scholarly journals Curcumin Prevents Cyclophosphamide-Induced Lung Injury in Rats by Suppressing Oxidative Stress and Apoptosis

Processes ◽  
2020 ◽  
Vol 8 (2) ◽  
pp. 127 ◽  
Author(s):  
Sultan A. M. Saghir ◽  
Sulaiman A. Alharbi ◽  
Maged A. Al-Garadi ◽  
Naif Al-Gabri ◽  
Hagar Y. Rady ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Caspase 3 ◽  
Protein Carbonyl ◽  
Albino Rats ◽  
Protective Effects ◽  
Pulmonary Injury ◽  
Pharmacological Activities ◽  
Ancient Times ◽  
Inflammatory Edema ◽  
Alveolar Septa

Curcumin (CUR) has been used since ancient times to treat several ailments as it possesses many pharmacological activities. This study intended to explore the mechanism underlying the protective effects of CUR in remodeling oxidative stress and apoptotic signals in cyclophosphamide (CP)-induced pulmonary injury in albino rats. CUR was administered at a dose of 300 mg/kg/day for 7 days and on the seventh day a single dose of CP (200 mg/kg) was given. Histopathological and ultrastructural examinations of CP-intoxicated rats showed complete alveolar obstruction, thickened inter-alveolar septa, enlarged blood vessels, severe inflammatory edema with pyknotic nuclei, and disappearance of cytoplasmic organelles. Significant increases in caspase-3, malondialdehyde (MDA), and protein carbonyl (PCO) and significant decreases in superoxide dismutase (SOD) and glutathione peroxidase (GPx) were observed. In contrast, rats that received CUR showed clear and empty lumina with single row of pneumocytes, disappearance of edema, and no interstitial electron dense bodies in rats’ lung tissues. Additionally, CUR significantly reduced caspase-3, MDA, and PCO and increased SOD and GPx. In conclusion, these findings revealed the protective effects of CUR against CP-induced pulmonary injury in rats through suppressing oxidative damage and apoptosis.

Attenuation of erythrocyte membrane oxidative stress bySesbania grandiflorain streptozotocin-induced diabetic rats

2015 ◽  
Vol 93 (4) ◽  
pp. 385-395 ◽  
Author(s):  
Chandrabose Sureka ◽  
Thiyagarajan Ramesh ◽  
Vavamohaideen Hazeena Begum
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Blood Glucose ◽  
Erythrocyte Membrane ◽  
Osmotic Fragility ◽  
Diabetic Rats ◽  
Glycosylated Haemoglobin ◽  
Albino Rats ◽  
Enzymatic Antioxidants ◽  
Protective Effects

The aim of the present study was to investigate the protective effects of Sesbania grandiflora flower (SGF) extract on erythrocyte membrane in Streptozotocin (STZ)-induced diabetic rats. Adult male albino rats of Wistar strain, weighing 190–220 g, were made diabetic by an intraperitonial administration of STZ (45 mg/kg). Normal and diabetic rats were treated with SGF, and diabetic rats were also treated with glibenclamide as drug control, for 45 days. In this study plasma insulin and haemoglobin levels were decreased and blood glucose, glycosylated haemoglobin, protein oxidation, lipid peroxidation markers, and osmotic fragility levels were increased in diabetic rats. Moreover, erythrocytes antioxidant enzymes such as superoxide dismutase, catalase, glutathione peroxide, glutathione reductase, glutathione-S-transferase, and glucose-6-phosphate dehydrogenase activities and non-enzymatic antioxidants such as vitamin C, vitamin E, reduced glutathione (GSH), and oxidized glutathione (GSSG) levels were altered. Similarly, the activities of total ATPases, Na+/K+-ATPase, Ca2+-ATPase, and Mg2+-ATPase were also decreased in the erythrocytes of diabetic rats. Administration of SGF to STZ-induced diabetic rats reduced blood glucose and glycosylated haemoglobin levels with increased levels of insulin and haemoglobin. Moreover, SGF reversed the protein and lipid peroxidation markers, osmotic fragility, membrane-bound ATPases activities, and antioxidant status in STZ-induced diabetic rats. These results suggest that SGF could provide a protective effect on diabetes by decreasing oxidative stress-associated diabetic complications.

