scholarly journals Toxic effect comparison of three typical sterilization nanoparticles on oxidative stress and immune inflammation response in rats

2015 ◽  
Vol 4 (2) ◽  
pp. 486-493 ◽  
Author(s):  
Huan-Liang Liu ◽  
Hong-Lian Yang ◽  
Ben-Cheng Lin ◽  
Wei Zhang ◽  
Lei Tian ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Toxic Effect ◽  
Inflammation Response ◽  
Immune Inflammation

Three typical sterilization nanoparticles can cause oxidative stress and immune inflammation response to rats, and their toxicities showed significant differences.

scholarly journals Modulatory effect of Syzygium aromaticum and Pelargonium graveolens on oxidative stress and inflammation

2018 ◽  
Author(s):  
Ilias Marmouzi ◽  
El Mostafa Karym ◽  
Rachid Alami ◽  
Meryem El Jemli ◽  
Mourad Kharbach ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Essential Oils ◽  
Toxic Effect ◽  
Tetrahymena Pyriformis ◽  
Syzygium Aromaticum ◽  
Minimal Risk ◽  
Pelargonium Graveolens ◽  
Anti Inflammatory

AbstractBackgroundTherapy combination is defined as disease treatment with two or more medication to acheive efficacy with lower doses or lower toxicity. Regarding its reported toxicities and efficacy, the Essential Oils (EOs) from Syzygium aromaticum (SA) and Pelargonium graveolens (PG) were combined for in vitro and in vivo assays and toxicities.MethodsThe Essential Oils and mixture were tested for in vivo/in vitro antioxidant and anti-inflammatory activities. The assays included the animal model of acute inflammation (carrageenan model), the protective effect on H2O2/Sodium nitroprissude induced stress in Tetrahymena pyriformis, and the in vitro antioxidant assays.ResultsThe chemical analysis of the investigated Oils has lead to the identification of Eugenol (74.06%), Caryophyllene (11.52%) and Carvacrol acetate (7.82%) as the major element in SA; while PG was much higher in Citronellol (30.77%), 10-epi-γ-Eudesmol (22.59%), and Geraniol (13.95%). In our pharmacological screening of samples, both Oils demonstrated good antioxidant effects. In vivo investigation of the antioxidant activity in the protozoa model (T. pyriformis) demonstrated a lesser toxic effect of EOs mixture with no significant differences when oxidative stress markers and antioxidant enzymes (MDA, SOD and CAT) were evaluated. On the other hand the in vivo model of inflammatory response to carrageenan demonstrated a good inhibitory potential of both EOs. The EOs Mixture demonstrated equivalent bioactivity with lower toxic effect and minimal risk for each compound.ConclusionsThe results from this study indicate that EOs mixture from SA and PG demonstrated promising modulatory antioxidant/anti-inflammatory effect, which suggest an efficient association for therapy.

scholarly journals Folate Reverses NF-κB p65/Rela/IL-6 Level Induced by Hyperhomocysteinemia in Spontaneously Hypertensive Rats

2021 ◽  
Vol 12 ◽  
Author(s):  
Lihua Zhang ◽  
Zhongliang Li ◽  
Changcheng Xing ◽  
Ning Gao ◽  
Rui Xu
Keyword(s):  
Oxidative Stress ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Expression Levels ◽  
Relative Expression ◽  
Abnormal Metabolism ◽  
Rat Thoracic Aorta ◽  
Immune Inflammation ◽  
Arterial Damage ◽  
Rat Tail

Hyperhomocysteinemia (HHcy) is derived from the abnormal metabolism of homocysteine (Hcy) and is related to metabolic-related diseases. In addition, HHcy combined with hypertension increases the risk of cardiovascular diseases (CVD). However, the mechanism of HHcy aggravating hypertensive arterial damage and the efficacy of folate (FA) as a beneficial supplement have not been fully elucidated. In this study, we established a rat HHcy model and a hypertension combined with HHcy model. Rat tail artery blood pressure (BP), plasma Hcy, serum superoxide dismutase (SOD), and malondialdehyde (MDA) were measured. Rat thoracic aorta was for pathological analysis after 12 weeks of the experiment. The relative expression levels of oxidative stress and immune/inflammation in rat arterial tissues were detected by quantitative real-time polymerase chain reaction (qRT-PCR) and western blotting. The results demonstrated that the relative expression levels of oxidative stress and immune/inflammation were the highest in the hypertension combined with HHcy group, followed by the hypertension group. Compared with the hypertension group, the hypertension combined with HHcy group up-regulated the expression levels of interleukin-6 (IL-6) and nuclear factor-κ-gene binding (NF-κB) p65/Rela, but not NADPH oxidase (Nox). Furthermore, folate inhibited the expression of IL-6 and NF-κB p65/Rela, reduced the levels of MDA and HHcy, but significantly increased the SOD level. In conclusion, HHcy synergistically aggravated the arterial damage factor of hypertension through immune/inflammatory response. However, folate demonstrated anti-inflammatory properties and reversed the NF-κB p65/Rela/IL-6 level induced by HHcy in hypertensive rats.

