scholarly journals Gastro-Protective and Anti-Oxidant Potential of Althaea officinalis and Solanum nigrum on Pyloric Ligation/Indomethacin-Induced Ulceration in Rats

Antioxidants ◽  
2019 ◽  
Vol 8 (11) ◽  
pp. 512
Author(s):  
Sameh S. Zaghlool ◽  
Ali A. Abo-Seif ◽  
Mohamed A. Rabeh ◽  
Usama Ramadan Abdelmohsen ◽  
Basim A. S. Messiha
Keyword(s):  
Normal Control ◽  
Lipid Peroxide ◽  
Solanum Nigrum ◽  
Gastric Ulceration ◽  
Control Group ◽  
Heme Oxygenase 1 ◽  
Anti Oxidant ◽  
Althaea Officinalis ◽  
Pyloric Ligation

Recently, an alternative disease treatment approach is the research of medicaments from traditional medicine. Plants with anti-oxidant capabilities are used as herbal treatments for ulcer diseases. Medicinal/herbal extracts containing phytoconstituents have significant anti-ulcer activities in in vivo experiments on animal models, compared to reference drugs. The current study aims to inspect gastro-protective as well as in vitro and in vivo anti-oxidant potential of Althaea officinalis and Solanum nigrum extracts on pyloric-ligation/indomethacin-induced gastric-ulceration in rats. Rats were divided into six groups: normal control, gastric ulcer control, two standard pretreatment groups receiving omeprazole and misoprostol, and two test pretreatment groups receiving Althaea officinalis and Solanum nigrum. Pretreatments were administrated orally for 14 days. On the 15th day, animals, excluding the normal control group, were exposed to pyloric-ligation followed by indomethacin injection. After four hours, the rat’s stomachs were removed and gastric juice and blood samples were collected. Pyloric-ligation/indomethacin administration caused considerable elevation in ulcer number, ulcer index, acid and pepsin productivity, aggressive factors, and gastric mucosal lipid-peroxide contents. Moreover, reduction in titratable acidity, gastric mucosal nitric-oxide, anti-oxidant contents, and protective factors accompanied gastric-ulceration. Additionally, elevation in pro-inflammatory cytokines content and reduction in cystathionine-β-synthase and heme-oxygenase-1 expression was witnessed. Omeprazole, misoprostol, Althaea officinalis, and Solanum nigrum pretreatments fixed blood and tissue biomarkers, thereby protecting them from pyloric-ligation/indomethacin-induced gastric-ulceration in rats, which is hopeful for clinical examinations.

Protective role of melatonin in myocardial oxidative damage induced by mercury in murine model

2010 ◽  
Vol 30 (10) ◽  
pp. 1489-1500 ◽  
Author(s):  
Mitali Jindal ◽  
Gobind Rai Garg ◽  
Pramod Kumari Mediratta ◽  
Mohammad Fahim
Keyword(s):  
Drinking Water ◽  
Mercuric Chloride ◽  
Diastolic Pressure ◽  
Lipid Peroxide ◽  
Left Ventricular ◽  
Control Group ◽  
Albino Rats ◽  
Mercury Intoxication ◽  
Cardiovascular Functions

