Carvacrol exerts nephroprotective effect in rat model of diclofenac-induced renal injury through regulation of oxidative stress and suppression of inflammatory response

Objective. The aim of this study was to explore the pharmacological effects of curcumin on oxidative stress and inflammatory response of renal dysfunction induced by renal ischemia/reperfusion (RIRI). Methods. Fifty male SD rats (Sprague Dawley) were randomly divided into the sham group, RIRI group, and curcumin group (low, medium, and high). The RIRI model was established by clipping the left renal artery for 45 min and then reperfusion for 24 h and resection of the contralateral kidney. In the curcumin group, curcumin was intraperitoneally injected once a day for 3 consecutive days using different dosage regimens. The RIRI group was intraperitoneally administered with normal saline. Renal injury was evaluated by measuring the concentration of creatinine (Cr) and urea nitrogen (BUN) in serum. Oxidative stress was assessed by assessing the level of malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione (GSH), and iron reduction/antioxidant capacity (FRAP) in tissues. In addition, the protective effect of RIRI was investigated by measuring Paller scores, the level of serum inflammatory factors and caspase-3, and the number of apoptotic cells. Results. Ischemia/reperfusion resulted in increased levels of Cr and BUN in serum and MDA in tissues and decreased levels of SOD, CAT, GPx, GSH, and FRAP. Curcumin pretreatment strikingly increased the level of SOD, CAT, GPx, GSH, IL-10, IFN-γ, and FRAP and significantly decreased MDA, Cr, BUN, IL-8, TNF-α, IL-6, and myeloperoxidase (MPO) expressions in tissues. Conclusion. Curcumin can relieve the degree of renal injury and improve renal function in ischemia-reperfusion, which may be related to the fact that curcumin can increase SOD content in serum and reduce MDA and FRAP levels in the rat model.

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A Novel Rat Model of Cardiac Donation After Circulatory Death Combined With Normothermic ex situ Heart Perfusion

Frontiers in Cardiovascular Medicine ◽

10.3389/fcvm.2021.639701 ◽

2021 ◽

Vol 8 ◽

Author(s):

Jiale Li ◽

Chuqing Xue ◽

Xiao Ling ◽

Yu Xie ◽

Desai Pavan ◽

...

Keyword(s):

Oxidative Stress ◽

Inflammatory Response ◽

Rat Model ◽

Energy State ◽

Ex Situ ◽

Cell Swelling ◽

Donation After Circulatory Death ◽

Histopathological Changes ◽

Heart Perfusion ◽

Circulatory Death

Background: In heart transplantation, the adoption of hearts from donation after circulatory death (DCD) is considered to be a promising approach to expanding the donor pool. Normothermic ex situ heart perfusion (ESHP) is emerging as a novel preservation strategy for DCD hearts. Therefore, pre-clinical animal models of ESHP are essential to address some key issues before efficient clinical translation. We aim to develop a novel, reproducible, and economical rat model of DCD protocol combined with normothermic ESHP.Methods: Circulatory death of the anesthetized rats in the DCD group was declared when systolic blood pressure below 30 mmHg or asystole was observed after asphyxiation. Additional 15 min of standoff period was allowed to elapse. After perfusion of cold cardioplegia, the DCD hearts were excised and perfused with allogenic blood-based perfusate at constant flow for 90 min in the normothermic ESHP system. Functional assessment and blood gas analysis were performed every 30 min during ESHP. The alteration of DCD hearts submitted to different durations of ESHP (30, 60, and 90 min) in oxidative stress, apoptosis, tissue energy state, inflammatory response, histopathology, cell swelling, and myocardial infarction during ESHP was evaluated. Rats in the non-DCD group were treated similarly but not exposed to warm ischemia and preserved by the normothermic ESHP system for 90 min.Results: The DCD hearts showed compromised function at the beginning of ESHP and recovered over time, while non-DCD hearts presented better cardiac function during ESHP. The alteration of DCD hearts in oxidative stress, apoptosis, tissue energy state, histopathological changes, cell swelling, and inflammatory response didn't differ among different durations of ESHP. At the end of 90-min ESHP, DCD, and non-DCD hearts presented similarly in apoptosis, oxidative stress, inflammatory response, myocardial infarction, and histopathological changes. Moreover, the DCD hearts had lower energy storage and more evident cell swelling compared to the non-DCD hearts.Conclusion: We established a reproducible, clinically relevant, and economical rat model of DCD protocol combined with normothermic ESHP, where the DCD hearts can maintain a stable state during 90-min ESHP.

