Antioxidant and Anti-Inflammatory Effects of Coenzyme Q10 on L-Arginine-Induced Acute Pancreatitis in Rat

This study was aimed at evaluating the protective effect of coenzyme Q10 on L-arginine-induced acute pancreatitis in rats regarding biomarkers and morphologic changes. Thirty-two male Sprague-Dawley rats were divided into 4 equal groups. Control group received intraperitoneal normal saline, while in sham and experimental groups 1 and 2 pancreatitis was induced with L-arginine. E1 and E2 groups were treated with a single dose of 100 and 200 mg/kg Q10, respectively. Serum lipase and amylase, along with pancreas IL-10, IL-1β, and TNF-α, were measured. For evaluation of oxidative stress, pancreatic superoxide dismutase (SOD), glutathione (GSH), malondialdehyde (MDA), and myeloperoxidase (MPO) were assessed. Histopathological examination for morphologic investigation was conducted. Serum amylase and lipase, as well as TNF-αand IL-1βcytokines, reverted with administration of Q10 in consistence with dosage. In contrast, Q10 assisted in boosting of IL-10 with higher dosage (200 mg/kg). A similar pattern for oxidative stress markers was noticed. Both MDA and MPO levels declined with increased dosage, contrary to elevation of SOD and GSH. Histopathology was in favor of protective effects of Q10. Our findings proved the amelioration of pancreatic injury by Q10, which suggest the anti-inflammatory and antioxidant property of Q10 and its potential therapeutic role.

Download Full-text

P1572EFFECTIVENESS OF COENZYME Q10-MICELLE COMPARED WITH COENZYME Q10 ON TACROLIMUS-INDUCED RENAL INJURY

Nephrology Dialysis Transplantation ◽

10.1093/ndt/gfaa142.p1572 ◽

2020 ◽

Vol 35 (Supplement_3) ◽

Author(s):

Sheng Cui ◽

Kang Luo ◽

Yi Quan ◽

Sun Woo Lim ◽

Chul-Woo Yang

Keyword(s):

Oxidative Stress ◽

Coenzyme Q10 ◽

Renal Injury ◽

Apoptotic Cell ◽

Oxidative Stress Marker ◽

Protective Effects ◽

Sprague Dawley ◽

Male Adult ◽

Sprague Dawley Rats ◽

Pathologic Lesions

Abstract Background and Aims We and others have recently demonstrated that Coenzyme Q10 (CoQ10) has protective effects against diabetes mellitus and various types of renal injury. This study investigated whether CoQ10-micelle treatment would affords superior renoprotection compared with CoQ10 in the governing tacrolimus (Tacrolimus)-induced renal injury in the rats. Method Male adult Sprague-dawley Rats were treated daily with Tacrolimus (1.5mg/kg/day, subcutaneous), CoQ10 (20mg/kg/day, oral), and CoQ10-micelle (20 mg/kg/day, oral) for 4 weeks. The effects of CoQ10 orCoQ10-micelle on Tac-induced renal injury were assessed in terms of renal function, histopathology, oxidative stress and apoptotic cell death. Results After 4 weeks of Tacrolimus treatment to rats caused renal dysfunction, typical pathologic lesions, and oxidative stress marker. The serum creatinine was reduced by Tac co-treatment with CoQ10 or CoQ10-micelle groups compared with the Tac and VH group (0.31 ± 0.03 in the VH group vs. 0.43 ± 0.041 in the Tac group vs.0.37 ± 0.031 in the Tac+CoQ10 group 0.30 ± 0.02123 in the Tac+CoQ10-micellegroup; 1P<0.05 vs. VH. 2P<0.05 vs. TAC. . 3P<0.05 vs. TAC+C.) The administration of CoQ10-micelle improved renal immunoreactivity, which was accompanied by reductions in oxidative stress and apoptosis. Assessment of the mitochondrial ultrastructure by electron microscopy revealed that tacrolimus co-treatment with CoQ10-micelle increased the size and number of mitochondria more than co-treatment with CoQ10, compared with that induced by TAC treatment alone. Conclusion These findings suggest that both CoQ10 and CoQ10-micelle effectively attenuates Tac-induced renal injury, and CoQ10-micelle provides more benefits than that of CoQ10.

