scholarly journals Sinapic Acid Ameliorates Oxidative Stress, Inflammation, and Apoptosis in Acute Doxorubicin-Induced Cardiotoxicity via the NF-κB-Mediated Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-10 ◽  
Author(s):  
Yousef A. Bin Jardan ◽  
Mushtaq Ahmad Ansari ◽  
Mohammad Raish ◽  
Khalid M. Alkharfy ◽  
Abdul Ahad ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Caspase 3 ◽  
Cardiac Tissue ◽  
Interleukin 1 ◽  
Sinapic Acid ◽  
Serum Levels ◽  
Daily Administration ◽  
Control Group ◽  
Group I ◽  
Male Wistar Rats

In the present study, we explored SA’s activity against DOX-induced cardiotoxicity and revealed its underlying mechanisms. Male Wistar rats (weight, 190-210g; n=6) were randomly divided into four groups: group I, normal control; group II, DOX 15 mg/kg via intraperitoneal (ip) route; group III, administered DOX+SA 20 mg/kg; and group IV, administered DOX+captopril (CAP 30 mg/kg). SA and CAP were administered orally for seven days, and DOX (15 mg/kg) was injected intraperitoneally an hour before SA treatment on the fifth day. Forty-eight hours after DOX administration, animals were anesthetized and sacrificed for molecular and histology experiments. SA significantly mitigated the myocardial effects of DOX, and following daily administration, it reduced serum levels of lactate dehydrogenase (LDH) and creatine kinase isoenzyme-MB to near normal values. Levels of oxidative stress markers, glutathione-peroxidase, superoxide dismutase, and catalase, in the cardiac tissue were significantly increased, whereas malondialdehyde levels decreased after SA treatment in DOX-administered rats. Furthermore, DOX caused an inflammatory reaction by elevating the levels of proinflammatory cytokines, tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and endothelin- (ET-) 1, as well as nuclear factor kappa-B (NF-κB) expression. Daily administration of SA significantly repressed TNF-α, IL-1β, ET-1, and NF-κB levels. caspase-3 and Bax expression, bcl-2-like protein and caspase-3 activities and levels. Overall, we found that SA could inhibit DOX-induced cardiotoxicity by inhibiting oxidative stress, inflammation, and apoptotic damage.

scholarly journals Effects of l-Carnitine on the Follicle-Stimulating Hormone, Luteinizing Hormone, Testosterone, and Testicular Tissue Oxidative Stress Levels in Streptozotocin-Induced Diabetic Rats

2018 ◽  
Vol 23 ◽  
pp. 2515690X1879605 ◽  
Author(s):  
Nourollah Rezaei ◽  
Tahereh Mardanshahi ◽  
Majid Malekzadeh Shafaroudi ◽  
Saeed Abedian ◽  
Hamid Mohammadi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Luteinizing Hormone ◽  
Follicle Stimulating Hormone ◽  
Serum Levels ◽  
Diabetic Rats ◽  
Diabetic Group ◽  
Control Group ◽  
Group Vi ◽  
Group I ◽  
Stimulating Hormone

The present study was designed to investigate the antioxidant property of l-carnitine (LC) on serum levels of follicle-stimulating hormone (FSH), luteinizing hormone (LH), testosterone (TH) and testis oxidative stress in streptozotocin (STZ)-induced diabetic rats. The rats were divided into the following groups: group I, control; group II, LC 100 mg/kg/d; group III, diabetic; and groups IV to VI, diabetic rats treated with 50, 100, and 200 mg/kg/d of LC, respectively. Daily injections were given intraperitoneally for 7 weeks. At the end of experimental period, after sacrificing the rats, FSH, LH, TH, total antioxidant capacity (TAC), malondialdehyde (MDA), glutathione (GSH), catalase (CAT), mitochondrial function (MTT), protein carbonyl (PC), and reactive oxygen species (ROS) levels were measured. STZ caused an elevation of MDA, ROS, and PC ( P < .001) with reduction of GSH, CAT, TAC, and MTT ( P < .001) in the serum levels. Group VI had significantly increased FSH, LH, and TH levels versus the untreated diabetic group ( P < .001). Although groups V and VI significantly decreased MDA ( P < .001), PC ( P < .01), and ROS ( P < .01) compared with the untreated diabetic group; only in group VI, the activity of GSH ( P < .001), CAT ( P < .01), TAC ( P < .001), and MTT ( P < .001) significantly increased. The results of the present study suggest that LC decreased diabetes-induced oxidative stress complications and also improved serum level of FSH, LH, and TH by reducing levels of lipid peroxidation and increasing antioxidant enzymes.

