scholarly journals Vasorelaxant-Mediated Antihypertensive Effect of the Leaf Aqueous Extract from Stephania abyssinica (Dillon & A. Rich) Walp (Menispermaceae) in Rat

2021 ◽  
Vol 2021 ◽  
pp. 1-14
Author(s):  
Chamberlin Fodem ◽  
Elvine Pami Nguelefack-Mbuyo ◽  
Magloire Kanyou Ndjenda II ◽  
Albert Kamanyi ◽  
Télesphore Benoit Nguelefack
Keyword(s):  
Nitric Oxide ◽  
Heart Rate ◽  
Methylene Blue ◽  
Aqueous Extract ◽  
Calcium Release ◽  
Inhibitory Effect ◽  
Antihypertensive Activity ◽  
Phytochemical Analysis

Stephania abyssinica is a medicinal plant used in Cameroon alternative medicine to treat arterial hypertension (AHT). Previous in vitro studies demonstrated the endothelium nitric oxide-independent vasorelaxant property of the aqueous extract from Stephania abyssinica (AESA). But its effect on AHT is unknown. The present study was undertaken to explore other vasorelaxant mechanisms and to determine the antihypertensive effects of AESA in male Wistar rats. Phytochemical analysis of AESA was carried out using the liquid chromatography-mass spectrometry (LC-MS) method. The vasorelaxant effects of AESA (1-1000 μg/mL) were studied on rat isolated thoracic aorta rings, in the absence or presence of indomethacin (10 μM) or methylene blue (10 μM). The inhibitory effect of AESA on phenylephrine (PE, 10 μM) or KCl- (60 mM) induced contraction as well as the intracellular calcium release was also evaluated. The in vivo antihypertensive activity of AESA (43, 86, or 172 mg/kg/day) or captopril (20 mg/kg/day) administered orally was assessed in L-NAME- (40 mg/kg/day) treated rats. Blood pressure and heart rate (HR) were measured at the end of each week while serum or urinary nitric oxide (NO), creatinine, and glomerular filtration rate (GFR) were determined at the end of the 6 weeks of treatment, as well as histological analysis of the heart and the kidney. The LC-MS profiling of AESA identified 9 compounds including 7 alkaloids. AESA produced a concentration-dependent relaxation on contraction induced either by PE and KCl, which was significantly reduced in endothelium-denuded vessels, as well as in vessels pretreated with indomethacin and methylene blue. Moreover, AESA inhibited the intracellular Ca2+ release-induced contraction. In vivo, AESA reduced the AHT, heart rate (HR), and ventricular hypertrophy and increased serum NO, urine creatinine, and GFR. AESA also ameliorated heart and kidney lesions as compared to the L-NAME group. These findings supported the use of AESA as a potential antihypertensive drug.

Comparison of the hemodynamic effects of nitric oxide and endothelium-dependent vasodilators in intact lungs

1990 ◽  
Vol 68 (2) ◽  
pp. 735-747 ◽  
Author(s):  
S. L. Archer ◽  
K. Rist ◽  
D. P. Nelson ◽  
E. G. DeMaster ◽  
N. Cowan ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Methylene Blue ◽  
Pulmonary Hypertension ◽  
Feedback Inhibition ◽  
Pressor Response ◽  
Pulmonary Vasculature ◽  
Hemodynamic Effects ◽  
Isolated Lung

