scholarly journals Gastroprotective Activity of Sterculia striata A. St. Hil. & Naudin (Malvaceae) in Rodents

2012 ◽  
Vol 67 (3-4) ◽  
pp. 163-171
Author(s):  
Joubert A. Sousa ◽  
Irisdalva S. Oliveira ◽  
Francilene V. Silva ◽  
Danielly A. Costa ◽  
Mariana H. Chaves ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Methyl Ester ◽  
Gastric Secretion ◽  
Catalase Activity ◽  
Gastric Lesion ◽  
Ischemia Reperfusion ◽  
Ethanolic Extract ◽  
Antioxidant Compounds ◽  
Gastric Lesions ◽  
Gastroprotective Activity

The Sterculia striata ethanolic extract (Ss-EtOH) inhibited gastric lesions induced by ethanol, HCl/ethanol, and ischemia/reperfusion, but not those induced by indomethacin, and did not alter the gastric secretion. Ss-EtOH restored the catalase activity and content of nonprotein sulfhydryl groups in the stomach of mice treated with ethanol. The gastroprotection induced by Ss-EtOH in the ethanol-induced gastric lesion model was abolished by NG-nitro- L-arginine methyl ester (L-NAME) pretreatment, suggesting the involvement of nitric oxide and antioxidant compounds, but not prostaglandins, in this activity. Lupeol obtained from Ss-EtOH promoted gastroprotection as well as the extract at the same dose, and it must therefore contribute to the observed effects

scholarly journals Gastroprotection of Calein D against Ethanol-Induced Gastric Lesions in Mice: Role of Prostaglandins, Nitric Oxide and Sulfhydryls

Molecules ◽  
2019 ◽  
Vol 24 (3) ◽  
pp. 622 ◽  
Author(s):  
María Sánchez-Mendoza ◽  
Yaraset López-Lorenzo ◽  
Leticia Cruz-Antonio ◽  
Audifás-Salvador Matus-Meza ◽  
Yolanda Sánchez-Mendoza ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Methyl Ester ◽  
Oral Treatment ◽  
Control Group ◽  
Peptic Ulcers ◽  
Gastric Lesions ◽  
Gastroprotective Activity ◽  
Reference Drug ◽  
Sulfhydryl Compounds

Peptic ulcers are currently treated with various drugs, all having serious side effects. The aim of this study was to evaluate the gastroprotective activity of calein D (from Calea urticifolia), a sesquiterpene lactone with a germacrane skeleton. Gastric lesions were induced in mice by administering ethanol (0.2 mL) after oral treatment with calein D at 3, 10 and 30 mg/kg, resulting in 13.15 ± 3.44%, 77.65 ± 7.38% and 95.76 ± 2.18% gastroprotection, respectively, to be compared with that of the control group. The effect found for 30 mg/kg of calein D was not reversed by pretreatment with NG-nitro-l-arginine methyl ester (l-NAME, 70 mg/kg, ip), indomethacin (10 mg/kg, sc) or N-ethylmaleimide (NEM, 10 mg/kg, sc). Hence, the mechanism of action of calein D does not involve NO, prostaglandins or sulfhydryl compounds. Calein D was more potent than carbenoxolone, the reference drug. The findings for the latter are in agreement with previous reports.

Nitric oxide attenuates endothelin-1-induced vasoconstriction in canine stomach

1996 ◽  
Vol 271 (1) ◽  
pp. G27-G35
Author(s):  
J. G. Wood ◽  
Q. Zhang ◽  
Z. Y. Yan ◽  
L. Y. Cheung
Keyword(s):  
Nitric Oxide ◽  
Methyl Ester ◽  
Ischemia Reperfusion ◽  
Nitric Oxide Donor ◽  
Question Mark ◽  
Endothelin 1 ◽  
Vasoconstrictor Response ◽  
Anesthetized Dogs ◽  
Spermine Nonoate

We previously observed that endothelin-1 (ET-1)-induced gastric vasoconstriction is enhanced after ischemia-reperfusion. The purpose of our present study was to examine the role of nitric oxide in regulating ET-1-induced vasoconstriction under normal conditions and after ischemia-reperfusion. Using a mechanically perfused stomach segment from chloralose-anesthetized dogs, we examined 1) responses to NG-nitro-L-arginine methyl ester (L-NAME) alone and in combination with L-arginine, 2) whether L-NAME affects ET-1-induced vasoconstriction under normal conditions and after ischemia-reperfusion, and 3) if spermine NONOate inverted question mark1,3-propanediamine-N-[4-1-(3-aminopropyl)-2-hydroxy-2-nitrosohydrazi no] butyl; a nitric oxide donor inverted question mark attenuates the augmented response to ET-1 after ischemia-reperfusion. Our results show that 1) L-NAME significantly increased baseline vascular resistance and this response was reduced by L-arginine, 2) ET-1-induced vasoconstriction was enhanced by L-NAME, and 3) administration of spermine NONOate during reperfusion largely attenuated the vasoconstrictor response to ET-1 after ischemia-reperfusion. Our findings are consistent with the hypothesis that nitric oxide modulates responses to ET-1 under normal conditions, and loss of this vasodilator after ischemia-reperfusion results in an augmented response to ET-1.

