Tissue Total Antioxidant Capacity Research Articles

The Effects of Thymus Caramanicus Jalas Extract and Its Main Constituent Carvacrol Against Cisplatin-Induced Nephrotoxicity in Mice.

Cisplatin, an anti-cancer chemotherapy drug, has nephrotoxic effects. Thymus caramanicus Jalas (TCJ) has antioxidant effects due to its main components. In the current research, we assessed the impact of TCJ extract and its main compound on cisplatin-induced nephrotoxicity in mice. Forty-two male mice were used in the study. Depending on their group, the animals received saline, carvacrol (10 mg/kg), or TCJ extract (50, 100, and 150 mg/kg) for 10 days. On the fifth day, mice received cisplatin (7.5 mg/kg, i.p.). After 10 days, serum creatinine (Cr) and blood urea nitrogen (BUN) levels were measured. Additionally, malondialdehyde (MDA) and glutathione (GSH) contents, as well as the activity levels of superoxide dismutase (SOD), catalase, and glutathione peroxidase (GPx), and total antioxidant capacity (TAC) were measured in the kidney tissues. The western blotting method was used to determine the kidney's expression of cleaved caspase-3, Bax, Bcl-2, nuclear factor kappa-B (NF-κB), and tumor necrosis factor-alpha (TNF-α). Kidney tissue damage score (KTDS) was assessed using the hematoxylin-eosin (H&E) staining method. Cisplatin significantly increased serum Cr, KTDS, MDA, BUN levels, NF-κB, TNF-α, cleaved caspase-3, and Bax protein expression in the cisplatin group compared to the control group (P < 0.01). Additionally, cisplatin significantly decreased the kidney tissue's TAC and GSH content, activity levels of SOD, catalase, and GPx indicators, and expression of Bcl-2 protein (P < 0.05). TCJ and carvacrol significantly ameliorated these indicators in the cisplatin + TCJ (150 mg/kg) and cisplatin + carvacrol (10 mg/kg) groups compared to the cisplatin group (P < 0.05). TCJ (150 mg/kg) and its main component, carvacrol, could somewhat reduce cisplatin-induced nephrotoxicity through their anti-inflammatory, antioxidant, and anti-apoptotic effects.

MTOR inhibition modulates apoptosis and oxidative stress in hindlimb ischemia/reperfusion injury

Purpose: Ischemia/reperfusion (I/R)-induced injuries represent serious clinical events regarding profound target organ destructions followed by remote organ complications due to the loss of oxidant/antioxidant balance and apoptosis. Recent studies examining the mammalian target of rapamycin (mTOR) during I/R injury in different organs have remained a matter of debate. The current study aimed to explore further the protective and underlying antiapoptotic and antioxidant mechanisms of mammalian target of rapamycin (mTOR) inhibition in hindlimb (HL) schemia/reperfusion (I/R)injury. &#x0D; Materials and Methods: Occlusion of bilateral hindlimbs for 4 h with tourniquets was carried out under anesthesia to induce I/R for 4 h in rats. Rapamycin (1 mg/kg) or saline (4 mL/kg) was injected intraperitoneally 1 h before reperfusion. Gastrocnemius muscle, kidney, and blood were collected at the end of the experiments for analysis. Muscle and kidney damages were evaluated by measuring protein expression and/or phosphorylation of eukaryotic initiation factor 4E-binding protein 1 (4EBP1), ribosomal protein S6 (rpS6), B-cell lymphoma 2 (Bcl-2), caspase-3, and Bcl-2-associated X protein (Bax) with NADPH oxidase level and total antioxidant capacity in tissues or sera. &#x0D; Results: I/R-induced organ damages were demonstrated by enhanced phosphorylation and/or expression of rpS6, 4EBP1, caspase-3, and Bax with a significant reduction in Bcl-2 accompanied by a decreased total antioxidant capacity and increased level of NADPH oxidase. Administration of rapamycin, an inhibitor mTOR, protected against I/R-mediated injuries. &#x0D; Conclusion: Our findings suggest that the activation of mTOR signaling plays a crucial role in HL I/R-triggered organ damages presumably through the activation of apoptosis as a result of oxidant/antioxidant imbalance.