The effects of endothelium-dependent vasodilation on pulmonary vascular hemodynamics were evaluated in a variety of in vivo and in vitro models to determine 1) the comparability of the hemodynamic effects of acetylcholine (ACh), bradykinin (BK), nitric oxide (NO), and 8-bromo-guanosine 3′,5′-cyclic monophosphate (cGMP), 2) whether methylene blue is a useful inhibitor of endothelium-dependent relaxing factor (EDRF) activity in vivo, and 3) the effect of monocrotaline-induced pulmonary hypertension on the responsiveness of the pulmonary vasculature to ACh. In isolated rat lungs, which were preconstricted with hypoxia, ACh, BK, NO, and 8-bromo-cGMP caused pulmonary vasodilation, which was not inhibited by maximum tolerable doses of methylene blue. Methylene blue did not inhibit EDRF activity in any model, despite causing increased pulmonary vascular tone and responsiveness to various constrictor agents. There were significant differences in the hemodynamic characteristics of ACh, BK, and NO. In the isolated lung, BK and NO caused transient decreases of hypoxic vasoconstriction, whereas ACh caused more prolonged vasodilation. Pretreatment of these lungs with NO did not significantly inhibit ACh-induced vasodilation but caused BK to produce vasoconstriction. Tachyphylaxis, which was agonist specific, developed with repeated administration of ACh or BK but not NO. Tachyphylaxis probably resulted from inhibition of the endothelium-dependent vasodilation pathway proximal to NO synthesis, because it could be overcome by exogenous NO. Pretreatment with 8-bromo-cGMP decreased hypoxic pulmonary vasoconstriction and, even when the hypoxic pressor response had largely recovered, subsequent doses of ACh and NO failed to cause vasodilation, although BK produced vasoconstriction. These findings are compatible with the existence of feedback inhibition of the endothelium-dependent relaxation by elevation of cGMP levels. Responsiveness to ACh was retained in lungs with severe monocrotaline-induced pulmonary hypertension. Many of these findings would not have been predicted based on in vitro studies and illustrate the importance for expanding studies of EDRF to in vivo and ex vivo models.

Hydrogen sulfide downregulates the aortic l-arginine/nitric oxide pathway in rats

2007 ◽  
Vol 293 (4) ◽  
pp. R1608-R1618 ◽  
Author(s):  
Bin Geng ◽  
Yuying Cui ◽  
Jing Zhao ◽  
Fang Yu ◽  
Yi Zhu ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Hydrogen Sulfide ◽  
Umbilical Vein ◽  
Transcript Abundance ◽  
Inhibitory Effect ◽  
Akt Phosphorylation ◽  
Enos Activity ◽  
Nos Inhibitors

The aim of the present study was to investigate the effect of hydrogen sulfide (H2S) signaling by nitric oxide (NO) in isolated rat aortas and cultured human umbilical vein endothelial cells (HUVECs). Both administration of H2S and NaHS, as well as endogenous H2S, reduced NO formation, endothelial nitric oxide synthase (eNOS) activity, eNOS transcript abundance, and l-arginine (l-Arg) transport (all P < 0.01). The kinetics analysis of eNOS activity and l-Arg transport showed that H2S reduced Vmax values (all P < 0.01) without modifying Km parameters. Use of selective NOS inhibitors verified that eNOS [vs. inducible NOS (iNOS) and neuronal NOS (nNOS)] was the specific target of H2S regulation. H2S treatment (100 μmol/l) reduced Akt phosphorylation and decreased eNOS phosphorylation at Ser1177. H2S reduced l-Arg uptake by inhibition of a system y+ transporter and decreased the CAT-1 transcript. H2S treatment reduced protein expression of eNOS but not of nNOS and iNOS. Pinacidil (KATP channel opener) exhibited the similar inhibitory effects on the l-Arg/NOS/NO pathway. Glibenclamide (KATP channel inhibitor) partly blocked the inhibitory effect of H2S and pinacidil. An in vivo experiment revealed that H2S downregulated the vascular l-Arg/eNOS/NO pathway after intraperitoneal injection of NaHS (14 μmol/kg) in rats. Taken together, our findings suggest that H2S downregulates the vascular l-Arg/NOS/NO pathway in vitro and in vivo, and the KATP channel could be involved in the regulatory mechanism of H2S.

scholarly journals Inhibitory effect of nitric oxide on the replication of a murine retrovirus in vitro and in vivo.

1995 ◽  
Vol 69 (11) ◽  
pp. 7001-7005 ◽  
Author(s):  
K Akarid ◽  
M Sinet ◽  
B Desforges ◽  
M A Gougerot-Pocidalo
Keyword(s):  
Nitric Oxide ◽  
Inhibitory Effect

Nitric oxide as a putative nonadrenergic noncholinergic inhibitory transmitter in the canine pylorus in vivo

1992 ◽  
Vol 262 (4) ◽  
pp. G695-G702 ◽  
Author(s):  
H. D. Allescher ◽  
G. Tougas ◽  
P. Vergara ◽  
S. Lu ◽  
E. E. Daniel
Keyword(s):  
Nitric Oxide ◽  
Sodium Nitroprusside ◽  
Vagal Stimulation ◽  
Inhibitory Effect ◽  
Field Stimulation ◽  
Neural Inhibition ◽  
Anesthetized Dogs ◽  
Inhibitory Transmitter