scholarly journals Pharmacoprophylaxis of liver diseases: creating a new hepatoprotector

2020 ◽  
Vol 17 ◽  
pp. 00061
Author(s):  
Svetlana Zykova ◽  
Sergey Shurov ◽  
Aleksey Savinkov ◽  
Nino Gugushvili ◽  
Vladimir Talismanov
Keyword(s):  
Oxidative Stress ◽  
Carbon Tetrachloride ◽  
Toxic Effect ◽  
Alanine Aminotransferase ◽  
Liver Diseases ◽  
Hepatoprotective Activity ◽  
Control Group ◽  
Biochemical Indicators ◽  
Intact Group ◽  
Biochemical Studies

The article presents a study of the hepatoprotective activity of a tricyclic heterocycle, which refers to 5, 6, 7, 8-tetrahydroquinolines. The effect of 8, 8-dimethyl-5-p-tolyl-8, 9-dihydro-2H-pyrido [4, 3, 2-de] cinnolin-3 (7H) was studied on rats under the influence of the model of toxic hepatosis induced by carbon tetrachloride to find out the indicators of peroxidation and biochemical indicators. Biochemical studies have shown that modelling toxic fat hepatosis caused by the inception of carbon tetrachloride to rats increased the activity of alanine aminotransferase by 2.5 times more compared with the intact group, indicating the development of oxidative stress induced by the treatment of pyrido [4, 3, 2] Cinnol I that reduced the toxic effect of CTC by 79.9 %. Mexidol had a less pronounced hepatoprotective effect: the activity of Alanine aminotransferase on animals of the second group was lower by 29.2 % than on rats from the control group. Thus, a new compound with hepatoprotective activity has been developed and studied.

scholarly journals TrxR2 overexpression alleviates inflammation-mediated neuronal death via reducing the oxidative stress and activating the Akt–Parkin pathway

2019 ◽  
Vol 8 (5) ◽  
pp. 641-653 ◽  
Author(s):  
Jinbao Gao ◽  
Yunjun Li ◽  
Wende Li ◽  
Haijiang Wang
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Cell Viability ◽  
Western Blotting ◽  
Neuronal Death ◽  
Protective Effects ◽  
Mitochondrial Apoptosis ◽  
Inflammation Response ◽  
N2a Cells

Abstract Neuronal death caused by inflammatory cytokine-mediated neuroinflammation is being extensively explored. Thioredoxin reductase (TrxR) 2 is a novel mediator of inflammation response. In the current study, we focus on the mechanisms of TrxR2 overexpression in inflammation-mediated neuronal death. LPS was used to induce neuroinflammation in N2a cells in vitro. Adenovirus-loaded TrxR2 was transfected into N2a cells to up-regulate TrxR2 expression. Then, cell viability was determined via MTT assay and TUNEL assay. Apoptosis was measured via western blotting and ELISA. Oxidative stress was detected via ELISA and flow cytometry. A pathway inhibitor was used to verify the role of the Akt–Parkin pathway in the LPS-mediated N2a cell death in the presence of TrxR2 overexpression. With the help of immunofluorescence assay and western blotting, we found that TrxR2 expression was significantly reduced in response to LPS treatment, and this effect was associated with N2a cell death via apoptosis. At the molecular level, TrxR2 overexpression elevated the activity of the Akt–Parkin pathway, as evidenced by the increased expression of p-Akt and Parkin. Interestingly, inhibition of the Akt–Parkin pathway abolished the regulatory effect of TrxR2 on LPS-treated N2a cells, as evidenced by the decreased cell viability and increased apoptotic ratio. Besides, TrxR2 overexpression also reduced oxidative stress, inflammation factor transcription and mitochondrial apoptosis. However, inhibition of Akt–Parkin axis abrogated the protective effects of TrxR2 on redox balance, mitochondrial performance and cell survival. LPS-mediated neuronal death was linked to a drop in TrxR2 overexpression and the inactivation of the Akt–Parkin pathway. Overexpression of TrxR2 sustained mitochondrial function, inhibited oxidative stress, repressed inflammation response, and blocked mitochondrial apoptosis, finally sending a pro-survival signal for the N2a cells in the setting of LPS-mediated inflammation environment.