34 Assessing the Ability to Immunomodulate the Innate Immune System and Oxidative Status of Weaned Pigs Through a Prenatal Lipopolysaccharide Challenge

Abstract Gastrointestinal immunity and antioxidant defenses may be bolstered in young animals through prenatal immune system stimulation (PIS), but this is largely uninvestigated in swine. The objective of this experiment was to determine if a low dose of lipopolysaccharide (LPS) administered to late-gestating sows would alter the immune response and oxidative status of subsequent offspring. On d 78 ± 1.8 of gestation, 14 Camborough sows (Parity = 2.6±1.4) of the same farrowing group were blocked by body weight and randomly assigned to one of two treatments: intramuscular injection of saline (CON) or LPS from E. coli O111:B4 (2.5 µg/kg of BW). Sow rectal temperatures (RT) and sickness behavior scores (SBS) were recorded every 0.5 h from -0.5 h to 8 h and every 8 h from 8 to 48 h post-treatment. A subset of 34 weaned barrows (n = 17 CON, LPS; weaning age 21 ± 1.3 d) from the experimental sow group were transported on d -7 to an environmentally controlled facility where they were individually housed with ad libitum access to water and feed. On d -1, pigs were anesthetized for placement of a subcutaneous temperature logger and a jugular catheter. On d 0, all pigs were challenged intravenously with the same LPS strain (10 µg/kg of BW) previously administered to sows. Body temperature was measured at 5-min intervals from the time of logger placement. Blood samples were collected at -2, 0, 1, 2, 4, 6, 8, 12, and 24 h relative to LPS administration at 0 h. After the 24 h blood collection, pigs were necropsied for ileal and jejunal tissue. Plasma samples, jejunal and ileal tissues were analyzed for total antioxidant capacity (TAC) and malondialdehyde (MDA). Data were analyzed as a linear mixed model using PROC MIXED (SAS 9.4) with treatment and time as fixed effects. A dependent covariance structure was used for repeated measurements. Sows administered LPS had elevated RT from 2 to 16-h post-challenge with return to baseline by h 24, indicating mild immune stimulation (treatment × time; P &amp;lt; 0.01). Similarly, sows exposed to LPS had increased SBS from 2 to 3.5 h post-challenge (treatment × time; P &amp;lt; 0.01). Pigs exposed to PIS had greater body temperature than CON at 1 and 2 h post-LPS (treatment × time; P &amp;lt; 0.01). An increase in plasma TAC at 2 and 4 h post-LPS was observed in pigs exposed to PIS relative to CON (treatment × time; P &amp;lt; 0.01). Irrespective of treatment, LPS increased plasma MDA from 2 to 24 h post-challenge (time; P &amp;lt; 0.01). There was no effect of PIS on ileal or jejunal tissue TAC (P ≥ 0.40), but weaned pigs exposed to PIS had decreased jejunal MDA (P &amp;lt; 0.05). Collectively, it appears PIS may alter the innate immune response and oxidative status of the weaned pig during LPS challenge.

Anti-inflammatory and anti-oxidant role of ursolic acid in cerulein-induced acute pancreatitis in rats.

Ursolic acid (UA) is found in many plants, and has been reported to have anti-protease, antioxidant, anti-inflammatory, antimicrobial, nephroprotective, hepatoprotective, and cardioprotective effects. The purpose of this study was to investigate the effects of ursolic acid in cerulein-induced acute pancreatitis (AP). Thirty-two Wistar albino rats were randomly assigned to 4 equal groups: Sham, acute pancreatitis, treatment, and ursolic acid group. Serum amylase levels in the AP and treatment groups were significantly higher than in the others (p < 0.05). In addition, serum IL-1β, IL-6, and TNF-α levels were significantly higher in the AP group in comparison with the treatment group. Although pancreatic tissue total oxidant activity in the AP and treatment groups was similar, pancreatic tissue total antioxidant capacity was significantly higher in the treatment group than in the AP group. Damage to the pancreas and remote organs in AP was observed to be reduced by UA. In addition, oxidative stress was observed to be decreased by the effect of UA.

Association of Oxidative Stress with Kidney Injury in a Hyperandrogenemic Female Rat Model.

Polycystic ovary syndrome (PCOS) is the most common reproductive dysfunction in premenopausal women. PCOS is associated with oxidative stress (OS), which is the main risk factor for renal diseases. This study aimed to investigate the mechanisms responsible for renal injury in a hyperandrogenemic female rat model. This study was conducted from December 2019 to September 2021 at Shiraz Nephro-Urology Research Centre, Shiraz University of Medical Sciences (Shiraz, Iran). Thirty female Sprague-Dawley rats were randomly divided into three groups (n=10), namely control, sham, and dehydroepiandrosterone (DHEA). Plasma total testosterone, plasma creatinine (Cr), and blood urea nitrogen (BUN) levels were measured. In addition, total oxidant status (TOS), total antioxidant capacity (TAC), oxidative stress index (OSI), and histopathological changes in the ovaries and kidneys were determined. Data were analyzed using the GraphPad Prism software, and P<0.05 was considered statistically significant. Plasma total testosterone levels increased by nine-fold in DHEA-treated rats compared to controls (P=0.0001). Administration of DHEA increased Cr and BUN levels and caused severe renal tubular cell injury. In addition, plasma and tissue (kidney and ovary) TAC levels decreased significantly, but TOS levels and OSI values were significantly increased (P=0.019). Significant damage to both glomerular and tubular parts of the kidney and ovarian follicular structure was observed in the DHEA group. Hyperandrogenemia caused systemic abnormalities through OS-related mechanisms and damaged renal and ovarian tissues. DHEA treatment in rat models is recommended to study the mechanisms that mediate PCOS-associated renal injury.

