scholarly journals TIME COURSE STUDY OF COMBINED N-ACETYL-P-AMINOPHENOL AND DICLOPHENAC INDUCED-HEPATOTOXICITY AND OXIDATIVE STRESS IN WISTAR RATS

2021 ◽  
Vol 46 (2) ◽  
Author(s):  
O. A Dosumu ◽  
D. I. Akinloye ◽  
O. B. Onunkwor ◽  
F. C. Thomas ◽  
R. A. Adeyemo
Keyword(s):  
Oxidative Stress ◽  
Liver Damage ◽  
Wistar Rats ◽  
Time Course ◽  
Time Dependent ◽  
Control Group ◽  
Gamma Glutamyl Transferase ◽  
Dependent Manner ◽  
Glutamyl Transferase ◽  
And Oxidative Stress

The abuse of combined acetaminophen or N-acetyl-p-aminophenol (APAP) and diclofenac (DIC) due to their analgesics, anti-inflammatory and antipyretic properties is a predominant cause of hepatotoxicity and oxidative stress. This study investigated the time-course effects of APAP, DIC and their combination on biomarkers of hepatic function and oxidative stress in rats. Forty male Wistar rats were randomly divided into four groups of 10 animals each as follows; control (distilled water), APAP only, DIC only and APAP + DIC for 4 weeks. Indices of liver damage (serum ALT, alanine aminotransferase; AST, aspartate aminotransferase; ALP, alkaline phosphatase; GGT, gamma-glutamyl transferase and bilirubin) were measured. Oxidative stress biomarkers (MDA, malondialdehyde; NO, nitric oxide; CAT, Catalase activity; SOD, superoxide dismutase activity; GSH content, reduced glutathione), GR, glutathione reductase, and GST, glutathione-S-transferase) were also determined using spectrophotometric methods. Statistical analysis was done using one-way ANOVA with p < 0.05 considered significant. Acetaminophen and diclofenac caused marked liver damage as noted by time-dependent significant (p < 0.05) increased activities of serum ALT, AST, ALP, GGT, and bilirubin levels as well as significant (p < 0.05) increase in hepatic MDA and NO levels as compared to the control group. Hepatic GSH content, SOD, CAT, GPx, GST and GR activities were decreased significantly (p < 0.05) in all acetaminophen and diclofenac-treated groups compared to normal control in a time-dependent manner. These findings suggest that prolonged administration of diclofenac, acetaminophen or their combination may induce hepatotoxicity, oxidative stress and alteration of hepatic antioxidant status in a time-dependent manner.

scholarly journals NF-κB and FosB mediate inflammation and oxidative stress in the blast lung injury of rats exposed to shock waves

2021 ◽  
Author(s):  
Hong Wang ◽  
Wenjuan Zhang ◽  
Jinren Liu ◽  
Junhong Gao ◽  
Le Fang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lung Injury ◽  
Shock Waves ◽  
Time Dependent ◽  
Inflammatory Factors ◽  
Control Group ◽  
Dependent Manner ◽  
Total Antioxidant ◽  
Blast Lung Injury ◽  
And Oxidative Stress

Abstract Blast lung injury (BLI) is the major cause of death in explosion-derived shock waves; however, the mechanisms of BLI are not well understood. To identify the time-dependent manner of BLI, a model of lung injury of rats induced by shock waves was established by a fuel air explosive. The model was evaluated by hematoxylin and eosin staining and pathological score. The inflammation and oxidative stress of lung injury were also investigated. The pathological scores of rats’ lung injury at 2 h, 24 h, 3 days, and 7 days post-blast were 9.75±2.96, 13.00±1.85, 8.50±1.51, and 4.00±1.41, respectively, which were significantly increased compared with those in the control group (1.13±0.64; P&lt;0.05). The respiratory frequency and pause were increased significantly, while minute expiratory volume, inspiratory time, and inspiratory peak flow rate were decreased in a time-dependent manner at 2 and 24 h post-blast compared with those in the control group. In addition, the expressions of inflammatory factors such as interleukin (IL)-6, IL-8, FosB, and NF-κB were increased significantly at 2 h and peaked at 24 h, which gradually decreased after 3 days and returned to normal in 2 weeks. The levels of total antioxidant capacity, total superoxide dismutase, and glutathione peroxidase were significantly decreased 24 h after the shock wave blast. Conversely, the malondialdehyde level reached the peak at 24 h. These results indicated that inflammatory and oxidative stress induced by shock waves changed significantly in a time-dependent manner, which may be the important factors and novel therapeutic targets for the treatment of BLI.