This study was designed to investigate the electrophysiological, hemodynamic and biochemical parameters of mercuric chloride and methylmercury exposure on cardiovascular functions and its modulation by melatonin in vivo. Wistar albino rats were divided into six group containing 10 animals each. Mercuric chloride (3.75 µM/L) in drinking water and methylmercury (0.5 mg/kg/day) through gavage, given for 1 month, induced a statistically significant increase ( p < 0.001) in left ventricular end diastolic pressure, blood and cardiac tissue mercury content and myocardial lipid peroxides compared to control. Significant attenuation ( p < 0.05) of baroreflex sensitivity and depletion of myocardial endogenous antioxidants ( p < 0.001) viz. Reduced glutathione (GSH) and superoxide dismutase (SOD) were also found in the mercury-exposed groups as compared to control group. Mercury exposure followed by subacute treatment with melatonin (4 µg/mL/day) in drinking water for 1 month significantly lowered ( p < 0.01) left ventricular end diastolic pressure and lipid peroxide levels and increased baroreceptor sensitivity ( p < 0.001) and also levels of GSH and SOD ( p < 0.001) as compared to mercury-exposed rats. The results of our study provide clear evidence that elevated oxidative stress and altered baroreflex mechanisms caused by mercury intoxication may be the contributing factors responsible for impairment of cardiovascular functions and melatonin may exhibit cardioprotective property against subacute heavy metal intoxication and enhance the antioxidant defense against mercury-induced oxidative myocardial injury in rats.

scholarly journals Oral Administration of Cystine and Theanine Attenuates 5-Fluorouracil-Induced Intestinal Mucositis and Diarrhea by Suppressing Both Glutathione Level Decrease and ROS Production in the Small Intestine of Mucositis Mouse Model

2021 ◽  
Author(s):  
Junya Yoneda ◽  
Sachiko Nishikawa ◽  
Shigekazu Kurihara
Keyword(s):  
Small Intestine ◽  
Mouse Model ◽  
Oral Administration ◽  
Normal Control ◽  
Control Group ◽  
Basal Region ◽  
Ros Production ◽  
Mucosal Tissue ◽  
Intestinal Mucositis

Abstract Background Chemotherapy is frequently used in cancer treatment; however, it may cause adverse events, which must be managed. Reactive oxygen species (ROS) have been reported to be involved in the induction of intestinal mucositis and diarrhea, which are common side effects of treatment with fluoropyrimidine 5-fluorouracil (5-FU). Our previous studies have shown that oral administration of cystine and theanine (CT) increases glutathione (GSH) production in vivo. In the present study, we hypothesized that CT might inhibit oxidative stress, including the overproduction of ROS, and attenuate 5-FU-induced mucositis and diarrhea. Methods We investigated the inhibitory effect of CT administration on mucositis and diarrhea, as well as its mechanism, using a mouse model of 5-FU-induced intestinal mucositis. Results CT administration suppressed 5-FU-induced diarrhea and weight loss in the studied mice. After 5-FU administration, the GSH level and the GSH/GSSG ratio in the small intestine mucosal tissue decreased compared to normal control group; but CT administration improved the GSH/GSSG ratio to normal control levels. 5-FU induced ROS production in the basal region of the crypt of the small intestine mucosal tissue, which was inhibited by CT. CT did not affect the antitumor effect of 5-FU. Conclusions CT administration suppressed intestinal mucositis and diarrhea in a mouse model. This finding might be associated with the antioxidant characteristics of CT, including the improved rate of GSH redox and the reduced rate of ROS production in the small intestine mucosal tissue. CT might be a suitable candidate for the treatment of gastrointestinal mucositis associated with chemotherapy.

scholarly journals Orosomucoid 1 Attenuates Doxorubicin-Induced Oxidative Stress and Apoptosis in Cardiomyocytes via Nrf2 Signaling

2020 ◽  
Vol 2020 ◽  
pp. 1-13
Author(s):  
Xiaoli Cheng ◽  
Dan Liu ◽  
Ruinan Xing ◽  
Haixu Song ◽  
Xiaoxiang Tian ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Caspase 3 ◽  
Acute Phase Protein ◽  
Control Group ◽  
Heme Oxygenase 1 ◽  
H9c2 Cells ◽  
Phase Protein ◽  
New Treatment