Resveratrol attenuates cardiac function impairment in plateau hypobaric hypoxia rats

Objective: To study the protective effects of resveratrol (RSV) on cardiac function in rats with high altitude hypobaric hypoxia and its mechanisms. Methods: Thirty-six rats were randomly divided into control group, hypobaric hypoxia group (HH) and hypobaric hypoxia + RSV group (HH+RSV) according to the random number, 12 rats in each group. Rats in the HH and HH+RSV groups were subjected to chronic long-term high altitude hypobaric hypoxia intervention for 8 weeks in a hypobaric chamber at a simulated altitude of 6 000 m for 20 h / d. The rats of HH + RSV were fed with RSV at a dose of 400 mg/(kg·d). The rats were tested once a week for body weight and twice a week for food intake. Before execution, the rats were tested by blood cell analyzer for routine blood parameters and echocardiogram for cardiac function parameters in each group. The routine blood indexes of each group were measured by blood cell analyzer, the cardiac function indexes of each group were measured by echocardiography, myocardial hypertrophy was evaluated by HE staining, myocardial tissue reactive oxygen levels were evaluated by dihydroethidium (DHE) staining. Oxidative stress was evaluated by serum and myocardial tissue total antioxidant capacity (T-AOC), superoxide dismutase activity (SOD) and malondialdehyde (MDA) content. Results: Compared with the C group, the body mass and food intake of rats were decreased significantly (P＜0.05) in HH group, while compared with the C group, RSV had no significant effects on the body mass and food intake of rats in the HH+RSV group (P＞0.05). Compared with the C group, the levels of erythrocytes and hemoglobin of rats in the HH group were increased significantly (P＜0.05), while the platelet concentration was decreased significantly(P＜0.05); compared with the HH group, the erythrocyte and hemoglobin levels were decreased significantly (P＜0.05) and platelet concentration was increased significantly(P＜0.05) in rats of the HH+RSV group. Compared with the C group, the cardiac coefficient, myocardial fiber diameter and thickness were significantly increased in the HH group (P＜0.05); compared with the HH group, the cardiac coefficient and myocardial fiber thickness were significantly decreased in the HH+RSV group (P＜0.05). Echocardiographic analysis showed a significant increase in ventricular wall thickness (P＜0.05) and a significant decrease in ejection fraction and cardiac output (P＜0.05) in the HH group compared with the C group, and a significant decrease in ventricular wall thickness and a significant improvement in cardiac function (P＜0.05) in the HH+RSV group compared with the HH group. The results of DHE staining showed that myocardial tissue reactive oxygen levels were increased significantly in the HH group compared with the C group (P＜0.05); myocardial tissue reactive oxygen levels were significantly restored in the HH+RSV group compared with the HH group (P＜0.05). The oxidative/antioxidant results showed that the serum and myocardial T-AOC and SOD activities were decreased significantly (P＜0.05) and the MDA level was increased significantly (P＜0.05) in the HH group compared with the C group; the serum and myocardial T-AOC and SOD activities were increased significantly (P＜0.05) and the MDA level was decreased significantly(P＜0.05) in the HH+RSV group compared with the HH group. Conclusion: Long-term plateau hypobaric hypoxia exposure leads to myocardial hypertrophy and reduced cardiac function in rats. Resveratrol intervention significantly improves myocardial hypertrophy and cardiac function in rats caused by altitude hypobaric hypoxia exposure, which is closely related to reducing of reactive oxygen species and improving myocardial oxidative stress levels.

MO279: Vitamin D Supplementation Attenuates Hyperandrogenemia-Associated Acute Kidney Injury in Female Sprague-Dawley Rats