scholarly journals Manganese Inhibits Indomethacin-Induced Hepatorenal Oxidative Stress in Wistar Rats

2020 ◽  
pp. 79-90
Author(s):  
Tijani Stephanie Abiola ◽  
Olori Ogaraya David ◽  
Farombi Ebenezer Olatunde
Keyword(s):  
Oxidative Stress ◽  
Density Lipoprotein ◽  
Treated Group ◽  
Control Group ◽  
Gamma Glutamyl Transferase ◽  
Cellular Processes ◽  
Concomitant Reduction ◽  
Liver And Kidney ◽  
Glutamyl Transferase ◽  
And Oxidative Stress

Aim: Manganese (Mn) is an essential trace element in many cellular processes. However, there is dearth of literature on its influence on indomethacin-induced hepatorenal damage. Therefore, this study was conducted to investigate the effect of manganese on indomethacin-induced hepatorenal damage in rats. Methods: Rats were divided into four groups of eight rats consisting of control group, indomethacin (IND) alone (20 mg/kg), Mn alone (10 mg/kg) and co-treated group that were treated orally for 14 consecutive days. Twenty four hours after treatment, under pentobarbital anesthesia, blood was collected and liver was excised to prepare homogenate and histology staining. Liver and kidney function tests aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), gamma glutamyl transferase (GGT), lactate dehydrogenase (LDH), malate dehydrogenase (MDH), glutamine dehydrogenase (GLDH), sorbitol dehydrogenase (SDH), glucose-6-phosphate dehydrogenase (G6PD), bilirubin (BIL), urea, creatinine, cholesterol (CHOL), triglycerides (TG), low and high density lipoprotein (LDL and HDL), electrolytes and oxidative stress superoxide dismutase (SOD), catalase (CAT), glutathione (GSH) and lipid peroxidation (LPO) biomarkers were assessed. Results: The results showed that indomethacin caused hepatorenal damage in rats manifested with increase in serum hepatic and renal function biomarkers. But co-administration of IND with Mn significantly (p < 0.05) decreased the level of hepatorenal biomarkers. Additionally, co-administration of IND with Mn improved the antioxidant status with concomitant reduction of LPO and restored the integrity of the liver and kidney histologically. Conclusion: The results of this study emphasize that co-administration of IND with Mn to rats alleviated IND-induced hepatorenal toxicities and oxidative stress in rats.

scholarly journals Methanol Extract of Chasmanthera dependens Stem Mitigates against Mechanisms Involved in Piroxicam-induced Liver Damage in Rat

2020 ◽  
pp. 16-28
Author(s):  
Tijani Stephanie Abiola ◽  
Olori Ogaraya David ◽  
Farombi Ebenezer Olatunde
Keyword(s):  
Oxidative Stress ◽  
Liver Function ◽  
Oral Administration ◽  
Inflammatory Cytokines ◽  
Control Group ◽  
Gamma Glutamyl Transferase ◽  
Dependent Manner ◽  
Apoptotic Markers ◽  
Glutamyl Transferase ◽  
Pro Inflammatory Cytokines