Download Full-text

Sulodexide Protects Contrast-Induced Nephropathy in Sprague-Dawley Rats

Cellular Physiology and Biochemistry ◽

10.1159/000452575 ◽

2016 ◽

Vol 40 (3-4) ◽

pp. 621-632 ◽

Cited By ~ 11

Author(s):

Qing Zhao ◽

Jianyong Yin ◽

Zeyuan Lu ◽

Yiwei Kong ◽

Guangyuan Zhang ◽

...

Keyword(s):

Oxidative Stress ◽

Caspase 3 ◽

Vehicle Group ◽

Control Group ◽

Therapeutic Effects ◽

Protective Effects ◽

Sprague Dawley ◽

Contrast Induced Nephropathy ◽

Sprague Dawley Rats ◽

Hk2 Cells

Background: Sulodexide is a powerful antithrombin agent with reno-protective property. However, whether it has beneficial effects on Contrast-Induced Nephropathy (CIN) remained elusive. In the current study, we evaluated the therapeutic effects of Sulodexide on CIN and investigated the potential mechanisms. Methods: CIN model was induced by intravenous injection of indomethacin, followed by Ioversol and L-NAME. Sprague-Dawley rats were divided into 4 groups: control group, CIN group, CIN+vehicle group (CIN rats pretreated with vehicle) and CIN+ Sulodexide (CIN rats pretreated with Sulodexide). Sulodexide or an equivalent volume of vehicle was intravenously delivered 30 min before the induction of CIN. All the animals were sacrificed at 24h after CIN and tissues were harvested to evaluate renal injury, kidney oxidative stress and apoptosis levels. Plasma antithrombin III (ATIII) activities were also measured. Results: Compared to the untreated CIN group, improved renal function, reduced tubular injury, decreased levels of oxidative stress and apoptosis were observed in CIN rats receiving Sulodexide injection. In addition, we also found that ATIII activity was significantly higher in Sulodexide-administered group than that in vehicle-injected CIN rats. For in vitro studies, HK2 cells were exposed to Ioversol and the cyto-protective effects of Sulodexide were also determined. Sulodexide pretreatment protected HK2 cells against the cytotoxicity of Ioversol via inhibiting caspase-3 activity. Preincubation with Sulodexide could also attenuate H2O2-induced increases in ROS, apoptosis and caspase-3 levels. Conclusions: Taken together, Sulodexide could protect against CIN through activating ATIII, and inhibiting oxidative stress, inflammation and apoptosis.

Download Full-text

Antioxidant and Anti-Inflammatory Effects of Curcumin Nanoparticles on Drug-Induced Acute Myocardial Infarction in Diabetic Rats

Antioxidants ◽

10.3390/antiox8100504 ◽

2019 ◽

Vol 8 (10) ◽

pp. 504 ◽

Cited By ~ 9

Author(s):

Boarescu ◽

Bocșan ◽

Gheban ◽

Bulboacă ◽

...

Keyword(s):

Oxidative Stress ◽

Myocardial Infarction ◽

Acute Myocardial Infarction ◽

Creatine Kinase ◽

Serum Levels ◽

Control Group ◽

Protective Effects ◽

Curcumin Nanoparticles ◽

Creatine Kinase Mb ◽

Anti Inflammatory

We have investigated the cardio-protective effects of pretreatment with curcumin nanoparticles (CUN) compared to conventional curcumin (CUS) on the changes in oxidative stress parameters and inflammatory cytokine levels during induced acute myocardial infarction (AMI) in rats with diabetes mellitus (DM). DM was induced with streptozotocin, and AMI with isoproterenol. Eight groups of seven Wister Bratislava rats were included in the study. The N-C was the normal control group, AMI-C was the group with AMI, DM-C was the group with DM, and DM-AMI-C was the group with DM and AMI. All four groups received saline solution orally during the whole experiment. S-DM-CUS-AMI and S-DM-CUN-AMI groups received saline for seven days prior to DM induction and continued with CUS (200 mg/kg bw, bw = body weight) for S-DM-CUS-AMI and CUN for S-DM-CUN-AMI (200 mg/kg bw) for 15 days before AMI induction. The CUS-DM-CUS-AMI group received CUS (200 mg/kg bw), while the CUN-DM-CUN-AMI received CUN (200 mg/kg bw) for seven days prior to DM induction, and both groups continued with administration in the same doses for 15 days before AMI induction. CUS and CUN prevented elevation of creatine kinase, creatine kinase-MB, lactate dehydrogenase in all groups, with better results in the CUN (S-DM-CUN-AMI and CUN-DM-CUN-AMI groups). CUS and CUN significantly reduced serum levels of oxidative stress markers (malondialdehyde, the indirect assessment of nitric oxide synthesis, and total oxidative status) and enhanced antioxidative markers (total antioxidative capacity and thiols, up to 2.5 times). All groups that received CUS or CUN showed significantly lower serum levels of tumor necrosis factor-alpha, interleukin-6, and interleukin-1β. The best antioxidative and anti-inflammatory effects were obtained for the group that received CUN before DM induction (CUN-DM-CUN-AMI group). Pretreatment with CUN proved higher cardio-protective effects exerting an important antioxidative and anti-inflammatory impact in the case of AMI in DM.