Abstract BACKGROUND AND AIMS Polycystic ovary syndrome (PCOS) is closely related to the onset and development of metabolic abnormalities. However, the correlation between PCOS and kidney injury has not been clarified, and the underlying mechanism remains unknown. Vitamin D therapy has beneficial effects in women with PCOS and renal injuries. Therefore, this study was designed to explain the mechanisms responsible for kidney damages in a model of hyperandrogenic rats and the healing effects of vitamin D. METHOD Female Sprague-Dawley rats were randomly divided into five groups (n = 10): (i) control, (ii) sham, (iii) dehydroepiandrosterone (DHEA, 6 mg/100 g day-1 S.Q.), (iv) DHEA + vitamin D (1000 IU/Kg; 3 days/week), and (v) vitamin D. Plasma total testosterone, plasma creatinine (Cr), blood urea nitrogen (BUN), plasma and tissue levels of total oxidant status (TOS), total antioxidant capacity (TAC) and oxidative stress index (OSI), and histopathological changes of ovary and kidney were determined. RESULTS Plasma testosterone increased 9-fold in DHEA-treated rats compared with controls. They also had increased Cr, BUN, and severe renal tubular injury. Plasma and tissue TAC levels showed significant decreases, whereas TOS and OSI showed significant increases in the DHEA group. A significant injury in the glomerular and tubular parts of the kidney and ovarian follicular structure was observed in DHEA-administered rats. Vitamin D treatment attenuated TOS levels and significantly improved TAC levels. Kidneys and ovaries histopathological changes were significantly improved by vitamin D treatment. CONCLUSION Hyperandrogenemia causes systemic abnormalities through oxidative stress-related mechanisms, followed by obvious destruction to renal and ovarian tissues. Vitamin D supplementation attenuated these hyperandrogenemia-associated acute kidney injuries.

Guanosine protects against glycerol-induced acute kidney injury via up-regulation of the klotho gene.

Objective(s):Acute Kidney Injury (AKI) is characterized by a rapid and reversible decline in renal function with a rapid decrease in Glomerular Filtration Rate (GFR), which is associated with high mortality. Rhabdomyolysis accounts for 10–40% of AKI, to which the therapeutic approach is limited. Klotho is a protein that modulates sodium-phosphate co-transporters, ion channels that have been reported to have a renal protective effect. Guanosine, a purine nucleoside, has already been reported to have a renal protective effect; however, the mechanism of such protection and its relation to Klotho modification has not been evaluated yet. This study aims to evaluate the mechanism of the protective effect of guanosine against rhabdomyolysis-induced AKI and its relation to the expression of the Klotho gene.Materials and Methods:In the current study, rats were divided into three groups: control, glycerol-induced AKI, and guanosine-treated. Serum urea and creatinine levels, renal tissue Total Antioxidant Capacity (TAC), and Klotho and Cystatin C genes expression were evaluated. Furthermore, caspase-3 immunostaining and histopathological evaluations were done. Results:Results showed that guanosine treatment resulted in a significant reduction in serum urea and creatinine, Cystatin C genes expression, and caspase-3 immunoexpression, and an increase in TAC and Klotho genes expression. Results also revealed an improvement of renal histopathology when compared with the glycerol-induced AKI group. Conclusion:Guanosine may be a promising agent in the treatment of rhabdomyolysis-induced AKI. The proposed mechanism for guanosine may be through its ability to enhance Klotho gene expression in renal tissue, with subsequent antioxidant and anti-apoptotic activity.

Effects of Stevia rebaudiana Bertoni extracts in the rat model of epilepsy induced by pentylenetetrazol: Sirt-1, at the crossroads between inflammation and apoptosis.

The current study investigated the effects of stevia extracts on a PTZ-induced epileptic rat model and its potential mechanism. Thirty male Sprague-Dawley rats were equally subdivided into 3 groups; (1) normal control (NC) group, (2) PTZ-group: received PTZ (50 mg/kg, i.p. every other day) for 2 weeks, and (3) PTZ+ Stevia group: received PTZ and stevia (200 mg/kg orally daily) for 4 weeks (2 weeks before the start of PTZ treatment and 2 weeks with PTZ administration). The first jerk latency and the seizure score were assessed in rats. Also, brain tissue samples were collected by the end of the experiment, and oxidative stress markers (catalase, MDA, and total antioxidant capacity (TAC)) were measured by biochemical analysis in hippocampal brain homogenates. Also, in the hippocampus, the expression of IL6 and Bcl-2 at the mRNA level and expression of Sirt-1, P53, caspase-3, GFAP, and NF-kB in CA3 hippocampal region by immunohistochemistry was investigated. PTZ substantially increased the seizure score and decreased the seizure latency. Also, PTZ significantly increased MDA, GFAP, IL-6, NF-kB, caspase-3, and p53 and significantly reduced Sirt-1, TAC, and Bcl-2 in hippocampal tissues compared to the control group (p < 0.01). However, Stevia Rebaudiana Bertoni (Stevia R.) significantly attenuated the PTZ-induced seizures, improved oxidative stress markers, downregulated GFAP, IL-6, NF-kB, caspase-3, and p53, and upregulated Sirt-1 and Bcl-2 in the CA3 hippocampal region (p < 0.01). In conclusion, Stevia R. exhibits neuroprotective and antiepileptic actions in PTZ-induced epilepsy due to its antioxidant, anti-apoptotic, and anti-inflammatory effects. Additionally, the Sirt-1 pathway might be involved in the antiepileptic and neuroprotective effects of stevia in PTZ-kindled epileptic rat model.

Protective Effects of Quercetin on Clothianidin-Induced Liver Damage in the Rat Model.