Chasmanthera dependens has been claimed by tradition healers as a therapeutic agent in many diseases including hepatotoxicity. This study sought to evaluate the possible mechanisms involved in the hepatoprotective potential of tannin-rich extract of Chasmanthera dependens stem (TRECDS). Thirty two male Wistar rats (100- 130 g) were divided into four groups of eight rats per group labelled as group 1,2,3  and 4. The rats were treated orally for ten days consecutively.  Group 1 served as control group and received normal saline, group 2 rats received 40 mg/kg piroxicam alone, groups 3-4 were treated with 40 mg/kg piroxicam and 200 and 400 mg/kg TREDS respectively concomitantly. All the experimental rats were fed with standard rat chows. Twenty four hours after, blood was collected to obtain serum; liver was excised to prepare homogenate and histology staining under pentobarbital sodium anaesthesia. Liver function test (aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), gamma glutamyl transferase (GGT)) and oxidative stress (superoxide dismutase (SOD), catalase (CAT), glutathione (GSH) and lipid peroxidation (LPO)) biomarkers were assessed. Pro-inflammatory cytokines (tumor necrosis factor-α (TNF- α), interleukin-1β (IL-1β)) and apoptotic markers; caspase-3 (CASP-3) and caspase-9 (CAPS-9), cytochrome-c (CYT-c)) were also assessed. The results showed that piroxicam administration caused hepatic damage as was evident in the histological assessment with increased serum activities of liver function markers, levels of pro-inflammatory cytokines and apoptotic markers. TRECDS also showed significant attenuation of the oxidative stress by decreasing the LPO level and increasing the activities of SOD, CAT and GSH level. Oral administration of TRECDS also restores the morphological structure of the liver in a dose-dependent manner. Conclusion: Oral administration of TRECDS exhibited protective potential against piroxicam-induced hepatotoxicity.

scholarly journals PROTECTIVE ROLE AND ANTIOXIDANT ACTIVITY OF AQUEOUS EXTRACT OF ROSMARINUS OFFICINALIS AGAINST TRICHLOROACETATE-INDUCED TOXICITY IN LIVER OF MALE RATS

2018 ◽  
Vol 11 (6) ◽  
pp. 420
Author(s):  
Medhat Mostafa Abozid ◽  
Hoda Ea Farid
Keyword(s):  
Aqueous Extract ◽  
Liver Damage ◽  
Protective Role ◽  
Rosmarinus Officinalis ◽  
Male Rats ◽  
Control Group ◽  
Albino Rats ◽  
Gamma Glutamyl Transferase ◽  
Group I ◽  
Glutamyl Transferase

 Objective: The current study was designed to estimate the potential protective role of the aqueous extract of rosemary (AER) (Rosmarinus officinalis) against trichloroacetic acid (TCA)-created hepatotoxicity in male albino rats.Methods: Forty male albino rats were separated into four groups of ten: Group I served as control; Group II was given AER (200 mg/kg/day) by gavage; Group III received TCA at the dose 50 mg/kg/day, and Group V was treated with AER (200 mg/kg/day) and received TCA (50 mg/kg/day). The experiment was carried out for 2 months.Results: The toxicity of TCA for rats was revealed by an elevation in liver marker enzymes activities (gamma-glutamyl transferase [GGT], alkaline phosphatase [ALP], aspartate transaminase [AST], alanine aminotransferase [ALT]) and conjugated bilirubin (CB) level, and a decrease in albumin and total protein (TP) levels. The TCA administration also caused a significant increase in the activities of catalase (CAT), glutathione peroxidase (GPx) and superoxide dismutase (SOD), and also malondialdehyde (MDA) level in liver tissues. These biochemical effects were accompanied by histological indicators of liver damage. Treatment with ARE recovered the liver damage instigated by TCA, as showed by perfection of liver enzyme markers (GGT, ALT, AST, ALP), CB, TP and albumin; as well as antioxidant parameters (CAT, SOD, GPx) and lipid peroxidation (MDA) and amelioration of histopathology changes in the liver tissues.Conclusion: It could be concluded that AER supplementation for 2 months in TCA-induced toxicity in rats benefited hepatic antioxidant status and improved liver injury and damage in male albino rats exposed to TCA.

scholarly journals Roles of Moringa oleifera Leaf Extract in Improving the Impact of High Dietary Intake of Monosodium Glutamate-Induced Liver Toxicity, Oxidative Stress, Genotoxicity, DNA Damage, and PCNA Alterations in Male Rats

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Tarfa Albrahim ◽  
Manal Abdulaziz Binobead
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Leaf Extract ◽  
Liver Toxicity ◽  
Monosodium Glutamate ◽  
Male Rats ◽  
Control Group ◽  
Gamma Glutamyl Transferase ◽  
Glutamyl Transferase ◽  
The Impact

