Benzo(a)pyrene induces lung toxicity and inflammation in mice: prevention by carvacrol

2017 ◽  
Vol 37 (7) ◽  
pp. 752-761 ◽  
Author(s):  
P Barnwal ◽  
A Vafa ◽  
SM Afzal ◽  
A Shahid ◽  
SK Hasan ◽  
...  
Keyword(s):  
Lung Tissue ◽  
Environmental Pollutant ◽  
Lung Toxicity ◽  
Antioxidant Enzyme Activities ◽  
Protective Agent ◽  
Protective Effects ◽  
Histopathological Changes ◽  
Membrane Oxidation ◽  
Protein Expressions ◽  
Cox 2

Benzo(a)pyrene (B(a)P) is an environmental pollutant which causes various lung toxicities. The present study was designed to evaluate the protective effects of carvacrol, a monoterpenic phenol against B(a)P-induced lung toxicity. In this study, Swiss albino mice were pretreated with carvacrol (25 mg/kg and 50 mg/kg) orally for 7 consecutive days before administering oral B(a)P (125 mg/kg). Preventive efficacy of carvacrol was assessed in terms of membrane oxidation, antioxidant enzyme activities, histopathological changes, and inflammatory (iNOS, NF-κB, and COX-2) markers. Carvacrol pretreatment in the two doses restored B(a)P-induced lipid peroxidation and increased the activities of antioxidant enzymes. Protein expressions of iNOS, NF-κB, and COX-2 in the lung tissue were found to be upregulated by B(a)P. Carvacrol treatment, however, downregulated their expressions by decreasing the marker of positive stained cells and restored the histopathological architecture of lung tissue. Our results suggest that carvacrol can be used as a protective agent against B(a)P-induced lung toxicity and inflammation.

scholarly journals Protective Effects of Polydatin on Septic Lung Injury in Mice via Upregulation of HO-1

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Xiao-hui Li ◽  
Xia Gong ◽  
Li Zhang ◽  
Rong Jiang ◽  
Hong-zhong Li ◽  
...  
Keyword(s):  
Lung Injury ◽  
Tumor Necrosis ◽  
Cecal Ligation ◽  
Protective Effects ◽  
Protein Expressions ◽  
Cox 2 ◽  
Oxide Synthase ◽  
Necrosis Factor ◽  
Serum Tumor Necrosis ◽  
Inducible Nitric Oxide

The present study was carried out to investigate the effects and mechanisms of polydatin (PD) in septic mice. The model of cecal ligation and puncture (CLP-)induced sepsis was employed. Pretreatment of mice with PD (15, 45, and 100 mg/kg) dose-dependently reduced sepsis-induced mortality and lung injury, as indicated by alleviated lung pathological changes and infiltration of proteins and leukocytes. In addition, PD inhibited CLP-induced serum tumor necrosis factor-α(TNF-α) and interleukin-6 (IL-6) production, lung cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase isoform (iNOS) protein expressions and NF-κB activation. Notably, PD upregulated the expression and activity of heme oxygenase (HO-)1 in lung tissue of septic mice. Further, the protective effects of PD on sepsis were abrogated by ZnPP IX, a specific HO-1 inhibitor. These findings indicated that PD might be an effective antisepsis drug.

Protective effects of casein-derived peptide VLPVPQK against hydrogen peroxide–induced dysfunction and cellular oxidative damage in rat osteoblastic cells

2017 ◽  
Vol 36 (9) ◽  
pp. 967-980 ◽  
Author(s):  
SB Mada ◽  
S Reddi ◽  
N Kumar ◽  
S Kapila ◽  
R Kapila
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Lipid Peroxidation ◽  
Oxidative Damage ◽  
Osteoblastic Cells ◽  
Antioxidant Enzyme Activities ◽  
Protective Agent ◽  
Protective Effects ◽  
Differentiation Markers