scholarly journals Protective Effect of Melatonin Against Radiotherapy-Induced Small Intestinal Oxidative Stress: Biochemical Evaluation

Medicina ◽  
2019 ◽  
Vol 55 (6) ◽  
pp. 308 ◽  
Author(s):  
Ahmed Eleojo Musa ◽  
Dheyauldeen Shabeeb ◽  
Haider Saadoon Qasim Alhilfi
Keyword(s):  
Oxidative Stress ◽  
Protective Effect ◽  
Radical Scavenging ◽  
Common Side Effect ◽  
Control Group ◽  
Intestinal Damage ◽  
Pelvic Malignancies ◽  
Group I ◽  
Male Wistar Rats ◽  
Small Intestinal

Background and Objectives: Radiation enteritis is a common side effect after radiotherapy for abdominal and pelvic malignancies. The aim of the present study was to investigate the protective effect of melatonin, known for its free radical scavenging ability, against radiotherapy-induced small intestinal oxidative damage. Materials and Methods: Thirty male Wistar rats were randomly assigned to six groups (5 rats in each) as follows: Group I (control group) rats received neither radiation nor melatonin; group II rats received only 8 Gy single dose of gamma radiation to their abdomen and pelvis regions; group III (administered with only 50 mg/kg melatonin); group IV (administered with only 100 mg/kg melatonin); group V (50 mg/kg melatonin + 8 Gy radiation), group VI (100 mg/kg melatonin + 8 Gy radiation). All rats were sacrificed after 5 days for biochemical assessments of their intestinal tissues. Results: Treatment with melatonin post irradiation significantly reduced malondialdehyde (MDA) levels as well as increased both superoxide dismutase (SOD) and catalase (CAT) activities of the irradiated intestinal tissues. In addition, melatonin administration with different doses pre irradiation led to protection of the tissues. Moreover, the 100 mg/kg dose was more effective compared to 50 mg/kg. Conclusions: The results of our study suggest that melatonin has a potent protective effect against radiotherapy-induced intestinal damage, by decreasing oxidative stress and increasing antioxidant enzymes. We recommend future clinical trials for more insights.

Protective Effects of Berberine as A Natural Antioxidant and Anti-Inflammatory Agent Against Nephrotoxicity Induced by Cyclophosphamide in Mice

2021 ◽  
Author(s):  
Mohammad Amin Mombeini ◽  
Hadi Kalantar ◽  
Elahe Sadeghi ◽  
Mehdi Goudarzi ◽  
Hamidreza Khalili ◽  
...  
Keyword(s):  
Interleukin 1 ◽  
Kidney Tissue ◽  
Kidney Injury ◽  
Serum Levels ◽  
Stress Factors ◽  
Control Group ◽  
Protective Effects ◽  
Group I ◽  
Tnf Α ◽  
Anti Inflammatory

Abstract Purpose Cyclophosphamide is an alkylating agent with nephrotoxicity that constraints its clinical application. Berberine is an isoquinoline derivative alkaloid with biological functions like antioxidant and anti-inflammatory. The current research intended to examine the nephroprotective impacts of berberine against cyclophosphamide-stimulated nephrotoxicity. Methods Forty animal subjects were randomly separated into five categories of control (Group I). Cyclophosphamide (200 mg/kg, i.p., on 7th day) (Group II), and groups III and IV that received berberine 50 and 100 mg/kg orally for seven days and a single injection of cyclophosphamide on 7th day. Group V as berberine (100 mg/kg, alone). On day 8, blood samples were drawn from the retro-orbital sinus to determine serum levels of blood urea nitrogen (BUN), creatinine (Cr), Neutrophil gelatinase-associated lipocalin (NGAL), and kidney injury molecule-1 (KIM-1) as biomarkers for kidney injury. Nitric oxide (NO), malondialdehyde (MDA) and glutathione (GSH) levels, catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx) activities as oxidative stress factors, tumor necrosis factor- α (TNF-α) and interleukin 1 beta (IL-1β) levels as inflammatory mediators were assessed in kidney tissue. Results The results of this study demonstrated that berberine was able to protect remarkably the kidney from CP-induced injury through decreasing the level of BUN, Cr, NGAL, KIM-1, NO, MDA TNF-α, IL-1β and increasing the level of GSH, CAT, SOD and GPx activities. Conclusion Berberine may be employed as a natural agent to prevent cyclophosphamide-induced nephrotoxicity through anti-oxidant and anti-inflammatory effects.