It is common for food to be made more palatable through the use of the flavour enhancer monosodium glutamate, also known as vetsin powder. The purpose of the study described in this paper was to explore how vetsin-induced hepatic toxicity, DNA fragmentation, damage, and oxidative stress modifications could be mitigated with moringa leaf extract (MLE). To that end, 40 male rats were separated into four groups: normal control, positive control or MLE, vetsin, and vetsin combined with MLE. Results indicated that, compared to the control group, the levels of serum alanine aminotransferase (ALT), aminotransferase (AST), alkaline phosphatase (ALP), gamma-glutamyl transferase (GGT), liver malondialdehyde (MDA), DNA damage, injury, PCNA, and P53 expressions were significantly enhanced by the administration of vetsin (P<0.05). However, the vetsin group had significantly reduced levels of albumin, globulin, total protein, liver glutathione (GSH), superoxide dismutase enzyme (SOD), catalase, and glutathione S-transferase (GST) enzyme activities (P<0.05) by comparison to control. Meanwhile, modifications in liver functions, oxidative stress, DNA damage, liver injury, and PCNA expression were alleviated when vetsin was administered alongside MLE. The authors conclude that vetsin may have many side effects and that MLE can ameliorate biochemical changes, oxidative stress, hepatic injury, PCNA, and P53 alterations induced by vetsin administration.

scholarly journals EVALUATION OF ANTIDEPRESSANT ACTIVITY OF ETHANOLIC EXTRACT OF LAGERSTROEMIA SPECIOSA LEAVES IN ALBINO WISTAR RATS

2019 ◽  
pp. 68-74
Author(s):  
VANITA KANASE ◽  
SUNITA VISHWAKARMA
Keyword(s):  
Oxidative Stress ◽  
Normal Saline ◽  
Restraint Stress ◽  
Wistar Rats ◽  
Ethanolic Extract ◽  
Antidepressant Activity ◽  
Control Group ◽  
Dependent Manner ◽  
Lagerstroemia Speciosa ◽  
Dose Dependent

Objective: The objective of the study was to evaluate the antidepressant activity of ethanolic extract of dried leaves of Lagerstroemia speciosa L. (EELS) on acute restraint stress (ARS)-induced depression-like behavior and biochemical alterations in albino Wistar rats. Methods: Thirty rats were randomly divided into five experimental groups. Group-I (normal control) rats received normal saline (2.0 ml/kg, p.o.) daily for 14 days; Group-II (stress control) rats received normal saline (2.0 ml/kg, p.o.) daily for 14 days and subjected to restraint stress on the 13th day. Group-III (standard drug-treated) rats received imipramine (15 mg/kg, p.o.) daily for 14 days and subjected to restraint stress on the 13th day. Groups-IV and V rats were treated with EELS (100 mg/kg and 300 mg/kg, p.o.) daily for 14 days subjected to ARS on the 13th day. Stress-like behavior was assessed by subjecting the rats to behavioral paradigms such as tail-suspension test (TST) and open field test (OFT), 40 min post-restraint stress procedure. Pretest of 10 min for forced swim test (FST) was also given to each rat simultaneously. Then, 23.5 h later, the relevant samples were administered and the main test performed 30 min later. Oxidative stress parameters such as superoxide dismutase (SOD), catalase (CAT), malondialdehyde (MDA), and extent of lipid peroxidation (LPO) were analyzed in restraint stress-induced animals and control group, following FST on the 15th day. Statistical Analysis: Expression of data was done as a mean standard error of the mean. The normally distributed data were subjected to one-way analysis of variance followed by Dunnett’s test. *p<0.05 was considered statistically significant. Results: It was observed that L. speciosa L. showed a significant dose-dependent decrease in duration of immobility time in TST and FST when compared with the control group in a dose-dependent manner. The results of OFT also showed a dose-dependent increase in locomotor activity. In addition to behavioral tests, EELS also normalized oxidative stress markers such as CAT, SOD, MDA, and LPO in a dose-dependent manner. Conclusion: The results suggest that the ethanolic extract of L. speciosa L. leaves possesses significant antidepressant property, may be recommended as a supplement for the antidepressant activity.