Oxidative stress inhibits osteoblast differentiation and function that lead to the development of osteoporosis. Casein-derived peptide VLPVPQK (PEP), a potent antioxidant, was isolated from β-casein of buffalo milk. We used an in vitro oxidative stress model induced by hydrogen peroxide (H2O2) in rat osteoblastic cells to investigate the protective effects of PEP against H2O2-induced dysfunction and oxidative damage. Cells were pretreated with PEP (50–200 ng/mL) for 2, 7 or 21 days followed by 0.3 mM H2O2 treatment for 24 h and then markers of osteogenic development, oxidative damage and apoptosis were examined. PEP significantly increased the viability and differentiation markers of osteoblast cells such as alkaline phosphatase and calcium mineralization. Moreover, PEP suppressed the production of reactive oxygen species (ROS), lipid peroxidation and ameliorated H2O2-induced reduction in glutathione, superoxide dismutase and catalase activities. In addition, PEP partially inhibited caspase-9 and-3 activities and reduced propidium iodide–positive cells. Altogether, our results demonstrated that PEP could protect rat osteoblast against H2O2-induced dysfunction and oxidative damage by reduction of ROS production, lipid peroxidation and increased antioxidant enzyme activities. Thus, our data suggest that PEP might be a valuable protective agent against oxidative stress–related diseases such as osteoporosis.

scholarly journals The Protective Effects of Maresin 1 in the OVA-Induced Asthma Mouse Model

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Guochun Ou ◽  
Qin Liu ◽  
Chengxiu Yu ◽  
Xiaoju Chen ◽  
Wenbo Zhang ◽  
...  
Keyword(s):  
Mouse Model ◽  
Signaling Pathway ◽  
Lung Tissue ◽  
Critical Role ◽  
Inflammatory Factors ◽  
High Dose ◽  
Protective Effects ◽  
Cox 2 ◽  
Maresin 1 ◽  
Asthma Mouse Model

Asthma is a chronic inflammatory disease that cannot be cured. Maresin 1 (MaR1) is a specific lipid synthesized by macrophages that exhibits powerful anti-inflammatory effects in various inflammatory diseases. The goal of this study was to evaluate the effect of MaR1 on allergic asthma using an ovalbumin- (OVA-) induced asthma model. Thirty BALB/c mice were randomly allocated to control, OVA, and MaR1 + OVA groups. Mice were sacrificed 24 hours after the end of the last challenge, and serum, bronchoalveolar lavage fluid (BALF), and lung tissue were collected for further analysis. Western blotting was used to measure the protein level of IκBα, the activation of the NF-κB signaling pathway, and the expression of NF-κB downstream inflammatory cytokines. Quantitative real-time polymerase chain reactions (qRT-PCRs) were used to evaluate the expression levels of COX-2 and ICAM-1 in lung tissues. We found that high doses of MaR1 were most effective in preventing OVA-induced inflammatory cell infiltration and excessive mucus production in lung tissue, reducing the number of inflammatory cells in the BALF and inhibiting the expression of serum or BALF-associated inflammatory factors. Furthermore, high-dose MaR1 treatment markedly suppressed the activation of the NF-κB signaling pathway, the degradation of IκBα, and the expression of inflammatory genes downstream of NF-κB, such as COX-2 and ICAM-1, in the OVA-induced asthma mouse model. Our findings indicate that MaR1 may play a critical role in OVA-induced asthma and may be therapeutically useful for the management of asthma.

Role of gambogenic acid in regulating PI3K/Akt/NF-kβ signaling pathways in rat model of acute hepatotoxicity

2021 ◽  
Vol 85 (3) ◽  
pp. 520-527
Author(s):  
Zhongyang Ding ◽  
Ying Li ◽  
Zhangfeng Tang ◽  
Xiaoyi Song ◽  
Fa Jing ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Caspase 3 ◽  
Nuclear Factor ◽  
Protective Effects ◽  
Histopathological Changes ◽  
Phosphatidylinositol 3 Kinase ◽  
Tnf Α ◽  
Protein Expressions ◽  
Apoptosis Markers