Download Full-text

Cacao powder supplementation attenuates oxidative stress, cholinergic impairment, and apoptosis in d-galactose-induced aging rat brain

Scientific Reports ◽

10.1038/s41598-021-96800-y ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Hyoeun Yoo ◽

Hyun-Sook Kim

Keyword(s):

Oxidative Stress ◽

Control Group ◽

Protective Effects ◽

Aging Male ◽

Sprague Dawley ◽

Advanced Glycation ◽

Age Related ◽

Sprague Dawley Rats ◽

Glycation End Products ◽

Aging Rat

AbstractAging, a critical risk factor of several diseases, including neurodegenerative disorders, affects an ever-growing number of people. Cacao supplementation has been suggested to improve age-related neuronal deficits. Therefore, this study investigated the protective effects of raw cacao powder on oxidative stress-induced aging. Male Sprague–Dawley rats were divided into 4 groups: Control (C), d-galactose-induced aging (G), d-galactose injection with 10% (LC), and 16% (HC) cacao powder mixed diet. d-galactose (300 mg/3 mL/kg) was intraperitoneally injected into all but the control group for 12 weeks. Cacao supplemented diets were provided for 8 weeks. The levels of serum Malondialdehyde (MDA), Advanced Glycation End-products (AGEs), brain and liver MDA, the indicators of the d-galactose induced oxidative stress were significantly decreased in LC and HC but increased in G. The Acetylcholinesterase (AChE) activity of brain showed that the cholinergic impairment was significantly lower in LC, and HC than G. Furthermore, the expression levels of catalase (CAT), phospho-Akt/Akt, and procaspase-3 were significantly increased in LC and HC. In conclusion, cacao consumption attenuated the effects of oxidative stress, cholinergic impairment and apoptosis, indicating its potential in future clinical studies.

Download Full-text

Bees’ Honey Attenuation of Metanil-Yellow-Induced Hepatotoxicity in Rats

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2013/614580 ◽

2013 ◽

Vol 2013 ◽

pp. 1-9 ◽

Cited By ~ 1

Author(s):

Abdulrahman L. Al-Malki ◽

Ahmed Amir Radwan Sayed

Keyword(s):

Oxidative Stress ◽

Inflammatory Markers ◽

Histopathological Examination ◽

Fatty Degeneration ◽

Control Group ◽

Cytoplasmic Vacuolization ◽

Liver Injuries ◽

Metanil Yellow ◽

Anti Inflammatory

The present study aims to investigate the protective effect of bees’ honey against metanil-yellow-induced hepatotoxicity in rats. Rats were divided into 7 groups: control group; three groups treated with 50, 100, and 200 mg/kg metanil yellow, and three groups treated with metanil yellow plus2.5 mg·kg-1·day-1bees’ honey for 8 weeks. The obtained data showed that the antioxidant/anti-inflammatory activity of bees’ honey reduced the oxidative stress in the liver tissue and downregulated the inflammatory markers. In addition, the elevated levels of AGE and the activated NF-κB in the metanil-yellow-treated animals were significantly attenuated. Moreover, the levels of TNF-αand IL-1βwere significantly attenuated as a result of bees’ honey administration. Furthermore, the histopathological examination of the liver showed that bees’ honey reduced fatty degeneration, cytoplasmic vacuolization, and necrosis in metanil-yellow-treated rats. In conclusion, the obtained data suggest that bees’ honey has hepatoprotective effect on acute liver injuries induced by metanil-yellowin vivo, and the results suggested that the effect of bees’ honey against metanil yellow-induced liver damage is related to its antioxidant/anti-inflammatory properties which attenuate the activation of NF-κB and its controlled genes like TNF-αand IL-1β.