scholarly journals EVALUATION OF “LEUCAS LANATA” AND ASSESSMENT OF ITS HEPATOPROTECTIVE EFFECTS ON ANTITUBERCULAR DRUG-INDUCED HEPATIC DAMAGE

2018 ◽  
Vol 11 (6) ◽  
pp. 451
Author(s):  
Pritt Verma ◽  
Sajal Srivastava ◽  
Ch. V. Rao
Keyword(s):  
Oxidative Stress ◽  
Interleukin 1 ◽  
Hepatoprotective Activity ◽  
Hepatic Damage ◽  
Control Group ◽  
Antitubercular Drug ◽  
Oxidative Stress Parameter ◽  
Traditional Use ◽  
Toxic Dose ◽  
Group I

Objective: The objective of this study was to investigate the hepatoprotective activity of ethanolic whole plant extract of Leucas lanata (family - Lamiaceae) against rifampicin+isoniazid (RIF+INH) induced hepatic damage in rats.Methods: Wistar rats of either sex were divided into five groups of six animals each and given orally the following treatment for 28 days. The normal control was given 1% CMC 1 ml/kg body weight (b.w.), RIF+INH antitubercular drug (ATT) at a dose of 50 mg/kg b.w., p.o. was given a toxic dose for inducing hepatotoxicity. Silymarin (100 mg/kg, p.o) was given as reference standard. Two different doses of Lucas lanata extract of 200 and 400 mg/kg, p.o were tested for hepatoprotective activity. At the end of the treatment, blood was collected from direct cardiac puncture and analyzed for numerous bodily fluid parameter such as alanine transaminase (ALT), aspartate aminotransferase (AST), alkaline phosphate (ALP), total protein (TP), and total bilirubin (TB) and oxidative stress parameter lipid peroxidation (LPO), superoxide dismutase (SOD), catalase, glutathione (GSH), malondialdehyde and also evaluated the hydroxyproline content, tumor necrosis factor alpha, and interleukin-1 beta in all groups. Livers were isolated for its essential estimation followed by histopathological studies.Results: Hepatic serum markers (ALT, AST, ALP, albumins, TP, and TB) were significant (p<0.01–p<0.001) protective effect was obtained against ATT-induced liver damage, and ATT treatment significantly decreased LPO, SOD, and GSH (p<0.001) levels compared with control Group I and given a Leucas lanata extract (LLE) (p<0.01–p<0.001), the oxidative stress markers were markedly reversed. Histopathology of liver tissue showed that LLE attenuated the hepatocellular necrosis, regeneration, and repair of cells toward normal. LLE which was standardized using high-performance thin-layer chromatography revealed the presence of some critical phenolic (gallic acid and quercetin) compound.Conclusion: The results of this study powerfully indicate the protecting result of LLE against liver injury which can be attributed to its hepatoprotective activity, and thereby scientifically support its traditional use.

scholarly journals Glutathione ameliorates liver markers, oxidative stress and inflammatory indices in rats with renal ischemia reperfusion injury

2018 ◽  
Vol 8 (2) ◽  
pp. 91-97 ◽  
Author(s):  
Hassan Ahmadvand ◽  
Esmaeel Babaeenezhad ◽  
Maryam Nasri ◽  
Leila Jafaripour ◽  
Reza Mohammadrezaei Khorramabadi
Keyword(s):  
Oxidative Stress ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Serum Levels ◽  
Renal Ischemia ◽  
Paraoxonase 1 ◽  
Pon1 Activity ◽  
Control Group ◽  
Group I ◽  
Liver Markers