ABSTRACT The purpose of this study is to investigate the protective effect of gambogenic acid (GA) in acetaminophen (APAP)-induced hepatotoxicity in rat models. GA (10 mg/kg) was administered intraperitoneal (i.p.) to rats for 7 consecutive days followed by APAP (500 mg/kg) single dose (i.p.) on the final day after GA administration. The levels of MDA, GSH, SOD, CAT, GPx, GST, ALP, AST, ALT, proinflammatory cytokines (TNF-α, IL-1β, IL-6), apoptosis markers (caspase-3 and -9, Bax, Bcl-2), 4-hydroxynonenal (4-HNE), and prostaglandin E2 (PGE2) were evaluated. Results exhibited protective effects of GA by inhibiting inflammation, preventing oxidative stress and apoptosis in APAP-induced liver. Histopathological changes caused by APAP were attenuated, protein expressions of phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) were upregulated, and nuclear factor–kappa β (NF-kβ) was downregulated by GA. In summary, GA significantly exerted anti-inflammatory and antiapoptotic effects against APAP-induced hepatotoxicity potentially through regulation of PI3K/Akt and NF-kβ signaling pathways.

scholarly journals Protective Effects of Lemon Juice on Alcohol-Induced Liver Injury in Mice

2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Tong Zhou ◽  
Yu-Jie Zhang ◽  
Dong-Ping Xu ◽  
Fang Wang ◽  
Yue Zhou ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Liver Injury ◽  
Antioxidant Capacity ◽  
Lemon Juice ◽  
Antioxidant Enzyme Activities ◽  
Dependent Manner ◽  
Protective Effects ◽  
Histopathological Changes ◽  
Excessive Alcohol Consumption

Chronic excessive alcohol consumption (more than 40–80 g/day for males and more than 20–40 g/day for females) could induce serious liver injury. In this study, effects of lemon juice on chronic alcohol-induced liver injury in mice were evaluated. The serum biochemical profiles and hepatic lipid peroxidation levels, triacylglycerol (TG) contents, antioxidant enzyme activities, and histopathological changes were examined for evaluating the hepatoprotective effects of lemon juice in mice. In addition, the in vitro antioxidant capacities of lemon juice were determined. The results showed that lemon juice significantly inhibited alcohol-induced increase of alanine transaminase (ALT), aspartate transaminase (AST), hepatic TG, and lipid peroxidation levels in a dose-dependent manner. Histopathological changes induced by alcohol were also remarkably improved by lemon juice treatment. These findings suggest that lemon juice has protective effects on alcohol-induced liver injury in mice. The protective effects might be related to the antioxidant capacity of lemon juice because lemon juice showed in vitro antioxidant capacity.

scholarly journals Effects of resveratrol against scattered radiation-induced testicular damage in rats

2020 ◽  
Vol 0 (0) ◽  
Author(s):  
Tarik Emre Sener ◽  
Beste Melek Atasoy ◽  
Ozge Cevik ◽  
Ozlem Tugce Cilingir Kaya ◽  
Sule Cetinel ◽  
...  
Keyword(s):  
Ionizing Radiation ◽  
Radiation Exposure ◽  
Scattered Radiation ◽  
Caspase 3 ◽  
Sirtuin 1 ◽  
Protective Agent ◽  
Testicular Damage ◽  
Testosterone Levels ◽  
Protein Expressions ◽  
Ionizing Radiation Exposure

AbstractObjectivesTo investigate the possible protective effects of resveratrol against oxidative testicular damage due to scattered radiation during pelvic ionizing radiation exposure in rats.MethodsRats were divided into 5 groups; control, radiation, and radiation + resveratrol therapy in early and late periods. Under anesthesia, 20 Gy ionizing radiation was applied to prostatic region. Resveratrol was administered (10 mg/kg/day) orally before ionizing radiation exposure. Animals were decapitated at the end of 1st and 10th weeks. Biochemical markers of oxidative stress; caspase-3 and sirtuin-1 protein expressions; testosterone levels were evaluated, histological examinations were performed.ResultsSignificant increases in malondialdehyde, 8-hydroxy-deoxyguanosine levels, myeloperoxidase, and caspase-3 activities were observed after ionizing radiation exposure, also superoxide dismutase and glutathione activities were significantly decreased. Radiotherapy increased caspase-3 and decreased sirtuin-1 protein expressions. Resveratrol treatment significantly reversed these parameters and also reversed the decrease in testosterone levels back to control levels in late period.ConclusionResveratrol showed antioxidant and sirtuin-activating properties against oxidative damage caused by scattered radiation to testis and provided hormonal protection. These results suggest that resveratrol may be an alternative protective agent on testicular tissues against the effects of scattered pelvic radiation.