Ameliorative effect of trimetazidine on cisplatin-induced hepatotoxicity in rats

2016 ◽  
Vol 94 (2) ◽  
pp. 225-230 ◽  
Author(s):  
Hayam Ateyya ◽  
Hala Yosef ◽  
Manar A. Nader
Keyword(s):  
Liver Damage ◽  
Antioxidant Defense System ◽  
Serum Levels ◽  
Control Group ◽  
Gamma Glutamyl Transferase ◽  
Protective Effects ◽  
Bax Protein ◽  
Ameliorative Effect ◽  
Glutamyl Transferase ◽  
Per Oral

This study was designed to evaluate the protective effects of trimetazidine (TMZ) against cisplatin (CP) induced liver damage in rats. Animals were distributed among 4 groups as follows: control group; TMZ group (20 mg/kg body mass, per oral), which was treated for 10 days; CP group (6 mg/kg, by intraperitoneal injection), which received a single injection; and the CP + TMZ group (20 mg/kg, per oral), which received TMZ 4 days before and 6 days after CP injection. The extent of hepatic damage was studied by assessing biochemical parameters and histopathological evaluation of the extracted liver tissue. The results revealed that liver enzymes were markedly elevated after injection of CP, as evident from significant increases in the serum levels of alanine transaminase (AST), alanine aminotransferase (ALT), gamma glutamyl transferase (γ-GT), and lactate dehydrogenase (LDH), as well as marked changes to the liver architecture, with a significant decrease in serum levels of albumin. There were also marked changes to the antioxidant defense system, as indicated by significant decreases in total antioxidants and hepatic levels of reduced glutathione (GSH) and superoxide dismutase (SOD), together with a significant increase in lipid peroxidation. However, there was a significant increase in the activity of hepatic nuclear factor kappa B (NF-κB) as well as hepatic Bax protein expression. We conclude that TMZ protects against CP-induced liver damage through scavenging free radicals and anti-inflammatory and antiapoptotic effects, as well as through reducing NF-κB activation.

Fluazifop-p-butyl, an aryloxyphenoxypropionate herbicide, diminishes renal and hepatic functions and triggers testicular oxidative stress in orally exposed rats

2016 ◽  
Vol 33 (5) ◽  
pp. 406-415 ◽  
Author(s):  
Ayokanmi Ore ◽  
Ebenezer Tunde Olayinka
Keyword(s):  
Oxidative Stress ◽  
Hepatic Function ◽  
Dependent Manner ◽  
Lactate Dehydrogenase Activity ◽  
Group I ◽  
Male Wistar Rats ◽  
Glutamyl Transferase ◽  
The Impact ◽  
Dose Dependent ◽  
And Oxidative Stress

Fluazifop- p-butyl (FPB) is a selective aryloxyphenoxypropionate herbicide. Its phytotoxicity mechanism involves inhibition of lipid biosynthesis, free-radical generation, and oxidative stress in vulnerable plants. This study evaluates the impact of orally administered FPB on selected tissues in non-target animal model. Twenty-four male wistar rats (160–180g) were randomized into groups (I–IV). Group-I served as control, while animals in groups II, III, and IV received FPB at 18.75, 37.5, and 75 mg/kg body weight/day p.o., respectively, for 21 days. FPB caused significant ( p < 0.05) increase in plasma biomarkers of renal and hepatic function (urea, creatinine, bilirubin, alkaline phosphatase, alanine aminotransferase, and aspartate aminotransferase) when compared to control. Significant reductions in testicular ascorbic acid, glutathione, and activities of glutathione-S transferase, superoxide dismutase, and catalase were observed in FPB-treated animals when compared to control, in a dose-dependent manner. This was accompanied by increased testicular lipid peroxidation in the treated groups. Furthermore, a significant decrease in testicular acid phosphatase and γ-glutamyl transferase activities was also observed in the FPB-treated groups in a dose-dependent manner compared to control. However, testicular lactate dehydrogenase activity was significantly increased in the FPB-treated rats when compared to control. Additionally, histopathological studies revealed severe interstitial oedema and congestion of testicular blood vessels in the FPB-treated groups. Overall, data from this study suggest that FPB induced hepatotoxicity, nephrotoxicity, and oxidative stress-mediated alteration of testicular functions in rat.