Download Full-text

Celecoxib Decrease Seizures Susceptibility in a Rat Model of Inflammation by Inhibiting HMGB1 Translocation

Pharmaceuticals ◽

10.3390/ph14040380 ◽

2021 ◽

Vol 14 (4) ◽

pp. 380

Author(s):

Hadeel Alsaegh ◽

Hala Eweis ◽

Fatemah Kamal ◽

Aziza Alrafiah

Keyword(s):

Oxidative Stress ◽

Inflammatory Cytokines ◽

Control Group ◽

Protective Effects ◽

Oxidative Stress Markers ◽

Stress Markers ◽

Inflammatory Models ◽

Anti Inflammatory ◽

Lung And Kidney ◽

Pro Inflammatory Cytokines

The risk of developing epilepsy is strongly linked to peripheral inflammatory disorders in humans. High-mobility group box protein 1 (HMGB1) has the most focus for being a suspect in this scenario. The current study aimed to detect the celecoxib effect, an anti-inflammatory drug, on decreasing seizure susceptibility and organ damage in lipopolysaccharides (LPS)/pilocarpine (PILO) pretreated Wistar rats. Rats were divided into 6 groups (8 each): group 1 (control), group 2 (PILO), group 3 (PILO+LPS), group 4 (PILO+LPS+(VPA) Valproic acid), group 5 (PILO+LPS+Celecoxib), and group 6 (PILO+LPS+VPA+Celecoxib). LPS was used to induce sepsis and PILO to induce seizures. Oxidative stress markers, pro-inflammatory cytokines, and HMGB1 levels in serum and brain homogenate were evaluated. Histopathological studies were conducted on the hippocampus, liver, lung, and kidney. Treatment with celecoxib either alone or in combination with VPA significantly reduced Racine score and delays latency to generalized tonic-clonic seizures onset with a significant decrease in hippocampal levels of pro-inflammatory cytokines, oxidative stress markers, and increase in reduced glutathione. In addition, celecoxib treatment either alone or in combination with VPA suppressed HMGB1translocation into peripheral circulation more than treatment with VPA alone. Furthermore, hippocampus, liver, lung, and kidney histopathological changes were improved in contrast to other epileptic groups. Celecoxib either alone or combined with VPA has antiepileptic and multiorgan protective effects on acute seizures and inflammatory models induced by PILO with LPS. It decreased histopathological findings, oxidative, and inflammatory effects induced by VPA and LPS. This might be due to its anti-oxidative, anti-inflammatory and anti-HMGB1 mediated effects.

Download Full-text

Cardioprotection of Sodium–Glucose Cotransporter 2 Inhibition in Rats With Isoproterenol-Induced Cardiomyopathy

10.21203/rs.3.rs-242853/v1 ◽

2021 ◽

Author(s):

Fang-Zheng Wang ◽

Wen-Bo Wei ◽

Xin Li ◽

Jun-Yu Huo ◽

Wan-Ying Jiang ◽

...

Keyword(s):