scholarly journals Neurological Alterations and Testicular Damages in Aging Induced by D-Galactose and Neuro and Testicular Protective Effects of Combinations of Chitosan Nanoparticles, Resveratrol and Quercetin in Male Mice

Coatings ◽  
2021 ◽  
Vol 11 (4) ◽  
pp. 435
Author(s):  
Reham Z. Hamza ◽  
Mohammad S. Al-Harbi ◽  
Munirah A. Al-Hazaa
Keyword(s):  
Oxidative Stress ◽  
Chitosan Nanoparticles ◽  
Oxidative Stress Marker ◽  
Control Group ◽  
Antioxidant Enzyme Activities ◽  
Enzymatic Antioxidants ◽  
Protective Effects ◽  
Biochemical Alterations ◽  
Wide Range ◽  
Neurological Alterations

Aging is a neurological disease that is afforded by incidence of oxidative stress. Chitosan has received global interests due to its wide medical uses. Quercetin (Q) is a bioflavonoid and widely distributed in vegetables and fruits. Resveratrol is considered as a potent antioxidant and is a component of a wide range of foods. The using of either chitosan nanopartciles (CH-NPs), querectin (Q), and resveratrol (RV) to reduce the oxidative stress and biochemical alterations on brain and testicular tissues induced by D-galactose (DG) (100 mg/Kg) were the aim of the present study. This study investigated the probable protective effects of CH-NPs in two doses (140,280 mg/Kg), Q (20 mg/Kg) and RV (20 mg/Kg), against DG induced aging and neurological alterations. Brain antioxidant capacity as malonaldehyde (MDA), catalase (CAT), and glutathione reductase (GRx), as well as histopathological damages of the brain and testicular tissues were measured. The DG treated group had significantly elevated the oxidative stress markers by 96% and 91.4% in brain and testicular tissues respectively and lower significantly the antioxidant enzyme activities of both brain and testicular tissues than those of the control group by 86.95%, 69.27%, 83.07%, and 69.43%. Groups of DG that treated with a combination of CH-NPs in two doses, Q and RV, the levels of oxidative stress marker declined significantly by 68.70%, 76.64% in brain tissues and by 74.07% and 76.61% in testicular tissues, and the enzymatic antioxidants increased significantly by 75.55%, 79.24%, 62.32%, and 61.97% as compared to the DG group. The present results indicate that CH-NPs, Q, and RV have protective effects against DG-induced brain and testis tissue damage at the biochemical and histopathological levels. Mechanisms of this protective effect of used compounds against neurological and testicular toxicity may be due to the enhanced brain and testis antioxidant capacities.

Protective role of protocatechuic acid in carbon tetrachloride-induced oxidative stress via modulation of proinflammatory cytokines levels in brain and liver of Wistar rats

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Anne A. Adeyanju ◽  
Folake O. Asejeje ◽  
Olorunfemi R. Molehin ◽  
Olatunde Owoeye ◽  
Esther O. Olatoye ◽  
...  
Keyword(s):  
Cholesterol Level ◽  
Protocatechuic Acid ◽  
Liver Toxicity ◽  
Total Cholesterol Level ◽  
Density Lipoprotein ◽  
Albino Rats ◽  
Antioxidant Enzyme Activities ◽  
Cox 2 ◽  
Anti Inflammatory ◽  
The Brain