Antropyloroduodenal motility was recorded in seven anesthetized dogs to assess the role of nitric oxide and L-arginine metabolites in nonadrenergic noncholinergic (NANC) mediation of pyloric relaxation. Pyloric activity induced by duodenal field stimulation was inhibited by antral field stimulation and electrical vagal stimulation. Intra-arterial NG-L-arginine-methyl-ester (L-NAME) reduced the inhibition from antral or vagal stimulation (P less than 0.05). Intravenous infusion of L-NAME also blocked the inhibitory effect of vagal and antral stimulation but left the tetrodotoxin-insensitive action of intra-arterial vasoactive intestinal peptide (VIP) and sodium nitroprusside unchanged. L-Arginine reversed the effect of L-NAME whereas D-arginine did not. L-NAME enhanced pyloric contractions to intra-arterial acetylcholine. The NANC inhibition of the substance P-stimulated pyloric response in vitro was blocked by L-NAME and reversed by addition of L-arginine. Sodium nitroprusside was effective as a relaxant in vitro but VIP was not. These data suggest that metabolites of L-arginine mediate neural inhibition of canine pyloric motor activity.

Effect of Peganum Harmala Seeds Extract on Nitric Oxide in U937 Monocytes and Macrophages

2020 ◽  
Author(s):  
Nima Rahmati ◽  
Fatemeh Hajighasemi
Keyword(s):  
Nitric Oxide ◽  
Aqueous Extract ◽  
Calf Serum ◽  
Peritoneal Macrophages ◽  
No Production ◽  
Peganum Harmala ◽  
Logarithmic Growth Phase ◽  
Anti Inflammatory

Background and Aims: Nitric oxide (NO) has an essential role in inflammation and has been related to pathogenesis and the progress of numerous inflammatory-based diseases, including some cancers. Peganum harmala (P. harmala) is a medicinal plant used for the treatment of numerous diseases such as several infections. Also, anti-inflammatory effects of P. harmala extracts and its derivatives (harmaline and harmine) by suppressing myeloperoxidase, NO, and other mediators have been demonstrated in vivo. In this study, the effect of P. harmala seeds aqueous extract on NO production in U937 monocytic cells and peritoneal macrophages has been evaluated in vitro. Materials and Methods: U937 and mice peritoneal macrophages were cultured in Roswell Park Memorial institute-1640 with 10% fetal calf serum. Then, the cells at the logarithmic growth phase were incubated with different concentrations of aqueous extract of P. harmala seeds (0.1-1 mg/ml) for 24 hours. Next, NO production was assessed by the Griess method in the culture medium. Results: P. harmala seeds aqueous extract did not significantly affect lipopolysaccharide-induced NO production in U937 cells and peritoneal macrophages after 24 hours incubation time compared with untreated control cells. Conclusion: These results suggest that the anti-inflammatory effects of P. harmala may be mediated through NO-independent mechanism(s). However, further studies are warranted to define the P. harmala aqueous extract impact on NO expression in other related normal and cancerous cells.

Aqueous Extract of Brassica rapa Exerts Antihyperglycemic Activity in Streptozotocin-induced Diabetic Rats

2021 ◽  
Vol 21 ◽  
Author(s):  
Ismail Bouadid ◽  
Ayoub Amssayef ◽  
Nadia Lahrach ◽  
Ahmed El-Haidani ◽  
Mohamed Eddouks
Keyword(s):  
Brassica Rapa ◽  
Aqueous Extract ◽  
Diabetic Rats ◽  
Lipid Profiles ◽  
Antioxidant Effect ◽  
Phytochemical Analysis ◽  
Glucose Levels ◽  
Blood Glucose Levels

Aims: The aim of the study was to assess the antihyperglycemic effect of Brassica rapa. Background: Brassica rapa (turnip) is used as an antidiabetic plant. Objective: This work aimed to evaluate the effect of the aqueous extract of Brassica rapa seeds (AEBRS) on glycemia in vivo. Methods: The effect of AEBRS (60 mg/kg) on glycemia and lipid profiles was evaluated. Besides, preliminary phytochemical analysis and the in vitro antioxidant effect were evaluated. Results: AEBRS caused a significant reduction in blood glucose levels in diabetic rats (p<0.0001). In contrast, no significant effect was observed on lipid profiles, whereas antioxidant potential of this extract has been shown. Phytochemical analysis showed the presence of many important phytochemical families. Conclusion: The present study shows that AEBRS has a potent antihyperglycemic ability in diabetic rats.