Doxorubicin (DOX) is an effective anticancer drug, but its therapeutic use is limited by its cardiotoxicity. The principal mechanisms of DOX-induced cardiotoxicity are oxidative stress and apoptosis in cardiomyocytes. Orosomucoid 1 (ORM1), an acute-phase protein, plays important roles in inflammation and ischemic stroke; however, the roles and mechanisms of ORM1 in DOX-induced cardiotoxicity remain unknown. Therefore, in the present study, we aimed to investigate the function of ORM1 in cardiomyocytes experiencing DOX-induced oxidative stress and apoptosis. A DOX-induced cardiotoxicity animal model was established in C57BL/6 mice by administering an intraperitoneal injection of DOX (20 mg/kg), and the control group was intraperitoneally injected with the same volume of sterilized saline. The effects were assessed after 7 d. Additionally, H9c2 cells were stimulated with DOX (10 μM) for 24 h. The results showed decreased ORM1 and increased oxidative stress and apoptosis after DOX stimulation in vivo and in vitro. ORM1 overexpression significantly reduced DOX-induced oxidative stress and apoptosis in H9c2 cells. ORM1 significantly increased the expression of nuclear factor-like 2 (Nrf2) and its downstream protein heme oxygenase 1 (HO-1) and reduced the expression of the lipid peroxidation end product 4-hydroxynonenal (4-HNE) and the level of cleaved caspase-3. In addition, Nrf2 silencing reversed the effects of ORM1 on DOX-induced oxidative stress and apoptosis in cardiomyocytes. In conclusion, ORM1 inhibited DOX-induced oxidative stress and apoptosis in cardiomyocytes by regulating the Nrf2/HO-1 pathway, which might provide a new treatment strategy for DOX-induced cardiotoxicity.

scholarly journals The Anti-Inflammatory and Antioxidant Effects of Sodium Propionate

2020 ◽  
Vol 21 (8) ◽  
pp. 3026 ◽  
Author(s):  
Alessia Filippone ◽  
Marika Lanza ◽  
Michela Campolo ◽  
Giovanna Casili ◽  
Irene Paterniti ◽  
...  
Keyword(s):  
Heme Oxygenase 1 ◽  
Dependent Manner ◽  
Sodium Propionate ◽  
Intraplantar Injection ◽  
Concentration Dependent Manner ◽  
In Vivo Models ◽  
Anti Oxidant ◽  
Anti Inflammatory

The major end-products of dietary fiber fermentation by gut microbiota are the short-chain fatty acids (SCFAs) acetate, propionate, and butyrate, which have been shown to modulate host metabolism via effects on metabolic pathways at different tissue sites. Several studies showed the inhibitory effects of sodium propionate (SP) on nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway. We carried out an in vitro model of inflammation on the J774-A1 cell line, by stimulation with lipopolysaccharide (LPS) and H2O2, followed by the pre-treatment with SP at 0.1, 1 mM and 10 mM. To evaluate the effect on acute inflammation and superoxide anion-induced pain, we performed a model of carrageenan (CAR)-induced rat paw inflammation and intraplantar injection of KO2 where rats received SP orally (10, 30, and 100 mg/kg). SP decreased in concentration-dependent-manner the expression of cicloxigenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) following LPS stimulation. SP was able to enhance anti-oxidant enzyme production such as manganese superoxide dismutase (MnSOD) and heme oxygenase-1 (HO-1) following H2O2 stimulation. In in vivo models, SP (30 and 100 mg/kg) reduced paw inflammation and tissue damage after CAR and KO2 injection. Our results demonstrated the anti-inflammatory and anti-oxidant properties of SP; therefore, we propose that SP may be an effective strategy for the treatment of inflammatory diseases.

scholarly journals Quercetin Suppresses AOM/DSS-Induced Colon Carcinogenesis through Its Anti-Inflammation Effects in Mice

2020 ◽  
Vol 2020 ◽  
pp. 1-10 ◽  
Author(s):  
Rui Lin ◽  
Meiyu Piao ◽  
Yan Song ◽  
Chunyan Liu
Keyword(s):  
Colorectal Cancer ◽  
Gentian Violet ◽  
Lipid Peroxide ◽  
Colon Carcinogenesis ◽  
Indoxyl Sulfate ◽  
Control Group ◽  
Mice Model ◽  
Anti Inflammation ◽  
Quercetin Treatment

