scholarly journals miR-155-5p Promotes Oxalate- and Calcium-Induced Kidney Oxidative Stress Injury by Suppressing MGP Expression

2020 ◽  
Vol 2020 ◽  
pp. 1-14 ◽  
Author(s):  
Kehua Jiang ◽  
Jianxin Hu ◽  
Guangheng Luo ◽  
Dalong Song ◽  
Peng Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Calcium Oxalate ◽  
Luciferase Reporter ◽  
Control Group ◽  
Ros Generation ◽  
High Dose ◽  
Positive Staining ◽  
Stress Injury ◽  
Oxidative Stress Injury ◽  
Ldh Release

Oxalate and calcium are the major risk factors for calcium oxalate (CaOx) stone formation. However, the exact mechanism remains unclear. This study was designed to confirm the potential function of miR-155-5p in the formation of CaOx induced by oxalate and calcium oxalate monohydrate (COM). The HK-2 cells were treated by the different concentrations of oxalate and COM for 48 h. We found that oxalate and COM treatment significantly increased ROS generation, LDH release, cellular MDA levels, and H2O2 concentration in HK-2 cells. The results of qRT-PCR and western blot showed that expression of NOX2 was upregulated, while that of SOD-2 was downregulated following the treatment with oxalate and COM in HK-2 cells. Moreover, the results of miRNA microarray analysis showed that miR-155-5p was significantly upregulated after oxalate and COM treated in HK-2 cells, but miR-155-5p inhibitor treatment significantly decreased ROS generation, LDH release, cellular MDA levels, and H2O2 concentration in HK-2 cells incubated with oxalate and COM. miR-155-5p negatively regulated the expression level of MGP via directly targeting its 3′-UTR, verified by the Dual-Luciferase Reporter System. In vivo, polarized light optical microphotography showed that CaOx crystal significantly increased in the high-dose oxalate and Ca2+ groups compared to the control group. Furthermore, IHC analyses showed strong positive staining intensity for the NOX-2 protein in the high-dose oxalate and Ca2+-treated mouse kidneys, and miR-155-5p overexpression can further enhance its expression. However, the expression of SOD-2 protein was weakly stained. In conclusion, our study indicates that miR-155-5p promotes oxalate- and COM-induced kidney oxidative stress injury by suppressing MGP expression.

scholarly journals Effect of total flavonoids of Cuscuta chinensis Lam. (Convolvulaceae) on oxidative stress injury in mouse testis and epididymis, and on serum levels of reproductive hormones in oligoasthenospermia mice model

2021 ◽  
Vol 18 (6) ◽  
pp. 1253-1258
Author(s):  
Hongliang Cui ◽  
Panpan Dong ◽  
Bin Chen
Keyword(s):  
Oxidative Stress ◽  
Sperm Quality ◽  
Serum Levels ◽  
Reproductive Hormones ◽  
Control Group ◽  
Total Flavonoids ◽  
Mice Model ◽  
Stress Injury ◽  
Oxidative Stress Injury ◽  
Cuscuta Chinensis

Purpose: To investigate the effect of total flavonoids of Cuscuta chinensis (TFCC) on oxidative stress injury in testis and epididymis, and serum levels of reproductive hormones in an oligoasthenospermia (OAS) mice model. Methods: Thirty male Wistar mice were randomly assigned to three groups of 10 mice each: control group, OAS group and TFCC group. With the exception of control group, OAS was orally induced in the mice with ornidazole. The TFCC group received TFCC. Reactive oxygen species (ROS), malondialdehyde (MDA) and superoxide dismutase (SOD) were determined. Serum levels of follicle stimulating hormone (FSH), luteinizing hormone (LH) and testosterone were also measured. Results: The levels of ROS and MDA in the testis and epididymis significantly increased in OAS group, when compared to control mice (p < 0.05). However, TFCC administration significantly reduced their levels in these tissues (p < 0.05). In contrast, SOD activity significantly decreased in the testis and epididymis of mice in OAS group, relative to control group, but increased significantly after TFCC exposure (p < 0.05). Serum FSH and LH were markedly elevated in OAS group, but treatment with TFCC significantly reduced the levels of these hormones (p < 0.05). Conclusion: These results suggest that TFCC effectively improves sperm quality and reduces oxidative damage in testis and epididymis of mice with oligoasthenospermia via a mechanism involving the regulation of serum levels of reproductive hormones. Thus, TFCC may be useful in the treatment of oligoasthenospermia.

