scholarly journals Protective Effects of Hydrogen-Rich Water Against Cartilage Damage in a Rat Model of Osteoarthritis by Inhibiting Oxidative Stress, Matrix Catabolism, and Apoptosis

2020 ◽  
Vol 26 ◽  
Author(s):  
ShaoWen Cheng ◽  
Lei Peng ◽  
BaiChao Xu ◽  
WenSheng Chen ◽  
YangPing Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Rat Model ◽  
Cartilage Damage ◽  
Protective Effects ◽  
Stress Matrix

scholarly journals Soluble CCR2 Gene Therapy Controls Joint Inflammation, Cartilage Damage, and the Progression of Osteoarthritis by Targeting MCP-1

2021 ◽  
Author(s):  
Hyun Sik Na ◽  
Seon-Yeong Lee ◽  
Dong Hwan Lee ◽  
Jin Seok Woo ◽  
Keun-Hyung Cho ◽  
...  
Keyword(s):  
Rat Model ◽  
Cartilage Damage ◽  
Gene Activation ◽  
Joint Inflammation ◽  
Therapeutic Effects ◽  
Low Grade ◽  
Intestinal Damage ◽  
Protective Effects ◽  
Micro Computed Tomography ◽  
Monosodium Iodoacetate

Abstract Background: Osteoarthritis (OA) is the most common type of degenerative arthritis and affects the entire joint, causing pain, joint inflammation, and cartilage damage. Various risk factors are implicated in causing OA, and in recent years, a lot of research and interest have been directed toward chronic low-grade inflammation in OA. Monocyte chemoattractant protein-1 (MCP-1; also called CCL2) acts through C-C chemokine receptor type 2 (CCR2) in monocytes and is a chemotactic factor of monocytes that plays an important role in the initiation of inflammation. The targeting of CCL2–CCR2 is being studied as part of various topics including the treatment of OA.Methods: In this study, we evaluated the potential therapeutic effects the sCCR2 E3 gene may exert on OA. The effects of sCCR2 E3 were investigated in animal experiments consisting of intra-articular injection of sCCR2 E3 in a monosodium iodoacetate (MIA)-induced OA rat model. The effects after intra-articular injection of sCCR2 E3 (fusion protein encoding 20 amino acids of the E3 domain of the CCL2 receptor) in a monosodium iodoacetate-induced OA rat model were compared to those in rats treated with empty vector (mock treatment) and full-length sCCR2.Results: Pain improved with expression of the sCCR2 gene. Improved bone resorption upon sCCR2 E3 gene activation was confirmed via bone analyses using micro-computed tomography. Histologic analyses showed that the sCCR2 E3 gene exerted protective effects against cartilage damage and anti-inflammatory effects on joints and the intestine.Conclusions: These results show that sCCR2 E3 therapy is effective in reducing pain severity, inhibiting cartilage destruction, and suppressing intestinal damage and inflammation. Thus, sCCR2 E3 may be a potential therapy for OA.

Protective Effects of Honey Bee Products against Oxidative Stress-Associated Carcinogenesis in a Rat Model of Colon Cancer

2019 ◽  
Vol 7 (2) ◽  
pp. 62-78
Author(s):  
Hajer Ibrahim Salim Al-Ajmi ◽  
◽  
Hassan Talib Al-Lawati ◽  
Mohammad Shafiur Rahman ◽  
Nejib Guizani
Keyword(s):  
Oxidative Stress ◽  
Colon Cancer ◽  
Honey Bee ◽  
Rat Model ◽  
Protective Effects

scholarly journals Protective effects of epifriedelinol in a rat model of traumatic brain injury assessed with histological and hematological markers

2018 ◽  
Vol 9 (1) ◽  
pp. 38-42 ◽  
Author(s):  
Shiping Li ◽  
Qiaoying Zhang ◽  
Peiwu Li
Keyword(s):  
Oxidative Stress ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Water Content ◽  
Rat Model ◽  
Protective Effects ◽  
Hematological Markers ◽  
Cytokine Levels ◽  
Factor Α ◽  
And Oxidative Stress