Radix Dipsaci extract protects against Rosiglitazone induced bone loss

2021 ◽  
Vol 8 (9) ◽  
pp. 15-21
Author(s):  
Khalid A Asseri ◽  
◽  
Yahya I Asiri ◽  
Ali Alqahtani ◽  
Krishnaraju Venkatesan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Bone Loss ◽  
Bone Fractures ◽  
Scientific Evidence ◽  
Streptozotocin Diabetes ◽  
Diabetic Control ◽  
Albino Rats ◽  
Protective Effects ◽  
Diabetes Group ◽  
Diabetic Osteoporosis

The dried root of Dipsacus asperoides is known as Radix Dipsaci extract(RDE). It's a kidney-toning herbal medication with a lengthy track record of safe usage in the treatment of bone fractures and joint disorders. The drug rosiglitazone (RSG) causes an imbalance in bone remodelling, which results in increased apoptotic death of osteogenic cells and decreased bone production. The goal of this study was to investigate the effects of RDE on RSGinduced bone loss in diabetic rats in a systematic way. Five groups of six Wistar albino rats were studied: control (vehicle therapy), Streptozotocin (diabetes) group, RDE group, Rosiglitazone, and Rosiglitazone +RDE group. Insulin, oxidative stress, and bone turnover markers in the blood were all detected using ELISA tests. When compared to diabetic control rats, RDE therapy significantly raised insulin and osteocalcin levels. RDE may be able to prevent diabetic osteoporosis by boosting osteogenesis and lowering oxidative stress in the bone.These findings support the use of RDE as a bone loss inhibiting in diabetics. Well-designed clinical trials are likely to yield further scientific evidence on its bone-protective effects and safety. Keywords: Radix Dipsaci, Diabetic osteoporosis, Rosiglitazone.

scholarly journals Tualang Honey Attenuates Noise Stress-Induced Memory Deficits in Aged Rats

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Khairunnuur Fairuz Azman ◽  
Rahimah Zakaria ◽  
Che Badariah Abdul Aziz ◽  
Zahiruddin Othman
Keyword(s):  
Oxidative Stress ◽  
Memory Performance ◽  
Acetylcholinesterase Activity ◽  
Protein Carbonyl ◽  
Protective Effects ◽  
Aged Rats ◽  
Stress Exposure ◽  
Object Recognition Test ◽  
Noise Stress ◽  
Tualang Honey

Ageing and stress exposure may lead to memory impairment while oxidative stress is thought to be one of the underlying mechanisms involved. This study aimed to investigate the potential protective effects of Tualang honey supplementation on memory performance in aged rats exposed to noise stress. Tualang honey supplementation was given orally, 200 mg/kg body weight for 28 days. Rats in the stress group were subjected to loud noise, 100 dB(A), 4 hours daily for 14 days. All rats were subjected to novel object recognition test for evaluation of memory performance. It was observed that the rats subjected to noise stress exhibited significantly lower memory performance and higher oxidative stress as evident by elevated malondialdehyde and protein carbonyl levels and reduction of antioxidant enzymes activities compared to the nonstressed rats. Tualang honey supplementation was able to improve memory performance, decrease oxidative stress levels, increase brain-derived neurotrophic factor (BDNF) concentration, decrease acetylcholinesterase activity, and enhance neuronal proliferation in the medial prefrontal cortex (mPFC) and hippocampus. In conclusion, Tualang honey protects against memory decline due to stress exposure and/or ageing via enhancement of mPFC and hippocampal morphology possibly secondary to reduction in brain oxidative stress and/or upregulation of BDNF concentration and cholinergic system.

scholarly journals Protective Effects of 3-benzoyl-7-hydroxy Coumarin on Liver of Adult Rat Exposed to Aluminium Chloride