scholarly journals Metformin Protects against Oxidative Stress Injury Induced by Ischemia/Reperfusion via Regulation of the lncRNA-H19/miR-148a-3p/Rock2 Axis

2019 ◽  
Vol 2019 ◽  
pp. 1-18 ◽  
Author(s):  
Jing Zeng ◽  
Long Zhu ◽  
Jing Liu ◽  
Tao Zhu ◽  
Zhaohui Xie ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ischemic Stroke ◽  
Cerebral Ischemia ◽  
Ischemia Reperfusion ◽  
Luciferase Reporter ◽  
Neuroprotective Effects ◽  
Stress Injury ◽  
Oxidative Stress Injury

Previous studies have shown that metformin not only is a hypoglycemic agent but also has neuroprotective effects. However, the mechanism of action of metformin in ischemic stroke is unclear. Oxidative stress is an important factor in the pathogenesis of cerebral ischemia-reperfusion injury. It has been reported that metformin is associated with stroke risk in the clinical population. This study is aimed at investigating the effect and mechanism of metformin in an experimental model of oxidative stress induced by ischemia/reperfusion (I/R) in vivo and oxygen glucose deprivation/reperfusion (OGD/R) in vitro. Metformin (100, 200, and 300 mg/kg) was administered intraperitoneally immediately after induction of cerebral ischemia. The indicators of oxidative stress selected were antioxidant enzyme activities of catalase, malondialdehyde (MDA), nitric oxide (NO), superoxide dismutase (SOD), and glutathione peroxidation enzyme (GSHPx). First, we demonstrated that metformin can significantly alleviate acute and chronic cerebral I/R injury and it has a strong regulatory effect on stroke-induced oxidative stress. It can reduce the elevated activities of MDA and NO and increase the levels of GSHPx and SOD in the cerebrum of mice and N2a cells exposed to I/R. Furthermore, real-time PCR and western blot were used to detect the expression of long noncoding RNA H19 (lncRNA-H19), microRNA-148a-3p (miR-148a-3p), and Rho-associated protein kinase 2 (Rock2). The direct interaction of lncRNA-H19, miR-148a-3p, and Rock2 was tested using a dual luciferase reporter assay. lncRNA-H19 altered OGD/R-induced oxidative stress by modulating miR-148a-3p to increase Rock2 expression. The expression of lncRNA-H19 and Rock2 could be downregulated with metformin in vivo and in vitro. In conclusion, our study confirmed that metformin exerts neuroprotective effects by regulating ischemic stroke-induced oxidative stress injury via the lncRNA-H19/miR-148a-3p/Rock2 axis. These results provide new evidence that metformin may represent a potential treatment for stroke-related brain injury.

scholarly journals Tanshinone IIA attenuates renal injury during hypothermic preservation via the MEK/ERK1/2/GSK-3β pathway

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Linhao Xu ◽  
Yizhou Xu ◽  
Zhoujing Zhu ◽  
Huiquan Gu ◽  
Chaofeng Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Tanshinone Iia ◽  
Control Group ◽  
Mitochondrial Morphology ◽  
Renal Cells ◽  
Stress Injury ◽  
Sd Rats ◽  
Hypothermic Preservation ◽  
Oxidative Stress Injury ◽  
Gsk 3Β