Colorectal cancer (CRC) is the fourth leading cause of tumor-related deaths worldwide. In this study, we explored the in vivo effects of quercetin, a plant flavonol from the flavonoid group of polyphenols with antioxidant effects, on colon carcinogenesis induced by azoxymethane/dextran sodium sulfate (AOM/DSS). Thirty mice were randomly assigned into three groups: the control group, the AOM/DSS group, and the quercetin+AOM/DSS group. CRC was induced by AOM injection and a solution of 2% DSS in the drinking water. In the AOM/DSS-induced colon cancer mice model, quercetin treatment dramatically reduced the number and size of colon tumors. In addition, quercetin significantly restored the leukocyte counts by decreasing the inflammation caused by AOM/DSS. We also observed that the expression of oxidative stress markers, such as lipid peroxide (LPO), nitric oxide (NO), superoxide dismutase (SOD), glucose-6-phosphate (G6PD), and glutathione (GSH), could be reduced by quercetin, suggesting that the anti-inflammatory function of quercetin comes from its antioxidant effect. Moreover, potential biomarkers were identified with serum metabolite profiling. Increased levels of 2-hydroxybutyrate, 2-aminobutyrate, and 2-oxobutyrate and decreased levels of gentian violet, indole-3-methyl acetate, N-acetyl-5-hydroxytryptamine, indoxyl sulfate, and indoxyl were also found in the AOM/DSS-treated mice. However, quercetin treatment successfully decreased the levels of 2-hydroxybutyrate, 2-aminobutyrate, 2-oxobutyrate, endocannabinoids, and sphinganine and increased the levels of gentian violet, N-acetyl-5-hydroxytryptamine, indoxyl sulfate, and indoxyl. Together, our data demonstrated that quercetin could maintain relatively potent antitumor activities against colorectal cancer in vivo through its anti-inflammation effect.

scholarly journals Diesel Engine Exhaust Initiates a Sequence of Pulmonary and Cardiovascular Effects in Rats

2010 ◽  
Vol 2010 ◽  
pp. 1-12 ◽  
Author(s):  
Ingeborg M. Kooter ◽  
Miriam E. Gerlofs-Nijland ◽  
A. John F. Boere ◽  
Daan L. A. C. Leseman ◽  
Paul H. B. Fokkens ◽  
...  
Keyword(s):  
Diesel Engine ◽  
Heme Oxygenase ◽  
Heme Oxygenase 1 ◽  
Defense Gene Expression ◽  
Engine Exhaust ◽  
Inhalation Study ◽  
Diesel Engine Exhaust ◽  
Sequence Of Events ◽  
Anti Oxidant

This study was designed to determine the sequence of events leading to cardiopulmonary effects following acute inhalation of diesel engine exhaust in rats. Rats were exposed for 2 h to diesel engine exhaust (1.9 mg/m3), and biological parameters related to antioxidant defense, inflammation, and procoagulation were examined after 4, 18, 24, 48, and 72 h. This in vivo inhalation study showed a pulmonary anti-oxidant response (an increased activity of the anti-oxidant enzymes glutathione peroxidase and superoxide dismutase and an increase in heme oxygenase-1 protein, heme oxygenase activity, and uric acid) which precedes the inflammatory response (an increase in IL-6 and TNF-α). In addition, increased plasma thrombogenicity and immediate anti-oxidant defense gene expression in aorta tissue shortly after the exposure might suggest direct translocation of diesel engine exhaust components to the vasculature but mediation by other pathways cannot be ruled out. This study therefore shows that different stages in oxidative stress are not only affected by dose increments but are also time dependent.

scholarly journals Sulforaphane Attenuates Contrast-Induced Nephropathy in Rats via Nrf2/HO-1 Pathway