Clothianidin (CTD) is a member of the neonicotinoid group of insecticides. This study was performed to determine the effect of quercetin on clothianidin-induced liver injury (CTD) in rats. Rats were randomly assigned to a normal control (saline), a CTD control-treated group (20 mg/kg) every 3 days for 21 days, and CTD + quercetin-treated groups (2.5, 5, and 10 mg/kg) for 35 days intraperitoneally. Enzyme activity, including alanine aminotransferase (ALT) and aspartate aminotransferase (AST), was measured by spectrophotometry in serum samples by an automatic biochemical analyzer using commercial kits. Total antioxidant capacity (TAC), malondialdehyde (MDA), and nitrate-nitrite were measured in homogeneous liver tissue samples of animals. A significant increase in ALT and AST enzyme activity was observed in the CTD group in comparison with that of the control groups. In the clothianidin + quercetin (10 mg/kg) group, the ALT and AST enzyme levels decreased compared to the clothianidin control group significantly (P < 0.05). The MDA value of the liver increased in the clothianidin-treated group compared to that of the control groups (P < 0.05). Decreased tissue TAC level was observed in the CTD-treated group in comparison with that of the control groups (P < 0.05). The MDA level of the liver decreased in the clothianidin + quercetin (10 mg/kg) group compared to that of the CTD control group (P < 0.05). Quercetin significantly raised the level of TAC in the liver tissue of the clothianidin + quercetin (10 mg/kg) treated group compared to that of the clothianidin control group (P < 0.05). Liver nitrate-nitrite measurement showed a significant increase in the clothianidin group compared to that of the normal control group (P < 0.05). Nitrate-nitrite level in the liver was decreased in clothianidin + quercetin (10 mg/kg) compared to that of the clothianidin control group significantly (P < 0.05). Histopathological investigation revealed that contact to the CTD induced tissue disorganization and inflammatory cell infiltration, but minor histopathological alterations in the liver tissues of rats treated with CTD and quercetin (10 mg/kg) were detected.

Protective effect of astaxanthin on experimental ovarian damage in rats.

This study aimed to investigate the protective effect of astaxanthin (AS) on 3-nitropropionic acid (3-NPA) induced experimental ovarian damage in rats. Thirty two female Wistar rats were divided into four equal groups of eight each: control group (C); phosphate-buffered saline, AS group; AS (80 mg/kg) for 14 days, 3-NPA group; 3-NPA (6.25 mg/kg) twice a day for 7 days, 3-NPA + AS group; administered AS (80 mg/kg) for 14 days and 3-NPA (6.25 mg/kg) for 7 days. All injections were administered intraperitoneally. Rats were fed ad libitum with standard rat chow and tap water. Plasma and ovarian tissue total antioxidant capacity (TAC), total oxidant capacity (TOC) and oxidative stress index (OSI) levels, whole blood reduced glutathione (GSH), plasma paraoxonase 1 (PON1) activity, lipid profile, malondialdehyde (MDA), nitric oxide (NO), total sialic acid (TSA) and total thiol (TT) concentrations were analysed spectrophotometrically. Also, ovarian tissue histopathology was performed. We observed 3-NPA-induced histopathological ovarian damagesignificantly decreased the TAC (p < 0.001), GSH (p < 0.001), high-density lipoprotein (p < 0.01) levels and PON1 activity (p < 0.01), and significantly increased TOC, OSI (p < 0.001), MDA, NO, TSA, cholesterol, low-density lipoprotein (p < 0.01) and triglyceride (p < 0.05) levels. In conclusion, cotreatment with AS restored the negative effect of 3-NPA on all biochemical parameters cited above and improved the histopathological ovarian damage. Ovarian toxicity induced by 3-NPA might be due to oxidative damage. The improvement of AS seems to be related to its antioxidant properties.

Nano-Seleniumoxide nanoparticles affect lipid peroxidation and tissue total antioxidant capacity (TAC) in skin injury

Nano-Seleniumoxide nanoparticles affect lipid peroxidation and tissue total antioxidant capacity (TAC) in skin injury

Anti-oxidant impact of Lisinopril and Enalapril against acute kidney injury induced by doxorubicin in male Wistar rats: involvement of kidney injury molecule-1