Abstract Background This study evaluated the protective effects of epifriedelinol (EFD) in a rat model of traumatic brain injury (TBI). Methodology TBI was induced by dropping a weight from a specific height. The animals were separated into control, TBI, and EFD 100 and 200 mg/kg groups. The latter received 100 and 200 mg/kg EFD, respectively, for 2 days beginning 30 min after inducing TBI. The neurological examination score, permeability of the blood–brain barrier (BBB), water content of the brain, cytokine levels, and oxidative stress parameters were measured in the rats. The effects of EFD on glial fibrillary acidic protein (GFAP)-positive cells were evaluated using immunohistochemistry. ResultThe EFD treatment significantly decreased the neurological score, permeability of the BBB, and water content of brain compared with the TBI group. The levels of interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and oxidative stress were significantly decreased in the EFD-treated groups. The number of GFAP-positive cells was also significantly reduced in the EFD-treated groups. ConclusionEFD attenuates the secondary injury in TBI rats by reducing the serum cytokine levels and oxidative stress.

scholarly journals MP67-07 THE PROTECTIVE EFFECTS OF PROPOLIS ON OXIDATIVE STRESS AND CRYSTAL DEPOSITION WITH HYPEROXALURIA INDUCED TUBULAR CELL INJURY IN RAT MODEL

2016 ◽  
Vol 195 (4S) ◽  
Author(s):  
Kamil Fehmi Narter ◽  
Alper Kafkasli ◽  
Oguz Ozturk ◽  
Ozgur Yazici ◽  
Bilal Hamarat ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Rat Model ◽  
Cell Injury ◽  
Tubular Cell ◽  
Protective Effects ◽  
Crystal Deposition

scholarly journals Protective Effects of Pterostilbene Against Cardiac Oxidative Stressand Dysfunctionin Nicotine-Induced Cardiac Injury Rat Model

2021 ◽  
Vol 14 (02) ◽  
pp. 623-633
Author(s):  
Ahmad Rohi Ghazali ◽  
Elancheleyen Mahindran ◽  
Anand Ramalingam ◽  
Liya Chee ◽  
Satirah Zainalabidin
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Rat Model ◽  
Systolic Dysfunction ◽  
Cardiac Injury ◽  
Left Ventricular ◽  
Study Endpoint ◽  
Tbars Level ◽  
Protective Effects ◽  
Sprague Dawley

Prolonged nicotine exposureescalates the onset and development of cardiovascular diseasesin both active and passive smokers via cardiac injury. Pterostilbene, a resveratrol derivative, has been shown to exhibit high anti-inflammatory,antioxidant and antitumor properties. Nevertheless, its role as a cardioprotective agent in a nicotine-induced rat model is still scarce. Therefore, our study was aimed to investigatethe effects of co-administered pterostilbene against nicotine-induced cardiac injury rat model.Twenty-six male Sprague-Dawley rats were randomly allotted and treated with nicotine (0.6 mg/kg)orin-combination with pterostilbene (10 mg/kg) for 28 consecutive days. Non-invasive tail cuff blood pressure measurements were taken atday-0, day-14 and day-28. Rat hearts were harvested at study endpoint and thechanges in cardiac function parameters and oxidative stress markers were evaluated. The findings have shown that pterostilbene co-administration significantly (P<0.05) reduced the blood pressure and ameliorated nicotine-induced cardiac systolic dysfunction by improving the left ventricular developed pressure (LVDP). In addition, pterostilbene also significantly (P <0.05)attenuatedthe thiobarbituric acid reactive substances (TBARS) level, indicative of protection against nicotine-induced cardiac oxidative stress. In summary, our findings suggest that pterostilbene has the potential to be developed as a natural alternative in protecting the cardiac injuryinduced by nicotine. However further studies are warranted to investigate its efficacy and the underlying mechanism in cardioprotection.

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