Introduction: Glutathione (GSH) protects the tissue and cell from oxidative injury. Objectives: In the current study, we investigated the possible effects of GSH on liver markers, oxidative stress and inflammatory indices in rat with renal ischemia reperfusion (RIR) injury. Materials and Methods: Twenty-four adult male Wistar rats were divided into 3 groups (n=8). Group I (the control group), group II (the RIR group) received saline (0.25 mL/d, intraperitoneally; i.p.), group III as the RIR group that received GSH (100 mg/kg/d, i.p.). The treatment with saline or GSH began daily 14 days before RIR induction. RIR was induced by clamping renal pedicles for 45 minutes and 24 hours of reperfusion. Results: RIR significantly increased the serum level of nitric oxide (NO), the serum activities of aspartate aminotransferase (AST), alkaline phosphatase (ALP), gamma-glutamyltransferase (GGT), the serum and renal levels of malondialdehyde (MDA), and the serum activity of myeloperoxidase (MPO). However, RIR significantly decreased the serum and renal levels of GSH, serum paraoxonase 1 (PON1) activity, and the serum and renal activities of catalase (CAT) and glutathione peroxidase (GPX). GSH administration could significantly improve the serum activities of AST, GGT, MPO, GPX and PON1 and serum levels of NO, renal MDA, GSH levels, and serum and also renal CAT activities. Conclusion: Our study indicated that GSH administration ameliorated RIR injury in rats by improving the activities of liver markers and antioxidant enzymes, the levels of MDA, NO, GSH and MPO activity.

In vivo effects of intravenous lipid emulsion on lung tissue in an experimental model of acute malathion intoxication

2018 ◽  
Vol 34 (2) ◽  
pp. 110-118 ◽  
Author(s):  
Murat Uysal ◽  
Serhat Karaman
Keyword(s):  
Oxidative Stress ◽  
Lung Tissue ◽  
Lipid Emulsion ◽  
Caspase 3 ◽  
Control Group ◽  
Albino Rats ◽  
Sod Activity ◽  
Expression Levels ◽  
Intravenous Lipid Emulsion ◽  
Group I

Malathion can be ingested, inhaled, or absorbed through the skin, but acute toxicity is maximized when administered orally. Intravenous lipid emulsion (ILE) treatment is used as a new therapeutic method in cases of systemic toxicity caused by some lipid soluble agents. This study aimed to examine the potential treatment effect of ILE on rat lung tissue in a toxicokinetic model of malathion exposure. Twenty-one adult Wistar albino rats were randomly divided into three equal groups. The groups were organized as group I (control), group II (malathion), and group III (malathion + ILE treatment). Malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) were evaluated in lung tissues. Immunohistochemical and Western blot analyses were performed to determine the bax, bcl-2, and caspase-3 expression levels. Tissue GSH-Px and SOD activities were decreased and MDA levels were increased in the malathion group. ILE administration increased GSH-Px and SOD activity and decreased MDA levels compared to the malathion group. Furthermore, expression of bax, bcl-2, and caspase-3 significantly increased in the malathion group, and ILE infusion reduced these expression levels. The present study revealed that acute oral malathion administration increased oxidative stress and apoptosis in the lung tissue of rats. ILE infusion prevented oxidative stress and decreased the deleterious effects of malathion. Taken together, the findings of our study suggest that lipid emulsion infusion has treatment efficacy on malathion-induced lung toxicity.

scholarly journals Caspase 3 in the pathogenesis of diabetic nephropathy: relationship with NF-κB gene expression and AOPP

2018 ◽  
Vol 9 (SPL1) ◽  
Author(s):  
Ferdous Abass Jaber ◽  
Anwar Jasib Almzaiel ◽  
Nawal khinteel Jabbar
Keyword(s):  
Oxidative Stress ◽  
Diabetic Nephropathy ◽  
Caspase 3 ◽  
Cell Damage ◽  
Colorimetric Method ◽  
Serum Levels ◽  
Control Group ◽  
Control Groups ◽  
Induced Apoptosis ◽  
And Control

