scholarly journals Effect of Duloxetine Pretreatment on 5-HTP and Dexfenfluramine Induced Behaviours in Albino Rats

2019 ◽  
Vol 12 (3) ◽  
pp. 1339-1343
Author(s):  
Vandana Milind Thorat ◽  
Chitra C Khanwelkar ◽  
Somnath Mallikarjun Matule ◽  
Pratibha Satish Salve ◽  
Smita Ajit Surle-Patil ◽  
...  
Keyword(s):  
Serotonin Transporter ◽  
Behavioural Syndrome ◽  
Albino Rats ◽  
Behavioral Syndrome ◽  
Serotonergic Receptors ◽  
Central Brain ◽  
Pre Treatment ◽  
Stimulation Of

Activation of central brain serotonergic receptors viz 5-HT1A and 5-HT2A by serotonin (5-HT) induces the 5-HT behavioural syndrome in rats. 5-HTP and dexfenfluramine produce 5-HT mediated behaviours. We have carried out the experiment with the aim to study the effect of duloxetine pretreatment on 5-hydroxytryptophan and dexfenfluramine induced behaviours in albino rats. Pre-treatment with 20 mg/kg duloxetine, a SNRI was found to potentiate 75 mg/kg 5-HTP mediated behavioural syndrome. However, 5, 10 and 20 mg/kg duloxetine had decreased the intensity of the behavioral syndrome produced by 10 mg/kg dexfenfluramine significantly. Duloxetine at 5, 10 and 20 mg/kg had produced inhibition of serotonin transporter (SERT) and inhibited dexfenfluramine uptake which had significantly antagonised its behavioural syndrome. Duloxetine at 5 and 10 mg/kg did not affect 5-HTP induced behavioral syndrome significantly where as 20 mg/kg duloxetine did significantly potentiate 5-HTP induced behavioral syndrome. This indicates 20 mg/kg dose of duloxetine blocks neuronal reuptake of 5-HT by blocking SERT and effectively increase its concentration to greater level in the synaptic gap which causes synergistic stimulation of the central postsynaptic 5-HT1A and 5-HT2A receptors and potentiation of 5-HTP behavioral syndrome.

scholarly journals Ethyl acetate fraction of Cola hispida leaf protects against doxorubicin-induced myocardial injury in male albino rats

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Chiemeka Lynda Umenwanne ◽  
Martins Obinna Ogugofor ◽  
Obioma U. Njoku
Keyword(s):  
Lipid Peroxidation ◽  
Antioxidant Enzymes ◽  
Ethyl Acetate ◽  
Myocardial Injury ◽  
Ethyl Acetate Fraction ◽  
Albino Rats ◽  
Cardiac Biomarker ◽  
Novel Drugs ◽  
Myxomatous Degeneration ◽  
Pre Treatment

Abstract Background Cardiovascular diseases have continued to be the leading cause of death globally. In addition, some of the drugs used in the treatment of the diseases present some adverse effects which limit the usefulness of such drugs. Thus, there is a need for novel drugs whose side effect is either minimal or non-existent. The presence of bioactive compounds in Cola hispida leaf is of great significance in the treatment and management of cardiovascular conditions. This study investigated the cardio-protective potential against doxorubicin (Dox)-induced cardiac infarction in rats. Results Dox induction resulted to muscle fiber degeneration in Dox-treated rats hence revealed significant (p < 0.05) elevation in the serum level of cardio biomarker enzymes and lipid peroxidation profile while significant (p < 0.05) fall in cardiac enzymatic antioxidant levels were observed relative to the normal control. Pre-treatment with ethyl acetate fraction of Cola hispida leaf expressed cardio-protective potentials against Dox-induced cardiotoxicity by significantly (p < 0.05) lowering the levels of cardiac biomarker enzymes towards normal, building up the activities of subdued antioxidant enzymes and depleting its malondialdehyde level. Histopathology photomicrograph of the heart tissues expressed myxomatous degeneration but was ameliorated through the administration of the fraction. Conclusion In accordance with the findings from this study, the administration of ethyl acetate fraction of Cola hispida leaf is effective against Dox-induced redox imbalance due to its enriched antioxidant phytoconstituents.