Doxorubicin (DOX) is a standard anticancer agent exerting devastating effects as nephrotoxicity, hepatotoxicity and cardiotoxicity. The purpose of this study was to increase the clinical use of DOX through decreasing its detrimental effects via combination with ACE inhibitors to ameliorate the induced acute kidney injury (AKI). AKI was induced by a single injection of DOX (7.5 mg/kg; i.p.) as Group 1; control (vehicle), Group 2; DOX (7.5 mg/kg; i.p.) single dose, Group 3 and 4; Lisinopril (Lis, 20 mg/kg) and Enalapril (Enal, 40 mg/kg) orally administration for 15 consecutive days after DOX injection, respectively. Serum samples were used to measure creatinine and BUN, tissue samples were extracted to determine myeloperoxidase (MPO), malondialdehyde (MDA), total antioxidant capacity (TAC) and kidney injury molecule (KIM-1) using ELISA technique. Heme oxygenase (HO-1) RNA expression was quantified in tissue using real time polymerase chain reaction (PCR). Parts of the kidney tissue were kept in formalin for immunohistochemical demonstration of Cleaved Caspase-3 and NF-κβ immune staining and the other part was used for pathological examination. Oral treatment with Lis (20 mg/kg) and Enal (40 mg/kg) for 15 consecutive days reversed DOX effects as they reduced the serum creatinine and BUN, kidney levels of MPO and MDA, whereas the drugs increased tissue TAC. The administration of Lis and Enal with DOX also reduced KIM-1and HO-1 RNA expression. A significant decrease in cleaved caspase-3 and NF-κβ immunostainings in conjunction with pronounced amelioration in pathologies in the rat kidney were observed. We concluded that DOX adverse effects can be controlled by Lis and Enal.

Accelerated healing by topical administration of Salvia officinalis essential oil on Pseudomonas aeruginosa and Staphylococcus aureus infected wound model

BackgroundSalvia officinalis L. (Lamiaceae) is known to have antibacterial properties possibly conducive to the healing process of infected wounds. PurposeThe present study aimed to evaluate the effects of an ointment containing Salvia officinalis essential oil (SOO) on an infected wound model. MethodsEssential oil hydrodistillated from the dried leaves of the plant was analyzed by GC-FID and GC–MS. After creating two full-thickness cutaneous wounds, mice were classified into four groups, control, and animals treated with 2 % mupirocin® (standard positive drug), and 2 % and 4 % (w/w) of SOO. In order to evaluate the effects of SOO on the wound healing phases, the expression levels of interleukin-6 (IL-6), interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), cyclin-D1, Bcl-2, fibroblast growth factor-2 (FGF-2) and vascular endothelial growth factors (VEGF) were analyzed using qRT-PCR. Immunohistochemistry analysis, tissue total antioxidant capacity (TAC) and malondialdehyde (MDA) were further assessed in all groups. ResultsConcerning essential oil, the main compounds were found to be cis-thujone (26.8 %), camphor (16.4 %), trans-thujone (14.1 %) and 1,8-cineole (10.8 %). Our findings showed that the topical application of SOO was able to shorten the inflammatory phase and accelerate the cellular proliferation, re-vascularization, collagen deposition and re-epithelialization in comparison to the control group (p < 0.05). Moreover, increased mRNA levels of FGF-2 and VEGF, and up-regulation of cyclin-D1 and Bcl-2 were observed following the topical application of SOO compared to the control group (p < 0.05). The expression levels of IL-6, IL-1β and TNF-α were reduced in animals treated with SOO on days 3, 7 and 14 (p < 0.05). ConclusionsAdministration of SOO increased the TAC level and reduced the MDA content and levels of IL-1β and TNF-α. It is concluded that SOO is able to accelerate the wound healing process by regulating the expression of pro-inflammatory cytokines, growth factors, and antioxidant properties.

Differences in oxidative stress across seasons and ability to cope with environmental mismatch in muscle and brain of black‐capped chickadees Poecile atricapillus and rock pigeons Columba livia

Resident birds in temperate areas respond to seasonally fluctuating temperatures by adjusting their physiology so as to match thermogenic requirements of their environment. Climate change is predicted to increase the frequency of heat waves, increasing the likelihood that birds will face environmental mismatch. Changes in BMR due to seasonality or anomaly events should show effects to the oxidative stress system. We examined the effects of chronic and acute heat exposure on muscle and brain tissue total antioxidant capacity, enzymatic activities of catalase (CAT) and glutathione peroxidase (GPx) and lipid peroxidation (LPO) damage in two temperate bird species of differing body masses and ecological strategies, the black‐capped chickadee Poecile atricapillus and the rock pigeon Columba livia, across three seasons. We found that heat stress did not alter oxidative stress in either species or tissue. But, in muscle, rock pigeons and black‐capped chickadees demonstrated similar seasonal changes where peroxyl scavenging capacity was highest in the fall, hydroxyl scavenging capacity was higher in fall and summer. CAT activity was lowest in the fall and highest in the summer, GPx activity was highest in the fall, and LPO damage was highest in the summer but lowest in the fall. In brain, we found that scavenging capacity to hydroxyl radicals was highest in fall and summer for rock pigeons, whereas it was only elevated in the summer for black‐capped chickadees. Our data suggest that the oxidative stress system is slow to change seasonally.