scholarly journals Drug library screen identifies inhibitors of toxic astrogliosis

2020 ◽  
Author(s):  
Ruturaj R Masvekar ◽  
Peter R Kosa ◽  
Christopher Barbour ◽  
Joshua L Milstein ◽  
Bibiana Bielekova
Keyword(s):  
Multiple Sclerosis ◽  
Endoplasmic Reticulum ◽  
Cerebrospinal Fluid ◽  
Calcium Release ◽  
Ryanodine Receptors ◽  
Mammalian Target Of Rapamycin ◽  
Inhibitory Effect ◽  
Multiple Sclerosis Patients

Objective: Multiple sclerosis is a chronic neuroinflammatory disorder, in which activated immune cells directly or indirectly induce demyelination and axonal degradation. Inflammatory stimuli also change the phenotype of astrocytes, making them neurotoxic. The resulting toxic astrocyte phenotype has been observed in animal models of neuroinflammation and in multiple sclerosis lesions. Proteins secreted by toxic astrocytes are elevated in the cerebrospinal fluid of multiple sclerosis patients and reproducibly correlate with the rates of accumulation of neurological disability and brain atrophy. This suggests a pathogenic role for neurotoxic astrocytes in multiple sclerosis. Methods: Here, we applied a commercially available library of small molecules that are either Food and Drug Administration-approved or in clinical development to an in vitro model of toxic astrogliosis to identify drugs and signaling pathways that inhibit inflammatory transformation of astrocytes to a neurotoxic phenotype. Results: Inhibitors of three pathways related to the endoplasmic reticulum stress: 1) proteasome, 2) heat shock protein 90 and 3) mammalian target of rapamycin reproducibly decreased inflammation-induced conversion of astrocytes to toxic phenotype. Dantrolene, an anti-spasticity drug that inhibits calcium release through ryanodine receptors expressed in the endoplasmic reticulum of central nervous system cells, also exerted inhibitory effect at in vivo achievable concentrations. Finally, we established cerebrospinal fluid SERPINA3 as a relevant pharmacodynamic marker for inhibiting toxic astrocytes in clinical trials. Interpretation: Drug library screening provides mechanistic insight into the generation of toxic astrocytes and identifies candidates for immediate proof-of-principle clinical trial(s).

scholarly journals Evaluation of in vitro Cholesterol esterase inhibitory and in vivo Anti-hyperlipidemic activity of aqueous extract of Plukenetia conophora Mull. Arg. (Euphorbiaceae)

2019 ◽  
Vol 11 (1) ◽  
Author(s):  
Glory Oluremilekun Ajayi ◽  
Aleshe Modupe Nofisat ◽  
Bassey Mfon Jessica
Keyword(s):  
Aqueous Extract ◽  
Cholesterol Esterase ◽  
High Cholesterol Diet ◽  
Phytochemical Analysis ◽  
Cholesterol Diet ◽  
High Cholesterol ◽  
Edible Plant ◽  
Standard Drug

<p>Hyperlipidemia is a condition of abnormally high lipids levels in the blood which has been ranked as one of the greatest risk factors contributing to prevalence and severity of coronary heart disease. The available antihyperlipidemic drugs have been associated with some side effects however, herbal management of hyperlipidemia are relatively safe, cheap and readily available. <em>P. conophora</em> is an edible plant consumed in Nigeria as snack and speculated to have beneficial effect on blood lipid profile. The present study evaluates anti-hyperlipidemic effect of aqueous extract of cooked <em>P.  conophora </em>nut using <em>in vivo</em> and <em>in vitro</em> experimental models.</p><p>The anti-hyperlipidemic activity was evaluated using tyloxapol induced-hyperlipidemic rats by intraperitoneal injections of Tyloxapol at a dose of 300 mg/kg body weight and high cholesterol-diet induced rats by oral administration of high cholesterol diet for 60 days. Cholesterol esterase enzyme inhibition was used for the <em>in vitro</em> evaluation.</p><p class="Default">Aqueous extract of <em>P. conophora</em><em> </em>at varying doses, reduced the elevated lipid parameters in both models; the dose of 500 mg/kg showed comparable hypolipidemic effects with standard drug (Simvastatin) at 10 mg/kg (P&lt;0.01). The extract also inhibited cholesterol esterase enzyme with IC<sub>50</sub> value of 129.30±0.10μg/ml while Simvastatin with IC<sub>50</sub> value of 51.42±0.13μg/ml. Preliminary phytochemical analysis revealed the presence of; Flavonoids, saponin, cardiac glycoside, alkaloids, tannins, steroids and reducing sugar.</p><p class="Default"><em>P. conophora </em>extract<em> </em>exhibited strong hypolipidemic activity and the dose of 500mg/kg demonstrated equipotent activity as the standard drug; Simvastatin 10mg/kg. The extract also showed inhibitory activity against pancreatic cholesterol esterase enzyme; hence can be used to limit absorption of dietary cholesterol, prevent and treat hyperlipidemia.</p>