2021 ◽  
Vol 68 (1) ◽  
pp. 222-228
Author(s):  
Ahmet Özkaya ◽  
Kenan Türkan
Keyword(s):  
Oxidative Stress ◽  
Enzyme Activity ◽  
Aluminium Chloride ◽  
Control Group ◽  
Albino Rats ◽  
Activity Levels ◽  
Protective Effects ◽  
Adult Rat ◽  
Antioxidant Enzyme System ◽  
Hydroxy Coumarin

In this study, the effects of 3-benzoyl-7-hydroxy coumarin molecule on mineral and antioxidant enzymes were investigated in rat liver exposed to oxidative stress with aluminium chloride (AlCl3). Adult male Wistar albino rats were divided into four groups as Control, Coumarin, AlCl3, and Coumarin + AlCl3. Coumarin at the dose of 10 mg/kg and AlCl3 at the dose of 8.3 mg/kg were administered for 30 days every other day. In AlCl3 group, malondialdehyde (MDA), iron (Fe), aluminium (Al) and copper (Cu) levels increased compared to the control group, while glutathione (GSH) level, glutathione S-transferase (GST), and carboxylesterase (Ces) enzyme activity levels decreased. In Coumarin + AlCl3 group, MDA, Fe, Al and Cu levels decreased with the effect of coumarin compared to AlCl3 group, while GSH level, and GST enzyme activity levels increased. According to our results, AlCl3 generates oxidative stress in rat livers, and we believe that 3-benzoyl-7-hydroxy coumarin has an ameliorative effect on antioxidant enzyme system, Al, Fe and Cu levels.

scholarly journals Propolis Protective Effects Against Doxorubicin-Induced Multi-Organ Toxicity via Suppression of Oxidative Stress, Inflammation, Apoptosis, and Histopathological Alterations in Female Albino Rats

2021 ◽  
Vol 12 (2) ◽  
pp. 1762-1777
Keyword(s):  
Oxidative Stress ◽  
Large Scale ◽  
Protective Efficacy ◽  
Biological Activities ◽  
Female Rats ◽  
Control Group ◽  
Albino Rats ◽  
Protective Agent ◽  
Protective Effects ◽  
Treatment Protocols

Doxorubicin (DOX) is effective chemotherapy in several malignancies, but large-scale toxicities limit its clinical usefulness. Propolis has been reported to exhibit a broad spectrum of biological activities. We aim to assess the protective efficacy of propolis against DOX-induced multi-toxicity in female rats. Forty female rats were divided into four groups: control group; Group (P) were administrated oral propolis (100 mg/kg once daily for 28 days); Group (P+DOX) were injected with a single intraperitoneal dose of DOX (20 mg/kg i.p at 24th day after the propolis administration) and group (DOX) were injected with doxorubicin only. Estimation of cardiac, renal and hepatic injury markers, apoptosis and pro-inflammatory cytokines were done using sera. Also, liver and heart tissue samples were collected to determine GSH and MDA as oxidative stress markers. In addition to histopathological and immunohistochemical examination of Cytochrome-C and Connexin43 on lysed myocardium, liver, kidney and lung tissues. Doxorubicin toxicity caused marked deteriorations of measured parameters through the different mechanisms in different body organs. However, pre-treatment with propolis significantly ameliorated these alterations. Thus propolis can ameliorate the DOX-induced experimental multi-toxicity as cardiomyopathy, hepatotoxicity, nephritis and pneumonia. Thus, it could be a promising protective agent in DOX treatment protocols.

scholarly journals Protective effect of essential oil of Cinnamomum verum bark on hepatic and renal toxicity induced by carbon tetrachloride in rats

2019 ◽  
Vol 44 (6) ◽  
pp. 606-618 ◽  
Author(s):  
Khaled Bellassoued ◽  
Ferdaws Ghrab ◽  
Houda Hamed ◽  
Rim Kallel ◽  
Jos van Pelt ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Essential Oil ◽  
Renal Toxicity ◽  
Density Lipoprotein ◽  
Protein Carbonyl ◽  
Untreated Group ◽  
Protective Effects ◽  
Glutamyl Transferase