2016 ◽  
Vol 2016 ◽  
pp. 1-12 ◽  
Author(s):  
Zhihong Zhao ◽  
Guixiang Liao ◽  
Qin Zhou ◽  
Daoyuan Lv ◽  
Harry Holthfer ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Model ◽  
Renal Tissue ◽  
Antioxidant Defenses ◽  
Control Group ◽  
Heme Oxygenase 1 ◽  
Contrast Induced Nephropathy ◽  
Hk2 Cells

Background. Oxidative stress plays an important role in the pathogenesis of contrast-induced nephropathy (CIN). The aim of this study was to investigate the antioxidant effects of sulforaphane (SFN) in a rat model of CIN and a cell model of oxidative stress in HK2 cells.Methods. Rats were randomized into four groups (n=6per group): control group, Ioversol group (Ioversol-induced CIN), Ioversol + SFN group (CIN rats pretreated with SFN), and SFN group (rats treated with SFN). Renal function tests, malondialdehyde (MDA), and reactive oxygen species (ROS) were measured. Western blot, real-time polymerase chain reaction analysis, and immunohistochemical analysis were performed for nuclear factor erythroid-derived 2-like 2 (Nrf2) and heme oxygenase-1 (HO-1) detection.Results. Serum blood urea nitrogen (BUN), creatinine, and renal tissue MDA were increased after contrast exposure. Serum BUN, creatinine, and renal tissue MDA were decreased in the Ioversol + SFN group as compared with those in the Ioversol group. SFN increased the expression of Nrf2 and HO-1 in CIN rats and in Ioversol-induced injury HK2 cells. SFN increased cell viability and attenuated ROS level in vitro.Conclusions. SFN attenuates experimental CIN in vitro and in vivo. This effect is suggested to activate the Nrf2 antioxidant defenses pathway.

scholarly journals Endometriosis Susceptibility to Dapsone-Hydroxylamine-Induced Alterations Can Be Prevented by Licorice Intake: In Vivo and In Vitro Study

2021 ◽  
Vol 22 (16) ◽  
pp. 8476
Author(s):  
Chiara Sabbadin ◽  
Alessandra Andrisani ◽  
Gabriella Donà ◽  
Elena Tibaldi ◽  
Anna Maria Brunati ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
In Vitro Study ◽  
Carbonic Anhydrase Activity ◽  
Control Group ◽  
Beneficial Effects ◽  
Licorice Extract ◽  
Anti Oxidant ◽  
Gynecological Disease

Endometriosis, an estrogen-dependent chronic gynecological disease, is characterized by a systemic inflammation that affects circulating red blood cells (RBC), by reducing anti-oxidant defenses. The aim of this study was to investigate the potential beneficial effects of licorice intake to protect RBCs from dapsone hydroxylamine (DDS-NHOH), a harmful metabolite of dapsone, commonly used in the treatment of many diseases. A control group (CG, n = 12) and a patient group (PG, n = 18) were treated with licorice extract (25 mg/day), for a week. Blood samples before (T0) and after (T1) treatment were analyzed for: i) band 3 tyrosine phosphorylation and high molecular weight aggregates; and ii) glutathionylation and carbonic anhydrase activity, in the presence or absence of adjunctive oxidative stress induced by DDS-NHOH. Results were correlated with plasma glycyrrhetinic acid (GA) concentrations, measured by HPLC–MS. Results showed that licorice intake decreased the level of DDS-NHOH-related oxidative alterations in RBCs, and the reduction was directly correlated with plasma GA concentration. In conclusion, in PG, the inability to counteract oxidative stress is a serious concern in the evaluation of therapeutic approaches. GA, by protecting RBC from oxidative assault, as in dapsone therapy, might be considered as a new potential tool for preventing further switching into severe endometriosis.