scholarly journals Gastroprotective Effect of Geopropolis fromMelipona scutellarisIs Dependent on Production of Nitric Oxide and Prostaglandin

2015 ◽  
Vol 2015 ◽  
pp. 1-5 ◽  
Author(s):  
Jerônimo Aparecido Ribeiro-Junior ◽  
Marcelo Franchin ◽  
Miriam Elias Cavallini ◽  
Carina Denny ◽  
Severino Matias de Alencar ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Ethanolic Extract ◽  
Mechanisms Of Action ◽  
The Other ◽  
Medicine Use ◽  
Gastroprotective Activity ◽  
Sh Groups ◽  
Antisecretory Activity ◽  
Ulcerative Lesions ◽  
Prior Administration

The aim of this study was to evaluate the gastroprotective activity of ethanolic extract of geopropolis (EEGP) fromMelipona scutellarisand to investigate the possible mechanisms of action. The gastroprotective activity of the EEGP was evaluated using model ulcer induced by ethanol. To elucidate the possible mechanisms of action, we investigated the involvement of the nonprotein sulfhydryl (NP-SH) groups, nitric oxide and prostaglandins. In addition, the antisecretory activity of EEGP was also evaluated by pylorus ligated model. The EEGP orally administrated (300 mg/kg) reduced the ulcerative lesions induced by the ethanol (P<0.05). Regarding the mechanism of action, the prior administration of nitric oxide and prostaglandins antagonists suppressed the activity of gastroprotective EEGP (P<0.05). On the other hand the gastroprotective activity of EEGP was kept in the group pretreated with the antagonist of the NP-SH groups; furthermore the antisecretory activity was not significant (P>0.05). These results support the alternative medicine use of geopropolis as gastroprotective and the activities observed show to be related to nitric oxide and prostaglandins production.

Ischemic tolerance in skeletal muscle: role of nitric oxide

1998 ◽  
Vol 275 (1) ◽  
pp. H94-H99 ◽  
Author(s):  
S. Pudupakkam ◽  
K. A. Harris ◽  
W. G. Jamieson ◽  
G. DeRose ◽  
J. A. Scott ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Methyl Ester ◽  
Tissue Injury ◽  
Ischemia Reperfusion ◽  
Ischemic Event ◽  
Reperfusion Period ◽  
Male Wistar Rats ◽  
Edl Muscle

We tested the hypothesis that ischemic preconditioning (PC) of skeletal muscle provided tolerance to a subsequent ischemic event 24 h later, and that such protection was due to nitric oxide (NO). Male Wistar rats, anesthetized with halothane, were randomly assigned to groups: ischemic (no PC; n = 11), PC ( n = 11), PC + N-nitro-l-arginine methyl ester (l-NAME; 100 μmol/l; n = 5), PC + N-nitro-d-arginine methyl ester (100 μmol/l; n= 4), PC + aminoguanidine (AMG; 100 μmol/l; n = 4), ischemic +l-NAME ( n= 4), or ischemic + AMG ( n = 4). PC consisted of 5× 10 min of ischemia and reperfusion, and, 24 h later, 2 h of ischemia were induced by a tourniquet applied to the limb. With the use of intravital microscopy, the number of perfused capillaries ( N pc) in the extensor digitorum longus (EDL) muscle was measured over a 90-min reperfusion period. The ratio of ethidium bromide- to bisbenzimide-labeled nuclei was used to estimate tissue injury. PC preserved N pc(23.6 ± 2.5) following 2 h of ischemia compared with sham muscles (11.5 ± 5.1), significantly elevating inducible NO synthase (iNOS) activity (81% increase), but did not afford protection to the parenchyma.l-NAME and AMG prevented ischemia-reperfusion-induced reduction in N pc in muscles without PC. However, after 90 min of reperfusion,l-NAME ( N pc = 15.0 ± 1.7), but not AMG ( N pc = 22.8 ± 3.1), significantly reduced the microvascular protection afforded by PC. We conclude that PC of the EDL muscle resulted, 24 h later, in protection to microvascular perfusion only, and that such protection was due to NO from sources other than iNOS.