The inner bark of cinnamon (Cinnamomum verum) is widely used as a spice. Cinnamon plants are also a valuable source of essential oil used for medicinal purposes. The present study aimed to investigate the composition and in vitro antioxidant activity of essential oil of C. verum bark (CvEO) and its protective effects in vivo on CCl4-induced hepatic and renal toxicity in rats. Groups of animals were pretreated for 7 days with CvEO (70 or 100 mg/kg body weight) or received no treatment and on day 7 a single dose of CCl4 was used to induce oxidative stress. Twenty-four hours after CCl4 administration, the animals were euthanized. In the untreated group, CCl4 induced an increase in serum biochemical parameters and triggered oxidative stress in both liver and kidneys. CvEO (100 mg/kg) caused significant reductions in CCl4-elevated levels of alanine transaminase, aspartate transaminase, alkaline phosphatase, γ-glutamyl transferase, lactate dehydrogenase, total cholesterol, triglycerides, low-density lipoprotein, urea, and creatinine and increased the level of high-density lipoprotein compared with the untreated group. Moreover, pretreatment with CvEO at doses of 70 and 100 mg/kg before administration of CCl4 produced significant reductions in thiobarbituric acid reactive substances and protein carbonyl levels in liver and kidney tissues compared with the untreated group. The formation of pathological hepatic and kidney lesions induced by the administration of CCl4 was strongly prevented by CvEO at a dose of 100 mg/kg. Overall, this study suggests that administration of CvEO has high potential to quench free radicals and alleviate CCl4-induced hepatorenal toxicity in rats.

Effect of alpha-ketoglutarate and N-acetyl cysteine on cyanide-induced oxidative stress mediated cell death in PC12 cells

2010 ◽  
Vol 26 (5) ◽  
pp. 297-308 ◽  
Author(s):  
RM Satpute ◽  
J. Hariharakrishnan ◽  
R. Bhattacharya
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Pc12 Cells ◽  
Caspase 3 ◽  
Critical Role ◽  
Total Antioxidant Status ◽  
Protective Effects ◽  
Simultaneous Treatment ◽  
Acetyl Cysteine

Cyanide is a mitochondrial poison, which is ubiquitously present in the environment. Cyanide-induced oxidative stress is known to play a key role in mediating the neurotoxicity and cell death in rat pheochromocytoma (PC12) cells. PC12 cells are widely used as a model for neurotoxicity assays in vitro. In the present study, we investigated the protective effects of alpha-ketoglutarate (A-KG), a potential cyanide antidote, and N-acetyl cysteine (NAC), an antioxidant against toxicity of cyanide in PC12 cells. Cells were treated with various concentrations (0.625—1.25 mM) of potassium cyanide (KCN) for 4 hours, in the presence or absence of simultaneous treatment of A-KG (0.5 mM) and NAC (0.25 mM). Cyanide caused marked decrease in the levels of cellular antioxidants like superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and glutathione reductase (GR). Lipid peroxidation indicated by elevated levels of malondialdehyde (MDA) was found to be accompanied by decreased levels of reduced glutathione (GSH) and total antioxidant status (TAS) of the cells. Cyanide-treated cells showed notable increase in caspase-3 activity and induction of apoptotic type of cell death after 24 hours. A-KG and NAC alone were very effective in restoring the levels of GSH and TAS, but together they significantly resolved the effects of cyanide on antioxidant enzymes, MDA levels, and caspase-3 activity. The present study reveals that combination of A-KG and NAC has critical role in abbrogating the oxidative stress-mediated toxicity of cyanide in PC12 cells. The results suggest potential role of A-KG and NAC in cyanide antagonism.

scholarly journals Sulodexide Protects Contrast-Induced Nephropathy in Sprague-Dawley Rats

2016 ◽  
Vol 40 (3-4) ◽  
pp. 621-632 ◽  
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.

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