Abstract Background Oxidative stress-induced injury during hypothermic preservation is a universal problem that delays graft function and decrease the success of organ transplantation. Tanshinone IIA (Tan IIA) was reported to exhibit a variety of biochemical activities, including protection against oxidative stress. Therefore, the specific molecular pathway by which Tan IIA protects renal tissues during preservation was investigated in this study. Methods In vivo study, Sprague-Dawley (SD) rats were divided into twelve groups and the kidneys were isolated and preserved in different solutions for 0, 24 or 48 h, respectively: control group (Celsior solution) and Tan II groups (Celsior solution containing 10, 50,100 μM). In vitro study, primary renal cell from SD rats was cultured which was treated H2O2 (800 μM) for 6 h to mimic oxidative stress injury. Four groups were finally divided: control group; H2O2 group; H2O2 + Tan IIA group; H2O2 + Tan IIA + G15 group. Results In present study, we demonstrate data indicating that a significant increase in the superoxide dismutase (SOD) activity and a decrease in the reactive oxygen species (ROS) content were observed in the kidneys and renal cells preserved with Tan IIA compared with those preserved with the Celsior solution alone after 24 h and 48 h of hypothermic preservation (P < 0.01). The expression of phosphorylated mitogen-activated protein kinase kinase (MEK), phosphorylated extracellular signal-regulated protein kinases 1/2 (ERK1/2), phosphorylated glycogen synthase kinase-3β (GSK-3β) and cleaved caspase-3 was lower in the kidneys and renal cells preserved with Tan IIA than in those preserved with the Celsior solution alone after 24 h and 48 h of hypothermic preservation (P < 0.01). The mitochondrial morphology was rescued and adenosine triphophate (ATP) production and mitochondrial membrane potential were increased in the Tan IIA groups. Finally, Tan IIA also decreased cell apoptosis. Conclusion It suggests that the supplementation of the standard Celsior solution with Tan IIA may significantly improve long-term kidney preservation. Tan IIA attenuated oxidative stress injury and decreased apoptosis levels via activation of the MEK/ERK1/2/GSK-3β signaling pathway during kidney hypothermic preservation.

Establishment of a Mouse Asthenospermia Model through Triggering DGalactose Mediated Oxidative Stress Injury

2020 ◽  
Vol 20 ◽  
Author(s):  
Nanjun Liu ◽  
Qianxing Wang ◽  
Lin Li ◽  
Jian Lu
Keyword(s):  
Oxidative Stress ◽  
Survival Rate ◽  
Oxidative Damage ◽  
Dose Group ◽  
Low Dose ◽  
Control Group ◽  
High Dose ◽  
Stress Injury ◽  
Feed Addition ◽  
Motility Rate

Background: Asthenospermia is defined as forward motility of sperm less than 32%. Aim/Objective: This study aimed to establish mouse model of asthenospermia through triggering D-galactose mediated oxidative stress. Materials and methods: Total of 40 Kunming male mice were randomly divided into control group, low-dose group (administrating D-galactose at 60 mg/kg), high-dose group (administrating D-galactose at 120 mg/kg) and high-dose+feed addition group (administrating D-galactose at 120 mg/kg together with oral D-galactose). The testicular weight, testicular organ coefficient, sperm viability, sperm concentration and survival rate of tail of epididymis were measured. Oxidative damage of D-galactose to reproductive system of mice was evaluated by measuring superoxide dismutase (SOD) and malondialdehyde (MDA) in testicular homogenate of mice. Findings: The sperm motility, motility rate, concentration and survival rate of low-dose, high-dose and high-dose+feed addition group were decreased, compared to that in control group. However, there were significant difference between highdose group/high dose+feed group and control group (p<0.05). The forward motile sperm motility rate and total motility rate accorded with critical criteria of asthenospermia. Comparing with the control group, activity of SOD of model group mice significantly decreased, and MDA concentration significantly increased (p<0.05), excepting for low-dose versus control group for SOD activity. This suggests that testicular tissues suffered from oxidative damage. Conclusions: This study successfully established a mouse asthenospermia model through D-galactose mediated oxidative stress injury. The establishment of asthenospermia model in this study would provide a new promising insight and act as a potential approach for studying asthenospermia in vivo levels.

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