Effect of Vitamin D Supplementation on Doxorubicin-Induced Cardiotoxicity in Rats

Abstract Background Doxorubicin-induced cardiotoxicity is a worldwide problem. Vitamin D is a well-known beneficial vitamin for bone growth and calcium homeostasis but recently it is also known for its cardioprotective effects. The aim of this study is to investigate the potential protective role of vitamin D on the cardiac dysfunction induced by chronic doxorubicin exposure, and to throw more light on the possible underlying mechanism (s) for such effect. Materials and Methods: 70 female Albino-rats were divided into 4 groups; control group (C), Doxorubicin-treated group (Dox): given i.p. injection of Dox in a dose of 2.5 mg/kg body weight (cumulative dose: 15 mg/kg) over 3 weeks, vitamin Dsupplemented group (Vit D): given vitamin D by oral gavage in a dose of 500 IU/kg daily, 5 days a week, also for 3 weeks and the combined Doxorubicintreated+vitamin D-supplemented group (Dox+Vit D). At the end of the experiment, ECG was recorded and in vitro isolated heart study was performed on Langendoroff preparation to measure peak tension (PT), time to peak tension (TPT), half relaxation time (HRT) and myocardial flow rate (MFR). Body and cardiac weights, plasma levels of brain naturetic peptide (BNP), cardiac troponin I (cTnI), vitamin D and total calcium and cardiac tissue heat shock protein 20, total antioxidant capacity (TAC) and malondialdehyde (MDA) were measured. Also, cardiac tissues were histopathologically assessed. Results: Dox-treated rats showed significant decrease in the final body weight (fBW), significant prolongation of the P-R interval, QRS duration, observed Q-T (Q-TO) and corrected Q-T (Q-Tc) with significant depression of the R voltage. In addition, there was a significant decrease in the in vitro heart rate, significant depression in PT, PT/LV and MFR together with significant prolongation in TPT&amp; 3 HRT. These changes were accompanied by significant elevation of plasma BNP, cTnI and in cardiac tissue MDA and a significant decrease in plasma vit D, total calcium and cardiac tissue TAC and HSP20. Histopathological examination revealed markedly distorted muscle fibers with indistinct cell borders, bright eosinophilic cytoplasm, intra-cytoplasmic vacuoles and small pyknotic nuclei or absent nuclei, together with interstitial edema &amp; aggregates of inflammatory cells and thick irregular collagen fibers in between the muscle fibers. Concomitant supplementation of vitamin D to the doxorubicin treated rats resulted in significant decrease in PR interval, QRS duration, MDA and significant increase PT, PT/LV, MFR, MFR/LV, plasma vitamin D, total calcium and TAC compared to the Dox treated rats to be insignificantly different from the control group. Plasma BNP and cTnI were significantly decreased while cardiac HSP20 was significantly increased compared to the Dox-treated rats, yet these parameters were still significant from the control group. Meanwhile, fBW, Q-TO and Q-Tc intervals, and TPT remained insignificantly changed from the DOX group. These findings were associated by regaining the normal collagen fiber distribution between cardiac muscle fibers with resolution of interstitial edema. Conclusion: Vitamin D supplementation can partially mitigate cardiac dysfunction induced by chronic doxorubicin by improving the cardiac antioxidant state and heat shock protein 20 level. Key words: Doxorubicin, cardiac dysfunction, vitamin D, isolated heart studies, BNP, HSP20.

Topical application of Cinnamon verum essential oil accelerates infected wound healing process by increasing tissue antioxidant capacity and keratin biosynthesis.

Cinnamon essential oil is known to have antioxidant and antibacterial properties, which may accelerate, wound healing. This study was conducted to evaluate the effects of an ointment prepared from Cinnamon verum essential oil (C verum) in infected wound model. An experimentally excisional infected wound model was induced in mice. Circular excisional wound model of 5 mm surface area was surgically created and inoculated with 107 CFU of each of two bacterial strains of Staphylococcus aureus and Pseudomonas aeruginosa. The animals were divided into three groups and topically treated with soft yellow paraffin (control) and ointments containing 2% and 4% C verum. The mRNA levels of insulin-like growth factor I (IGF-1), fibroblast growth factor-2 (FGF-2) and vascular endothelial growth factor (VEGF), epidermal keratin, fibroblasts, fibrocytes, immune cells, and vascular distribution as well as epithelialization ratio were investigated in order to evaluate the effects of C verum on wound healing. Tissue total antioxidant capacity and malondialdehyde levels (MDA) were also evaluated. Topical administration of C verum remarkably shortened the inflammatory phase, increased fibroblast distribution, collagen deposition, and accelerated the cellular proliferation, reepithelialization and keratin synthesis. The mRNA levels of IGF-1, FGF-2 and VEGF were remarkably higher in C verum-treated groups (especially 2%) in comparison control group. Topical administration of C verum increased antioxidant power and reduced MDA content in comparison to control animals. C verum accelerates wound healing by upregulating the IGF-1, FGF-2, and VEGF expression and increasing cell proliferation, collagen synthesis, and reepithelialization ratio.