scholarly journals Oral administration of cystine and theanine attenuates 5-fluorouracil-induced intestinal mucositis and diarrhea by suppressing both glutathione level decrease and ROS production in the small intestine of mucositis mouse model

BMC Cancer ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Junya Yoneda ◽  
Sachiko Nishikawa ◽  
Shigekazu Kurihara
Keyword(s):  
Small Intestine ◽  
Mouse Model ◽  
Oral Administration ◽  
Normal Control ◽  
Control Group ◽  
Basal Region ◽  
Ros Production ◽  
Mucosal Tissue ◽  
Intestinal Mucositis

Abstract Background Chemotherapy is frequently used in cancer treatment; however, it may cause adverse events, which must be managed. Reactive oxygen species (ROS) have been reported to be involved in the induction of intestinal mucositis and diarrhea, which are common side effects of treatment with fluoropyrimidine 5-fluorouracil (5-FU). Our previous studies have shown that oral administration of cystine and theanine (CT) increases glutathione (GSH) production in vivo. In the present study, we hypothesized that CT might inhibit oxidative stress, including the overproduction of ROS, and attenuate 5-FU-induced mucositis and diarrhea. Methods We investigated the inhibitory effect of CT administration on mucositis and diarrhea, as well as its mechanism, using a mouse model of 5-FU-induced intestinal mucositis. Results CT administration suppressed 5-FU-induced diarrhea and weight loss in the studied mice. After 5-FU administration, the GSH level and the GSH/GSSG ratio in the small intestine mucosal tissue decreased compared to normal control group; but CT administration improved the GSH/GSSG ratio to normal control levels. 5-FU induced ROS production in the basal region of the crypt of the small intestine mucosal tissue, which was inhibited by CT. CT did not affect the antitumor effect of 5-FU. Conclusions CT administration suppressed intestinal mucositis and diarrhea in a mouse model. This finding might be associated with the antioxidant characteristics of CT, including the improved rate of GSH redox and the reduced rate of ROS production in the small intestine mucosal tissue. CT might be a suitable candidate for the treatment of gastrointestinal mucositis associated with chemotherapy.

scholarly journals Anti-Oxidant and Hepatoprotective Effects of Senecio biafrae on CCl4-induced Liver Damage in Rats

2019 ◽  
Vol 13 (2) ◽  
pp. 31-35
Author(s):  
Israel Oghenevwodoko Okoro ◽  
◽  
Helen Ejiro Kadiri ◽  
Keyword(s):  
Negative Control Group ◽  
Positive Control ◽  
Negative Control ◽  
Control Group ◽  
Albino Rats ◽  
Root Extract ◽  
Distilled Water ◽  
Standard Drug ◽  
Anti Oxidant

Background: The present study was performed to explore whether the aqueous extract of Senecio biafrae (S. biafrae) roots provide any in vivo protective activity against carbon tetrachloride (CCl4)-induced hepatotoxicity in male albino rats. Methods: Rats (150-200 grams) were grouped into five groups (A-E) of six rats each and were treated orally for twelve days with 72 hourly administration of CCl4 (1 mL/kg) as follows: Group A received distilled water only (negative control), Group B was administered distilled water plus CCl4 (positive control), Group C was administered 400 mg/kg extract and CCl4, Group D received 200 mg/extract and CCl4, while Group E was administered standard drug (Silymarin 25mg/kg, PO). Results: Pre-treatment with the extract of S. biafrae (200 or 400mg/kg) or Silymarin (25mg/kg) caused significant restoration in the biomarkers as evaluated by reducing the levels of malondialdehyde, transaminases and elevating the levels of superoxide dismutase, catalase and glutathione peroxidase activities, which were altered by CCl4 toxicity. The extract at a dose of 400mg/kg demonstrated similar activities comparable to the standard drug (Silymarin). Conclusion: The results of this study indicate that the root extract of S. biafrae possesses hepatoprotective and anti-oxidant properties which may be due to the presence of phytochemicals in it.

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