scholarly journals Vitamin C attenuates the toxic effect of aristolochic acid on renal tubular cells via decreasing oxidative stress-mediated cell death pathways

2015 ◽  
Vol 12 (4) ◽  
pp. 6086-6092 ◽  
Author(s):  
TSAI-KUN WU ◽  
CHYOU-WEI WEI ◽  
YING-RU PAN ◽  
SHUR-HUEIH CHERNG ◽  
WEI-JUNG CHANG ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Vitamin C ◽  
Toxic Effect ◽  
Aristolochic Acid ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Cell Death Pathways ◽  
Renal Tubular

scholarly journals SS-31 Protects Liver from Ischemia-Reperfusion Injury via Modulating Macrophage Polarization

2021 ◽  
Vol 2021 ◽  
pp. 1-16
Author(s):  
Longcheng Shang ◽  
Haozhen Ren ◽  
Shuai Wang ◽  
Hanyi Liu ◽  
Anyin Hu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Injury ◽  
Reperfusion Injury ◽  
Liver Damage ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Macrophage Polarization ◽  
Protective Effects ◽  
Inflammation Response ◽  
Stat3 Signaling

Ischemia-reperfusion injury (IRI) is a common complication in liver surgeries. It is a focus to discover effective treatments to reduce ischemia-reperfusion injury. Previous studies show that oxidative stress and inflammation response contribute to the liver damage during IRI. SS-31 is an innovated mitochondrial-targeted antioxidant peptide shown to scavenge reactive oxygen species and decrease oxidative stress, but the protective effects of SS-31 against hepatic IRI are not well understood. The aim of our study is to investigate whether SS-31 could protect the liver from damages induced by IRI and understand the protective mechanism. The results showed that SS-31 treatment can significantly attenuate liver injury during IRI, proved by HE staining, serum ALT/AST, and TUNEL staining which can assess the degree of liver damage. Meanwhile, we find that oxidative stress and inflammation were significantly suppressed after SS-31 administration. Furthermore, the mechanism revealed that SS-31 can directly decrease ROS production and regulate STAT1/STAT3 signaling in macrophages, thus inhibiting macrophage M1 polarization. The proinflammation cytokines are then significantly reduced, which suppress inflammation response in the liver. Taken together, our study discovered that SS-31 can regulate macrophage polarization through ROS scavenging and STAT1/STAT3 signaling to ameliorate liver injury; the protective effects against hepatic IRI suggest that SS-31 may be an appropriate treatment for liver IRI in the clinic.

Toxic effect of organophosphate compounds on the kidneys

2020 ◽  
Vol 22 (3) ◽  
pp. 199-205
Author(s):  
M. O. Sokolova ◽  
V. E. Sobolev ◽  
D. A. Reshetkina ◽  
O. A. Nagibovich
Keyword(s):  
Oxidative Stress ◽  
Toxic Effect ◽  
Kidney Injury ◽  
Pathological Process ◽  
Ultrastructural Changes ◽  
Systemic Hemodynamic ◽  
Organophosphate Compounds ◽  
Disease Epidemiology ◽  
Organophosphate Intoxication ◽  
Toxic Damage

Abstract. The study describes: the toxic effect of organophosphate intoxication compounds on the human and animal organism, the contribution of organophosphate to the chronic kidney disease epidemiology and the acute kidney poisoning pathophysiology caused by organophosphate compounds. The study shows oxidative stress and systemic hemodynamic disturbance in the pathogenesis of organophosphate-induced kidney injury. We summarized effects of organophosphate substances on the structural and functional kidneys tissue characteristics in humans and animals. Biomarkers useful for early diagnosis of kidneys toxic damage are shown. In study we considered microscopic and ultrastructural changes in the anatomical and histological kidney structures caused by acute and chronic organophosphate intoxication. The organophosphate compounds are highly toxic, easily overcome the epithelial integument, are able to penetrate cell membranes and the blood-brain barrier. These compounds are involved in the disruption of several key biological processes the acetylcholinesterase irreversible inhibition and the oxidative stress induction in the excretory organs cells. The kidneys are not the first target in the toxic effect of organophosphate compounds in the human body, but are actively involved in the pathological process. It was established that kidneys tissue damage by organophosphate compounds can manifest itself differently depending on the duration of exposure, type and concentration of the toxic compound. It was shown that the kidney injury pathogenesis during acute and chronic intoxication by organophosphate compounds remains not fully understood. Nephron dysfunction patterns depending from various doses and toxic agents exposure duration have not been identified.

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