scholarly journals BISPHENOL A DOSE- AND TIME-DEPENDENTLY INDUCES OXIDATIVE STRESS IN RAT LIVER MITOCHONDRIA EX VIVO

2018 ◽  
Vol 11 (9) ◽  
pp. 98 ◽  
Author(s):  
Mousumi Dutta ◽  
Goutam Paul
Keyword(s):  
Oxidative Stress ◽  
Bisphenol A ◽  
Rat Liver ◽  
Ex Vivo ◽  
Liver Mitochondria ◽  
Time Dependent ◽  
Incubation Mixture ◽  
Rat Liver Mitochondria ◽  
Control Group ◽  
Dependent Manner

Objective: The probable toxic effects of bisphenol A (BPA) on different physiological functions have been reported in animal models. The role of BPA in mitochondrial oxidative stress has not been reported till date. The present study is aimed to elucidate dose- and time-dependent oxidative stress generation by BPA, respectively, in rat liver mitochondria in ex vivo model. Methods: The incubation mixture of BPA-treated groups containing mitochondria, 50 mM potassium phosphate buffer (pH 7.4), and different concentrations of BPA (20–160 μM/ml) (dissolved in 12% DMSO) in a final volume of 1.0 ml was incubated at 37°C in incubator for different time durations (30 min–2 h). Whereas, the incubation mixture of control group contained DMSO (12%), mitochondria and 50 mM potassium phosphatebuffer (pH 7.4).’ will be replaced by ‘Whereas, the incubation mixture of control group contained the same constituents except BPA. Result: We have observed significant decrease in mitochondrial intactness incubated with BPA in dose- and time-dependent manner under bright field and confocal microscopic study compared to control. Further, we have observed a decrease in mitochondrial reduced glutathione (GSH) content and increase in lipid peroxidation and protein carbonylation levels in dose- and time-dependent manner in BPA-exposed mitochondria. We have found a significant increase in the activity of Mn-superoxide dismutase and decrease in the activities of GSH peroxidase, GSH reductase, pyruvate dehydrogenase, and other three enzymes of Kreb’s cycle dose and time dependently in BPA-exposed mitochondria. The results indicate that exposure to BPA leads to decrease in intactness of mitochondria and increase in oxidative stress in mitochondria isolated from rat liver in a dose- and time-dependent manner. Conclusion: It can be concluded that the incubation of mitochondria isolated from rat liver with BPA, caused oxidative stress-mediated damages in mitochondria in both dose- and time-dependent manners.

scholarly journals Human Urinary Kallidinogenase Reduces Lipopolysaccharide-Induced Neuroinflammation and Oxidative Stress in BV-2 Cells

2019 ◽  
Vol 2019 ◽  
pp. 1-6 ◽  
Author(s):  
Zhongyan Zhao ◽  
Zhiyu Xu ◽  
Tao Liu ◽  
Shixiong Huang ◽  
Huai Huang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Neurological Disorders ◽  
Interleukin 1 ◽  
Control Group ◽  
Tissue Kallikrein ◽  
Dependent Manner ◽  
Socioeconomic Burden ◽  
Dose Dependent ◽  
And Oxidative Stress ◽  
Necrosis Factor

Migraine is one of the most common neurological disorders which poses significant socioeconomic burden worldwide. Neuroinflammation and oxidative stress both play important roles in the pathogenesis of migraine. Human urinary kallidinogenase (UK) is a tissue kallikrein derived from human urine. Increasing evidence suggests that UK may protect against ischemic stroke, but UK’s treatment potential against migraine remains to be explored. Immortal BV-2 murine microglial cells were treated with UK (125 nM, 250 nM, and 500 nM) and then given lipopolysaccharides (LPS, 1000 ng/mL). Cell viability of BV-2 cells was tested by the CCK-8 assay. Expressions of tumor necrosis factor-α (TNFα), prostaglandin E2 (PGE2), interleukin-6 (IL-6), and interleukin-1β (IL-1β) were examined with the ELISA method and western blot. Intracellular reactive oxygen species (ROS) and malondialdehyde (MDA) were measured to determine oxidative stress. Our results showed that LPS administration increased the levels of proinflammatory cytokines (TNFα, PGE2, IL-6, and IL-1β) and oxidative stress (ROS and MDA) when compared with the control group and decreased significantly upon introduction with UK. Taken together, UK treatment reduced LPS-induced neuroinflammation and oxidative stress in a dose-dependent manner, which might be a potential treatment of migraine.

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