Gastroprotective activity of Pradosia huberi on experimentally induced gastric lesions in rodents: Role of endogenous sulphydryls and nitric oxide

2005 ◽  
Vol 101 (1-3) ◽  
pp. 61-67 ◽  
Author(s):  
Hélio Kushima ◽  
Clélia Akiko Hiruma-Lima ◽  
Maria Aparecida Santos ◽  
Elizabeth Viana ◽  
Márlia Coelho-Ferreira ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Gastric Lesions ◽  
Gastroprotective Activity ◽  
Experimentally Induced

Remifentanil Preconditioning Reduces Hepatic Ischemia–Reperfusion Injury in Rats via  Inducible Nitric Oxide Synthase Expression

2011 ◽  
Vol 114 (5) ◽  
pp. 1036-1047 ◽  
Author(s):  
Li-Qun Yang ◽  
Kun-Ming Tao ◽  
Yan-Tao Liu ◽  
Chi-Wai Cheung ◽  
Michael G. Irwin ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Methyl Ester ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Hepatic Ischemia ◽  
Hepatic Ischemia Reperfusion ◽  
Inducible Nos

Background Opioid preconditioning against ischemia reperfusion injury has been well studied in myocardial and neuronal tissues. The objective of this study was to determine whether remifentanil could attenuate hepatic injury and to investigate the mechanisms. Methods A rat model of hepatic ischemia reperfusion injury and a hepatocyte hypoxia reoxygenation (HR) injury model were used, respectively, in two series of experiments. Remifentanil was administered before ischemia or hypoxia and the experiments were repeated with previous administration of naloxone, L-arginine and N-ω-nitro-L-arginine methyl ester, a nonselective opioid receptor antagonist, a nitric oxide donor, and nitric oxide synthase (NOS) inhibitor, respectively. Serum aminotransferase, cytokines, and hepatic lipid peroxidation were measured. Histopathology examination and apoptotic cell detection were assessed. For the in vitro study, cell viability, intracellular nitric oxide, apoptosis, and NOS expression were evaluated. Results Remifentanil and L-arginine pretreatment reduced concentrations of serum aminotransferases and cytokines, decreased the concentrations of hepatic malondialdehyde and myeloperoxidase activity, and increased superoxide dismutase, nitric oxide, and inducible NOS expression in vivo. Decreased histologic damage and apoptosis were also seen in these two groups. These changes were prevented by previous administration of N-ω-nitro-L-arginine methyl ester but not naloxone. There was an increase in inducible NOS protein expression but not endogenous NOS in remifentanil and L-arginine pretreated groups compared with control, naloxone, and N-ω-nitro-L-arginine methyl ester groups. Conclusion Pretreatment with remifentanil can attenuate liver injury both in vivo and in vitro. Inducible NOS but not opioid receptors partly mediate this effect by exhausting reactive oxygen species and attenuating the inflammatory response.

scholarly journals Role of Prostaglandins, Nitric oxide, Sulfhydryls and Capsaicin-sensitive Neurons in Gastroprotection of Stigmasterol and β-Sitosterol

2008 ◽  
Vol 3 (4) ◽  
pp. 1934578X0800300
Author(s):  
María Elena Sánchez-Mendoza ◽  
Jesús Arrieta ◽  
Andrés Navarrete
Keyword(s):  
Nitric Oxide ◽  
Methyl Ester ◽  
Sensory Neurons ◽  
Tween 80 ◽  
Mucosal Damage ◽  
Gastric Mucosal Damage ◽  
Gastroprotective Activity ◽  
Model Drug ◽  
Dose Dependent

In this investigation the gastroprotective activity of stigmasterol and β-sitosterol was evaluated. Gastric mucosal damage was induced in rats by intragastric ethanol (1 mL/rat). Rats treated orally with stigmasterol suspended in Tween 80 at 10, 30, 100 and 300 mg kg−1 showed 26.2, 39.6, 58.3 and 70.7% gastroprotection, respectively. β-Sitosterol at 10, 30,100 and 300 mg kg−1 showed 21.6, 42.5, 48.5 and 71.2% gastroprotection, correspondingly. The gastroprotection observed at 30 mg kg−1 for stigmasterol and β-sitosterol was attenuated in rats pretreated with indomethacin, (10 mg kg−1, s. c.), NG-nitro-L-arginine methyl ester (L-NAME, 70 mg kg−1, i. p.) and capsaicin (125 mg kg−1, s. c), suggesting that the gastroprotective mechanism of these sterols involves, at least in part, the participation of prostaglandins, nitric oxide (NO) and capsaicin-sensitive sensory neurons (CPSN). The gastroprotection of β-sitosterol was also attenuated by the pretreatment with N-ethylmaleimide (NEM, 10 mg kg−1, s. c.) indicating that endogenous sulfrydryls may be involved in the gastrorpotection of this compound. Carbenoxolone was used as a gastroprotective model drug and showed a dose-dependent gastroprotective effect (25.7, 33.6 and 88.3% of gastroprotection, at 3, 10 and 30 mg kg−1, respectively). The partial participation of PGs, sulfhydryls and NO was observed in the gastroprotective mechanism of carbenoxolone.

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