Diabetic nephropathy (DN) is the most common and prevalent complication of diabetes mellitus (DM). Persistent hyperglycemia was induced oxidative stress,leading to cell damage and death by apoptosis,and enhanced the development of DN. However,the mechanism by which hyperglycemia induces apoptosis is not well understood. 60 patients (30 patients with Typ2 DM,30 patients with DN) and 30 healthy subjects as control group were enrolled in this study. Serum levels of advanced oxidation protein products (AOPPs) and CAT activity as indirect markers of oxidative stress were measured by the colorimetric method,level of serum caspase-3 as a proapoptotic biomarker was also measured by ELISA. Additionally,expression of the apoptotic genes,nuclear factor-B (NF-κB) in serum was investigated using qPCR. The level of AOPP was significantly increased in DN and DM group than control (P <0.05),while CAT activity in DN significantly decrease (P< 0.05) as compared with DM and control groups. Levels of caspase-3 in DN patients were significantly higher than DM and control groups (𝑃< 0.05),with upregulation of NF-κB mRNA gene expression.This study identified caspase-3 as a final common mediator of high glucose-induced apoptosis and have an important role in DN pathogenesis and progression. Apoptosis seems to be associated with an alteration in inflammatory mediators such as oxidative stress.

scholarly journals The beneficial effect of a phytonutrient-rich product against cadmium chloride-induced hepatorenal toxicity

2021 ◽  
pp. 26-35
Author(s):  
Omotayo Babatunde Ilesanmi ◽  
Ridwan Abiodun Lawal
Keyword(s):  
Oxidative Stress ◽  
Cadmium Chloride ◽  
Wistar Rats ◽  
Hepatic Injury ◽  
Hematological Parameters ◽  
Intraperitoneal Administration ◽  
Control Group ◽  
Group I ◽  
Male Wistar Rats ◽  
Liver And Kidney

Abstract. This study was designed to investigate the hepatorenal protective effects of trévo, on cadmium-induced renal and hepatic injury in male Wistar rats. Methods. Fifteen healthy male Wistar rats were divided into three groups of five rats per group. Group I (control); group II (35mg/kg cadmium chloride (CdCl2); Group III (2 ml/kg trévo+ CdCl2. The rats were treated with trévo (2ml/kg orally) and administered CdCl2 3 hrs later. Twenty-four hours after the last administration rats were sacrificed and blood was collected via cardiac puncture and processed for hematological parameters and assessment of urea, creatinine (CREA), and uric acid (UA), alanine aminotransferase (ALT), aspartate aminotransferase (AST), and albumin (ALB). The liver and kidney were excised and processed for markers of oxidative stress. Results intraperitoneal administration of 35 mg/kg of CdCl2 caused a significant increase in serum concentration of urea, CREA, UA, AST, ALT, while the concentration of ALB was significantly lower (P<0.0001). CdCl2 caused a significant reduction in packed cell volume, hemoglobin while the total white blood cell count, neutrophils, lymphocytes, monocytes, eosinophils, and basophils were increased. Oxidative stress was significantly pronounced in the liver and kidney of rats exposed to CdCl2 as observed in the high concentration of malondialdehyde, decreased concentration of glutathione, the activity of catalase, superoxide dismutase, and glutathione-S-transferase. Pretreatment with trévo was able to significantly prevent the anemic, oxidative damage, renal and hepatic injury initiated by CdCl2. Conclusions. The study reveals that trévo is effective in attenuating cadmium-induced hepatorenal toxicity in male Wistar rats.

scholarly journals Intraperitoneal Administration of Rosuvastatin Prevents Postoperative Peritoneal Adhesions by Decreasing the Release of Tumor Necrosis Factor

2018 ◽  
Vol 91 (1) ◽  
pp. 79-84 ◽  
Author(s):  
Stefan Chiorescu ◽  
Octavian Aurel Andercou ◽  
Nicolae Ovidiu Grad ◽  
Ion Aurel Mironiuc
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Interleukin 1 ◽  
Intraperitoneal Administration ◽  
Serum Levels ◽  
Control Group ◽  
Peritoneal Adhesions ◽  
Group I ◽  
Anti Inflammatory ◽  
Necrosis Factor