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Regulation of inflammatory response and oxidative stress by tocotrienol in a rat model of non-alcoholic fatty liver disease

Journal of Functional Foods ◽

10.1016/j.jff.2020.104209 ◽

2020 ◽

Vol 74 ◽

pp. 104209

Author(s):

Sok Kuan Wong ◽

Kok-Yong Chin ◽

Fairus Ahmad ◽

Soelaiman Ima-Nirwana

Keyword(s):

Oxidative Stress ◽

Liver Disease ◽

Inflammatory Response ◽

Fatty Liver ◽

Rat Model ◽

Fatty Liver Disease ◽

Alcoholic Fatty Liver ◽

And Oxidative Stress ◽

Alcoholic Fatty Liver Disease

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Ethyl Pyruvate Prevents Intestinal Inflammatory Response and Oxidative Stress in a Rat Model of Extrahepatic Cholestasis

Journal of Surgical Research ◽

10.1016/j.jss.2009.03.027 ◽

2010 ◽

Vol 160 (2) ◽

pp. 228-235 ◽

Cited By ~ 14

Author(s):

Pengfei Wang ◽

Guanwen Gong ◽

Zhiqing Wei ◽

Yousheng Li

Keyword(s):

Oxidative Stress ◽

Inflammatory Response ◽

Rat Model ◽

Ethyl Pyruvate ◽

Extrahepatic Cholestasis ◽

And Oxidative Stress

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The Nephroprotective Effect of TNF Receptor-Associated Factor 6 (TRAF6) Blockade on LPS-Induced Acute Renal Injury Through the Inhibition if Inflammation and Oxidative Stress

Medical Science Monitor ◽

10.12659/msm.919698 ◽

2020 ◽

Vol 26 ◽

Author(s):

Xuemei Chen ◽

Yiqing Zhao ◽

Jiajun Xu ◽

Jiachun Bao ◽

Junyao Zhao ◽

...

Keyword(s):

Oxidative Stress ◽

Renal Injury ◽

Tnf Receptor ◽

Acute Renal Injury ◽

Associated Factor ◽

Nephroprotective Effect ◽

And Oxidative Stress

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Explore the Effects of Fe3O4 Nanoparticles and Oxidative Stress and Neuroinflammatory Responses on the Intestinal Flora Based on a Parkinson Rat Model

Journal of Nanoscience and Nanotechnology ◽

10.1166/jnn.2021.18636 ◽

2021 ◽

Vol 21 (2) ◽

pp. 1176-1183

Author(s):

Li Xu ◽

Tuexun Mayila ◽

Jie Wang

Keyword(s):

Oxidative Stress ◽

Parkinson’S Disease ◽

Parkinson's Disease ◽

Nervous System ◽

Inflammatory Response ◽

Rat Model ◽

Clinical Symptoms ◽

Synergistic Effects ◽

Intestinal Flora ◽

And Oxidative Stress

Parkinson’s disease is a degenerative disease of the central nervous system, and it occurs in middle-aged and elderly people. Studies have shown that both the clinical symptoms and neuropathological evidence of Parkinson’s disease suggest that Parkinson’s disease may originate in the gut. Intestinal flora homeostasis plays an important role in maintaining normal functions of the brain and nervous system. It participates in changes in cellular flora through oxidative stress, inflammatory response, and immune response during metabolism. Intestinal flora disorders are closely related to the onset of neurological diseases such as Parkinson’s disease (PD). In order to better understand the relationship between intestinal flora and Parkinson’s disease, this article studies the correlation between PD rat models and intestinal flora, and analyzes the possible relationship between them. The 6-OHDA PD rat model is currently a better model preparation method, which is widely used in PD research. The experimental results show that using Fe3O4 nanoparticle technology to detect intestinal flora disorders in PD patients, and the role of intestinal flora disorders in Parkinson’s disease may include affecting inflammatory response and oxidative stress, α-synuclein Protein (α-syn), these modes of action are not independent, there are complex and synergistic effects, and the molecular simulation mechanism may play a key role in these effects. There is a certain relationship between intestinal flora and Parkinson’s disease, but the specific mechanism is not clear, and further research is needed to provide more directions for the early diagnosis and early treatment of PD.

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