 71 (1) ◽  
pp. 1-5 ◽  
Author(s):  
B.K. Oktar ◽  
M. Yüksel ◽  
İ. Alican
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen Species Production ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Cyclooxygenase Inhibition ◽  
Melanocyte Stimulating Hormone ◽  
Species Production ◽  
Stimulating Hormone

scholarly journals PINK1 deficiency impairs osteoblast differentiation through aberrant mitochondrial homeostasis

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
So-Young Lee ◽  
Hyun-Ju An ◽  
Jin Man Kim ◽  
Min-Ji Sung ◽  
Do Kyung Kim ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Quality Control ◽  
Reactive Oxygen Species Production ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Mitochondrial Quality Control ◽  
Mitochondrial Homeostasis ◽  
Ovariectomized Mice ◽  
Species Production

Abstract Background PTEN-induced kinase 1 (PINK1) is a serine/threonine-protein kinase in mitochondria that is critical for mitochondrial quality control. PINK1 triggers mitophagy, a selective autophagy of mitochondria, and is involved in mitochondrial regeneration. Although increments of mitochondrial biogenesis and activity are known to be crucial during differentiation, data regarding the specific role of PINK1 in osteogenic maturation and bone remodeling are limited. Methods We adopted an ovariectomy model in female wildtype and Pink1−/− mice. Ovariectomized mice were analyzed using micro-CT, H&E staining, Masson’s trichrome staining. RT-PCR, western blot, immunofluorescence, alkaline phosphatase, and alizarin red staining were performed to assess the expression of PINK1 and osteogenic markers in silencing of PINK1 MC3T3-E1 cells. Clinical relevance of PINK1 expression levels was determined via qRT-PCR analysis in normal and osteoporosis patients. Results A significant decrease in bone mass and collagen deposition was observed in the femurs of Pink1−/− mice after ovariectomy. Ex vivo, differentiation of osteoblasts was inhibited upon Pink1 downregulation, accompanied by impaired mitochondrial homeostasis, increased mitochondrial reactive oxygen species production, and defects in mitochondrial calcium handling. Furthermore, PINK1 expression was reduced in bones from patients with osteoporosis, which supports the practical role of PINK1 in human bone disease. Conclusions In this study, we demonstrated that activation of PINK1 is a requisite in osteoblasts during differentiation, which is related to mitochondrial quality control and low reactive oxygen species production. Enhancing PINK1 activity might be a possible treatment target in bone diseases as it can promote a healthy pool of functional mitochondria in osteoblasts.

scholarly journals Role of Renal DJ-1 in the Pathogenesis of Hypertension Associated With Increased Reactive Oxygen Species Production

Hypertension ◽  
2012 ◽  
Vol 59 (2) ◽  
pp. 446-452 ◽  
Author(s):  
Santiago Cuevas ◽  
Yanrong Zhang ◽  
Yu Yang ◽  
Crisanto Escano ◽  
Laureano Asico ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen Species Production ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Species Production

scholarly journals Protective Effect ofScutellaria litwinowiiExtract on Serum/Glucose-Deprived Cultured PC12 Cells and Determining the Role of Reactive Oxygen Species

2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Maryam Afsharzadeh ◽  
Zahra Tayarani-Najaran ◽  
Aryo Zare ◽  
Seyed Hadi Mousavi
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Pc12 Cells ◽  
Reactive Oxygen Species Production ◽  
Reactive Oxygen ◽  
Glucose Deprivation ◽  
Serum Glucose ◽  
Oxygen Species ◽  
Species Production

Considering the wide, positive reporting of the role of reactive oxygen species in ischemic brain injury, searching for antioxidant drugs within herbal remedies is logical. In this study, the protective effects ofScutellaria litwinowiiBornm. & Sint. on cell viability and reactive oxygen species production in cultured PC12 cells were investigated under serum/glucose-deprivation-induced cell death. After cells were seeded overnight, they were then deprived of serum/glucose for 24 h. Cells were treated with different concentrations ofS. litwinowiiextract (7.75–250 μg/mL). Cell viability was quantitated by MTT assay, and intracellular reactive oxygen species production was measured by flow cytometry. Serum/glucose-deprivation induced significant cell death after 24 h (P< 0.001). Treatment withS. litwinowii(7.75–250 μg/mL) reduced serum/glucose deprivation-induced cytotoxicity in PC12 cells after 24 h. A significant increase in intracellular reactive oxygen species production was seen following serum/glucose deprivation (P< 0.001).S. litwinowii(62 and 125 μg/mL,P< 0.01) treatment reversed the increased reactive oxygen species production following ischemic insult. This demonstrates thatS. litwinowiiextract protects PC12 cells against serum/glucose-deprivation-induced cell death by antioxidant mechanisms, which indicates the potential therapeutic application ofS. litwinowiiin managing cerebral ischemic and neurodegenerative disorders.

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