Oxidative Stress ◽

Cardiac Function ◽

Cumulative Risk ◽

Left Ventricular ◽

Control Group ◽

Protective Effects ◽

Sprague Dawley ◽

Risk Of Death ◽

Sodium Glucose Cotransporter ◽

Neprilysin Inhibitor

Abstract Background: Sodium-glucose cotransporter 2 inhibitor (SGLT2i) has been reported to improve glycaemic control in patients with type 2 diabetes. The aim of this study was to investigate the effect of SGLT2i Dapagliflozin (Dapa) on cardiomyopathy induced by isoproterenol (ISO) and its potential mechanism.Methods: Fifty male Sprague Dawley rats were randomly assigned to Control (n = 10) and ISO (2.5 mg/kg/day)-treated groups (n = 40). After 2 weeks, 28 survived rats with obvious left ventricular dysfunction in ISO group were randomized into three groups for medication including ARNI (angiotensin receptor neprilysin inhibitor, 68 mg/kg/day, n = 9), Dapa (3 mg/kg/day, n = 9) and ISO (saline, n = 10) for 4 weeks. After that, electrical programmed stimulation (EPS) was performed in all groups for the evaluation of the susceptibility of ventricular arrhythmias (VAs). Echocardiography was used to evaluate cardiac function. Results: Echocardiography revealed significant left ventricular (LV) dysfunction in rats with ISO treatment for 2 weeks compared to the control group. Dapa administration for 4 weeks reduced the cumulative risk of death, myocardial fibrosis, plasma angiotensin II level and its functional receptor AT1R protein expression in the heart, and proinflammatory cytokines levels in the cardiac tissue of ISO-treated rats. It also improved cardiac function and inhibited oxidative stress when compared to the ISO group. These effects were similar to ARNI. However, Dapa showed a greater efficacy than ARNI in reducing left ventricular end-diastolic volume, lowing heart rate and VAs, and decreasing body weight and plasma glucose in ISO-treated rats. Conclusion: Dapa effectively improved the myocardial remodelling and oxidative stress like ARNI in ISO-induced cardiomyopathy in rats, but Dapa may be more effectively in decreasing VAs, and improving cardiac function when compared to ARNI. The mechanisms by which Dapa exerts protective effects on cardiomyopathy may be related to its antioxidant capacity and hypoglycemic action.

Download Full-text

The anti-apoptotic, antioxidant and anti-inflammatory effects of curcumin on acrylamide-induced neurotoxicity in rats

10.21203/rs.2.16758/v1 ◽

2019 ◽

Author(s):

Jie Guo ◽

Xiaolu Cao ◽

Xianmin Hu ◽

Shulan Li ◽

Jun Wang

Keyword(s):

Oxidative Stress ◽

Terminal Deoxynucleotidyl Transferase ◽

Control Group ◽

Tunel Staining ◽

High Dose ◽

Sprague Dawley ◽

Curcumin Treatment ◽

Concurrent Administration ◽

Tnf Α ◽

Anti Inflammatory

Abstract Background: As a chemical extensively used in industrial areas as well as formed during heating of carbohydrate-rich food and tobacco, acrylamide (ACR) has been known as well-established neurotoxic pollutant. Although the precise mechanism is unclear, enhanced apoptosis, oxidative stress and inflammation have been demonstrated to contribute to the ACR-induced neurotoxicity. In this study, we assessed the possible anti-apoptotic, antioxidant and anti-inflammatory effects of curcumin, the most active component in a popular spice known as turmeric, on the neurotoxicity caused by ACR in rats. Methods: Curcumin at the dose of 50 and 100 mg/kg was orally given to ACR- intoxicated Sprague-Dawley rats exposed by ACR at 40mg/kg for 4 weeks. All rats were subjected to behavioral analysis. The HE staining and terminal deoxynucleotidyl transferase mediated dUTP nick end labelling (TUNEL) staining were used to detect histopathological changes and apoptotic cells, respectively. The mRNA and protein expressions of apoptosis-related molecule telomerase reverse transcriptase (TERT) were detected using real-time PCR and immunohistochemistry, respectively. The contents of malondialdehyde (MDA) and glutathione (GSH) as well as the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were measured as the indicators for evaluating the level of oxidative stress in brain. The levels of pro-inflammatory cytokinestumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in cerebral homogenates were detected using ELISA assay. Results: Concurrent administration of curcumin at the oral doses of 50 and 100 mg/kg with ACR significantly protected the rats from ACR-induced weigh loss and motor function deficits, and improved the pathological alterations in the ACR-intoxicated brains. Curcumin treatment especially at a high dose enhanced the TERT mRNA expression level and increased the number of TERT-positive nerve cells in cortex tissues of ACR intoxicated rats. The levels of MDA, TNF-α and IL-1β in the cerebral homogenates were reduced, the contents of GSH as well as the activities of SOD and GSH-Px were increased by curcumin treatment, compared to ACR control group. Conclusions: These data suggested the anti-apoptotic, antioxidant and anti-inflammatory effects of curcumin on ACR-induced neurotoxicity in rats. And maintaining TERT-related anti-apoptotic function might be one mechanism underlying the protective effect of curcumin on ACR-intoxicated brains.

Download Full-text

Hibiscus sabdariffa L. Extract Improved Plasma Catalase Activity but not Malondialdehyde Level in Hind Limb Immobilized Rats

International Journal of Research in Pharmaceutical Sciences ◽

10.26452/ijrps.v11i4.4569 ◽

2020 ◽

Vol 11 (4) ◽

pp. 7827-7832

Author(s):

Zainie Aboo Bakkar ◽

Nooraqilah Rubaai ◽

Nur Afiqah Mahazi ◽

Nurhanisah Hosni ◽

Nik Nur Nadia Nik Mat ◽

...