Activation of Liver X Receptors by GW3965 Attenuated Deoxycorticosterone Acetate-Salt Hypertension-Induced Cardiac Functional and Structural Changes.

In this study, the effect of liver X receptor (LXR) activation on hypertension-induced cardiac structural and functional alterations was investigated. Hypertension was induced by deoxycorticosterone acetate (DOCA)-salt administration in uninephrectomized rats for 6 weeks. LXR agonist GW3965 (3-{3-[(2-chloro-3-trifluoromethyl-benzyl)-(2,2-diphenyl-ethyl)-amino]-propoxy}-phenyl)-acetic acid was given for the past week. Rhythmic activity and contractions of the isolated heart tissues were recorded. Biochemical parameters were assessed in ventricular tissue and plasma samples. Cardiac expressions of various proteins were examined, and histopathological evaluation was performed in the left ventricle and liver. GW3965 reduced systolic blood pressure and enhanced noradrenaline-stimulated papillary muscle contraction induced by DOCA-salt + uninephrectomy. Plasma and tissue total antioxidant capacity (TAC) increased and tissue 4-hydroxynonenal (4-HNE) levels decreased in the DOCA-salt group. GW3965 elevated plasma and tissue TAC levels in both of groups. Glucose-regulated protein-78 (GRP78), phospho-dsRNA-activated-protein kinase-like ER kinase (p-PERK), matrix metalloproteinase-2 (MMP-2), and nuclear factor-κB p65 (NF-κB p65) expression was augmented, and inhibitor-κB-α (IκB-α) expression was reduced in hypertensive hearts. The altered levels of all these markers were reversed by GW3965. Also, GW3965 ameliorated DOCA-salt + uninephrectomy-induced cardiac and hepatic inflammation and fibrosis. However, GW3965 unchanged the plasma lipid levels and hepatic balloon degeneration score. These results demonstrated that LXR activation may improve hypertension-induced cardiac changes without undesired effects.

Kumiss Supplementation Reduces Oxidative Stress and Activates Sirtuin Deacetylases by Regulating Antioxidant System

It was aimed to investigate the effects of kumiss a fermented mare horse beverage on the sirtuin deacetylases in the oxidative stress which had been induced by 1,2-dimethyl hydrazine (DMH). Forty BALB/C male mice were divided into four groups as control, kumiss (2 × 108 cfu/mL), DMH (20 mg/kg), and kumiss + DMH (2 × 108 cfu/mL + 20 mg/kg). At the end of 20-week regimen, SIRT2, SIRT3 protein expressions by western blotting, immunolocalizations, and inhibitory anti-oxidant activity analysis in liver, colon, and kidney tissues were performed. SIRT2 and SIRT3 expressions in DMH group were decreased in liver, colon, and kidney tissues and the decrease further stimulated by kumiss reinforcement. SIRT3, a mitochondrial protein, immunostaining increased in cell nuclei of tissues in response to kumiss treatments. The oxidative stress induced by DMH was determined to increase plasma 8-OH-2-deoxyguanosine, tissue oxidative stress index, and total oxidant capacity levels. Kumiss supplement was identified to reduce these levels and increase tissue total antioxidant capacity and reduced glutathione levels. Clarifying the molecular relationship between intracellular changes in the locations of SIRT2 and SIRT3 and oxidative stress might be important with regards to developing new medical treatments in the future. The kumiss may show a protective effect against DMH-induced damage by regulating the expression of sirtuin proteins and by protecting antioxidant system.

Biochemical Study of Gender Effect on Thyroid Cancer in the Egyptian Population

Background and Objective: Thyroid is one of the largest glands; its hormones affect almost every cell in the body, the incidence of thyroid cancer has raised in recent years, About 52,070 new cases of thyroid cancer in the United States in 2018 only. This study was undertaken to determine if gender was associated with susceptibility of thyroid cancer.&#x0D; Materials and Methods: This study was carried out on 174 cases divided into 108 thyroid patients and 66 healthy as controls. The mean age of cases was (40.58±1.46) they include 48 female and 18 males. All participants were subjected to an estimation of thyroid stimulating hormone (TSH), free thyroxine (FT4), total antioxidant capacity (TAC), in addition to malondialdehyde (MDA).&#x0D; Results: For TSH results that was an obvious effect of gender on TC, while for FT4 there was an effect of gender on thyroiditis and TC, for TAC there was a biting effect on thyroiditis and TC, for MDA there was an effect also on thyroiditis and TC, for tissue TAC (TTAC) that was a clear effect of gender on both thyroiditis and TC, and for TMDA there was a little effect.&#x0D; Conclusion: Gender of TC patients effects on biochemical investigations of the thyroid.