Abstract Objectives Protocatechuic acid (PCA) possesses numerous pharmacological activities, including antioxidative and anti-inflammatory activities. This study seeks to investigate its underlying mechanism of action in the liver and brain toxicity induced by CCl4 in male albino rats. Methods Rats were given PCA at 10 and 20 mg/kg daily and orally as a pretreatment for seven days. A single injection of CCl4 was given 2 h later to induce brain and liver toxicity. Results CCl4 moderately elevated the activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP). PCA lowered AST level significantly when compared to control. Total protein and albumin levels presented insignificant changes (p>0.05) in all groups while lipid profile showed increased total cholesterol level and reduced high-density lipoprotein (HDL) by CCl4. PCA (10 mg/kg) significantly reduced the cholesterol level while the 20 mg/kg dose moderately prevented HDL reduction. There was an increased MDA production with a corresponding low GSH level in the group treated with CCl4. Activities of superoxide dismutase, catalase, and glutathione-S-transferase in both organs also declined. PCA, especially at 10 mg/kg attenuated lipid peroxidation by increasing GSH level in the organs. Biochemical assays revealed the improvement of antioxidant enzyme activities by PCA in these organs. Furthermore, PCA lowered the level of proinflammatory cytokine COX 2 in the brain and liver while NF-kB expression was inhibited in the brain. Histopathology reports validated the effects of PCA. Conclusions PCA exhibited protection against toxicity in these tissues through antioxidant and anti-inflammatory activities and the potential mechanism might be through modulation of the NF-κB/COX-2 pathway.

scholarly journals Protective Effect of Membrane-Free Stem Cells against Lipopolysaccharide and Interferon-Gamma-Stimulated Inflammatory Responses in RAW 264.7 Macrophages

2021 ◽  
Vol 22 (13) ◽  
pp. 6894
Author(s):  
Mei Tong He ◽  
Hye Sook Park ◽  
Young Sil Kim ◽  
Ah Young Lee ◽  
Eun Ju Cho
Keyword(s):  
Nitric Oxide ◽  
Stem Cells ◽  
Interferon Gamma ◽  
Mapk Signaling ◽  
Raw 264.7 ◽  
Raw 264.7 Macrophages ◽  
Protein Expressions ◽  
Ifn Γ ◽  
Cox 2 ◽  
Anti Inflammatory

Recently, adipose-derived stem cells (ADSCs) are considered to be ideal for application in cell therapy or tissue regeneration, mainly due to their wide availability and easy access. In this study, we examined the anti-inflammatory effects of membrane-free stem cell extract (MFSC-Ex) derived from ADSCs against lipopolysaccharide (LPS)/interferon-gamma (IFN-γ) on RAW 264.7 macrophage cells. Exposure of RAW macrophages to LPS and IFN-γ stimuli induced high levels of nitric oxide (NO), cyclooxygenase-2 (COX-2), and prostaglandin E2 (PGE2) production. However, pretreatment with MFSC-Ex inhibited LPS/IFN-γ-induced these pro-inflammatory mediators. To clarify the molecular mechanisms underlying the anti-inflammatory property of MFSC-Ex, we analyzed nuclear factor-kappa B (NF-κB) and mitogen-activated protein kinases (MAPKs) protein expressions by Western blotting. Our study showed that treatment of MFSC-Ex significantly down-regulated inducible nitric oxide synthase (iNOS) and COX-2 protein expressions. Furthermore, phosphorylation of extracellular signal-regulated kinase (ERK) and p38 was also blocked by treatment with MFSC-Ex, indicating that inhibitory effect of MFSC-Ex on MAPK signaling cascade may attribute to inactivation of NF-κB. From these findings, we suggest that MFSC-Ex exert anti-inflammatory activities, which suppressed LPS/IFN-γ-induced production of NO, COX-2 and PGE2 by regulation of NF-κB and MAPK signaling pathway in RAW 264.7 macrophages. In conclusion, MFSC-Ex might provide a new therapeutic opportunity to treatment of inflammatory-related diseases.

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