Keyword(s):

Oxidative Stress ◽

Dna Damage ◽

Catalase Activity ◽

Hind Limb ◽

Control Group ◽

Hibiscus Sabdariffa ◽

Protective Effects ◽

Sprague Dawley ◽

Group Control Group ◽

Limb Immobilization

Disused muscle atrophy (DMA) causes severe problems in aging society especially bedridden people. Oxidative stress is proposed to be involved in the pathogenesis of DMA. Hibiscus sabdariffa L. (HS) or roselle contains high flavonoids, a compound previously shown to be an effective antioxidant, antihypertensive and antidiabetic agent. Thus, the present study investigated the protective effects of HS against oxidative stress in the hind limb of immobilized rats. Twenty-eight male Sprague-Dawley rats were randomly divided into four groups (n=6 per group): Control group received no intervention; Immobilized group received unilateral hind limb immobilization for five days; HS group received 100 mg/kg/bw through oral force feeding for 28 days; Immobilized + HS group received unilateral hind limb immobilization for five days followed by 28-days HS treatment with the same dosage. Blood samples were collected and analysed for DNA damage, lipid peroxidation and oxidative enzyme. Data were presented as mean ± SEM and statistically analysed by ANOVA. The results showed a significant increase in percentage of mild DNA damage after HS treatment in hind limb immobilized rat (Control: 86.5±1.4%; Immobilized: 25.0±5.5%; HS: 37.0±3.5%; Immobilized + HS: 56.7±7.9%, P=0.003). There was also significant increase in plasma catalase activity after HS treatment (plasma [hydrogen peroxide] in Control: 72.5±0.3 µg/ml; Immobilized: 65.1±1.3 µg/ml; HS: 68.3±3.2 µg/ml; Immobilized + HS: 56.5±4.9 µg/ml, P=0.006) but not in plasma malondialdehyde (MDA) level. In conclusion, these findings suggested that HS treatment may prevent oxidative stress-induced DMA in the rats' hind limb immobilization model.

Download Full-text

Dexamethasone and losartan combination treatment protected cigarette smoke-induced COPD in rats

Human & Experimental Toxicology ◽

10.1177/0960327120950012 ◽

2020 ◽

pp. 096032712095001

Author(s):

Samia S Sokar ◽

Esraa H Afify ◽

Enass Y Osman

Keyword(s):

Oxidative Stress ◽

Lung Injury ◽

Cigarette Smoke ◽

Lavage Fluid ◽

Control Group ◽

Chronic Obstructive ◽

Protective Effects ◽

Sprague Dawley ◽

Obstructive Pulmonary Disease ◽

Sprague Dawley Rats

Chronic Obstructive Pulmonary Disease (COPD) is a dangerous prevalent smoking-related disease characterized by abnormal inflammation and oxidative stress and expected to be the third cause of death in the world next decade. Corticosteroids have low effects in decreasing numbers of inflammatory mediators specifically in long-term use. Our study designed to investigate the possible protective effects of combined dexamethasone (Dex) (2mg/kg) and losartan (Los) (30mg/kg angiotensin receptor blocker, it possesses antioxidant and anti-inflammatory properties in lung injury in mice) against cigarette -smoke (CS) induced COPD in rats compared with dexamethasone and losartan. Male Sprague Dawley rats (N = 40) divided into five groups (n = 8): control group, CS group, Dex group, Los group, and Dex +Los group. COPD induced in rats by CS exposure twice daily for 10 weeks. After the specified treatment period, bronchoalveolar lavage fluid (BALF) and lung tissue were collected for measurement of SOD, NO, MDA, ICAM-, MMP-9, CRP, NF-κB and histopathology scoring. Our results indicated that Los+Dex significantly prevent CS-induced COPD emphysema, congested alveoli, and elevation of lung injury parameters in BALF. They also showed a significant decrease in MDA, ICAM-1, MMP-9, CRP, and NF-κB and a significant increase in SOD and NO. In conclusion, adding Los to Dex potentiating their activity in inhibition the progression of COPD based on its activity on oxidative stress, inflammation, and NF-κB protein expression.

Download Full-text