Antihypertensive and Vasorelaxant Effects of Cinnamomum zeylanicum Stem Bark Aqueous Extract in Rats

2011 ◽  
Vol 8 (1) ◽  
Author(s):  
Paulin Nyadjeu ◽  
Alain Dongmo ◽  
Télesphore Benoît Nguelefack ◽  
Albert Kamanyi
Keyword(s):  
Nitric Oxide ◽  
Aqueous Extract ◽  
Katp Channels ◽  
Stem Bark ◽  
In Vitro Tests ◽  
Cinnamomum Zeylanicum ◽  
Arterial Blood ◽  
Pre Treatment

The present study was undertaken to evaluate the antihypertensive and vasorelaxant effects of Cinnamomum zeylanicum Blume stem bark aqueous extract in rats. The in vivo activities of the extract were evaluated on normotensive and three rat models of hypertension while the in vitro tests were assayed on rat isolated aorta rings. Acute intravenous injection of the extract (5, 10 and 20mg/kg) induced a significant reduction in mean arterial blood pressure in anaesthetised normotensive Wistar rats, salt-loaded hypertensive, L-NAME hypertensive and spontaneously hypertensive rats. Pre-treatment of rats with either propranolol or atropine significantly inhibited the hypotensive effects of the plant extract suggesting its possible action through the interferences with both cholinergic and sympathetic transmissions. Moreover, pre-treatment of rats with L-NAME inhibited the sustained plant antihypertensive effects, suggesting a possible active vasodilatation, which might be partly mediated by an endothelial l-arginine/nitric oxide pathway. In isolated rat aortic rings pre-contracted with KCl (60mM), the extract exhibited cumulative vasodilating effects, which were attenuated with either L-NAME, vascular endothelium removal or both tetraethylammonium and glibenclamide pre-treatments. The vasorelaxant effects may be involved in the extract antihypertensive mechanism, partially by increasing the endothelial nitric oxide and by activating the KATP channels in vascular smooth muscle.

scholarly journals A Review ofIn VitroandIn VivoStudies on the Efficacy of Herbal Medicines for Primary Dysmenorrhea

2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Kyoung-Sun Park ◽  
Kang-In Park ◽  
Deok-Sang Hwang ◽  
Jin-Moo Lee ◽  
Jun-Bock Jang ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Somatostatin Receptor ◽  
Herbal Medicines ◽  
Inhibitory Effect ◽  
Phospholipid Metabolism ◽  
Reproductive Age ◽  
Herbal Formula ◽  
Primary Dysmenorrhea

Purpose. Primary dysmenorrhea (PD) is a common gynecological complaint among adolescent girls and women of reproductive age. This study aims to review the findings of published articles on thein vitroandin vivoefficacy of herbal medicines for PD.Methods.In vitroandin vivostudies of herbal compounds, individual herbal extracts, or herbal formula decoctions published from their inception to April 2014 were included in this review.Results. A total of 18 studies involving herbal medicines exhibited their inhibitory effect on PD. The majority ofin vitrostudies investigated the inhibition of uterine contractions.In vivostudies suggest that herbal medicines exert a peripheral analgesic effect and a possible anti-inflammatory activity via the inhibition of prostaglandin (PG) synthesis. The mechanisms of herbal medicines for PD are associated with PG level reduction, suppression of cyclooxygenase-2 expression, superoxide dismutase activation and malondialdehyde reduction, nitric oxide, inducible nitric oxide synthase, and nuclear factor-kappa B reduction, stimulation of somatostatin receptor, intracellular Ca2+reduction, and recovery of phospholipid metabolism.Conclusions. Herbal medicines are thought to be promising sources for the development of effective therapeutic agents for PD. Further investigations on the appropriate herbal formula and their constituents are recommended.

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