Objectives. The purpose of this experimental study was to demonstrate the reduction of peritoneal adhesions formation in rats after intraperitoneal administration of rosuvastatin, due to its anti-inflammatory effect.Method. Peritoneal adhesions were induced in 120 Wistar-Bratislava rats divided into 4 groups (n=30), using a parietal and visceral (cecal) abrasion model. Group I was designated as control group; in group II, a saline solution was administered intraperitoneally; in groups III and IV, a single dose of rosuvastatin solution, 10 mg/kg and 5 mg/kg respectively, was injected intraperitoneally. The serum values of tumor necrosis factor (TNF-α) and interleukin-1 (IL-1α) were determined on day 1 and day 7 postoperatively (ELISA). Macroscopic assessment of the peritoneal adhesions was conducted on day 14.Results. Rosuvastatin therapy induced a significant decrease of tumor necrosis factor serum levels in groups III and IV, on day 1 and day 7 (p<0.01). Intraperitoneal administration of rosuvastatin correlated with a decrease of mean interleukin-1α levels on postoperative day 1 in groups III (p=0.0013) and IV (p=0.00011), but not on day 7, where the differences were no longer statistically significant (p=0.8) The reduction of postoperative peritoneal adhesions in the experimental rat model is supported by the anti-inflammatory effect of rosuvastatin, mediated mainly by the tumor necrosis factor.Conclusions. Rosuvastatin prevents the formation of postoperative peritoneal adhesions in rats. This effect may be linked to the inhibition of proinflammatory cytokines release in the early stages of adhesions formation. The present study suggests that rosuvastatin may be an efficient pharmacological agent in the prevention of postoperative peritoneal adhesions development, and requires further studies as it has a promising application value.

Ameliorative Effect of Cardamom Aqueous Extract on Doxorubicin-Induced Cardiotoxicity in Rats

2018 ◽  
Vol 206 (1-2) ◽  
pp. 62-72 ◽  
Author(s):  
Maha Abu Gazia ◽  
Mohammed Abu El-Magd
Keyword(s):  
Oxidative Stress ◽  
Elevated Serum ◽  
Myocardial Damage ◽  
Serum Levels ◽  
Control Group ◽  
Albino Rats ◽  
Loss Of Function ◽  
Group I ◽  
Ameliorative Effect ◽  
Fiber Deposition

This study was conducted to evaluate the potential cardioprotective effect of cardamom (CAR) against myocardial injuries induced by doxorubicin (DOX) in rats through investigation of histological alterations and the associated oxidative stress, apoptosis, inflammation, and angiogenesis. This study included 30 adult male albino rats that were randomized to 3 groups (n = 10/group): group I (control), group II (DOX) rats injected with DOX (2.5 mg/kg body weight [BW] i.p.) every other day for 2 weeks, and group III (CAR+DOX) received CAR extract (200 mg/kg BW) orally for 3 weeks, and 1 week later (starting from the 2nd week) they were injected with DOX (2.5 mg/kg BW i.p.) every other day for 2 weeks. Rats treated with DOX alone exhibited notable myocardial damage (discontinuity and disorganization of cardiac muscle fibers, mononuclear cell infiltration, and apparent increases in collagen fiber deposition) accompanied by loss of function (revealed by elevated serum levels of lactate dehydrogenase, creatine kinase, and cardiac troponin), induction of oxidative stress (indicated by higher levels of nitric oxide and malon­dialdehyde, and lower levels of superoxide dismutase, catalase, and glutathione peroxidase), apoptosis (evidenced by high caspase 3 activity and immunostaining), and inflammation (marked by high cardiac NFκB level). However, administration of CAR not only ameliorated all deleterious effects of DOX but also induced angiogenesis, as indicated by a significant increase in VEGF immunoreactivity. These data indicate that CAR could relieve DOX-induced cardiotoxicity, at least in part, via reductions in oxidative stress, apoptosis, and inflammation and increased tissue regeneration via induction of angiogenesis. Therefore, CAR could be a promising cytoprotective agent against DOX cardiotoxicity.

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