Ovine corticotrophin-releasing factor in dogs: dose-response relationships and effects of dexamethasone

1986 ◽  
Vol 112 (1) ◽  
pp. 12-19 ◽  
Author(s):  
R.J. Kemppainen ◽  
D. V. Filer ◽  
J. L. Sartin ◽  
R. B. Reed
Keyword(s):  
Dose Response ◽  
Plasma Cortisol ◽  
Peak Plasma ◽  
Cortisol Response ◽  
Corticotrophin Releasing Factor ◽  
Pre Treatment ◽  
The Relationship ◽  
Dose Dependent ◽  
Response Area ◽  
Stimulation Of

Abstract. Dose-response relationships between iv bolus injections (0, 0.1, 1 or 10 μg/kg) of synthetic ovine corticotropin-releasing factor (oCRF) and plasma immunoreactive (i) ACTH and cortisol concentrations were examined in healthy, conscious dogs. All doses of oCRF resulted in elevated plasma iACTH and cortisol levels over those of the controls. Maximum (or Peak) plasma iACTH concentrations were generally observed 20–30 min after oCRF and the magnitude of these peaks was a linear function (P<0.001) of the logarithm of the oCRF dose. The time of peak cortisol concentrations was more variable but the peak cortisol level was also linearly related (P< 0.001) to the logarithm of the oCRF dose. An estimate for the response areas for both hormones demonstrated a quadratic (P < 0.05) relationship with the logarithm of the oCRF dose. The relationship between oCRF and the iACTH response suggested a progressively greater response at increasing oCRF doses while a maximally effective oCRF dose was predicted in the cortisol response area relationship. Graded (0, 0.01, 0.1 or 1 mg/kg) bolus doses of dexamethasone produced a dose-dependent (P < 0.03) decline in baseline plasma iACTH levels and a non-dosedependent suppression in baseline plasma cortisol. Pre-treatment with 0.001 mg dexamethasone/kg 4 or 8 h before injection of 1 μg oCRF/kg did not alter the plasma iACTH or cortisol response; however, 0.1 mg dexarhethasone/kg administered at these times totally abolished the responses to oCRF. An intermediate dose (0.01 mg/kg) of dexamethasone inhibited the plasma iACTH response by an average of 79% (P<0.01) when administered 4 h before oCRF, but did not significantly alter this response when given 8 h prior to oCRF. The plasma cortisol response to oCRF was inhibited (P < 0.01) when 0.01 mg dexamethasone/kg was given as a 4 h, but not as a 8 h, pre-treatment. Iv administration of oCRF produces a profound, dose-dependent stimulation of the pituitary-adrenocortical axis of dogs and should prove useful in studies of this system.

scholarly journals Leptin inhibits insulin-stimulated incorporation of glucose into lipids and stimulates glucose decarboxylation in isolated rat adipocytes

1998 ◽  
Vol 158 (3) ◽  
pp. R7-R9 ◽  
Author(s):  
RB Ceddia ◽  
FB Lima ◽  
R Curi ◽  
Keyword(s):  
Energy Homeostasis ◽  
Biological Effects ◽  
Albino Rats ◽  
Mediated Effects ◽  
Glucose Incorporation ◽  
14Co2 Production ◽  
Isolated Adipocytes ◽  
Per Se ◽  
Isolated Rat ◽  
Stimulation Of

Leptin is an adipocyte hormone involved in the regulation of energy homeostasis. Generally accepted biological effects of leptin are inhibition of food intake and stimulation of metabolic rate in ob/ob mice, that are defective in the leptin gene. In contrast to these centrally mediated effects of leptin, we are reporting here on leptin effects on glucose incorporation into lipids and glucose decarboxylation in adipocytes isolated from male lean albino rats. Adipocytes previously cultivated (15 h) in the presence of leptin presented a 25% (P < 0.05) reduction of the insulin stimulated incorporation of glucose into lipids. Concurrently, the basal conversion of (U-14C)D-glucose into 14CO2 increased (110%) in the leptin cultivated adipocytes and reached values (1.54 nmol/10(5) cells) similar to the insulin stimulated group (not cultivated with leptin) (1.40 nmol/10(5) cells). In addition, in the presence of insulin, the leptin cultivated adipocytes elicited a 162% (P < 0.05) increase in 14CO2 production that was significantly higher than the increase observed for the not-leptin-cultivated insulin group (92%). We conclude that leptin: 1) directly inhibits the insulin stimulated glucose incorporation into lipids; 2) stimulates glucose decarboxylation, and also potentiates the effect of insulin on glucose decarboxylation in isolated adipocytes. Leptin per se does not alter glucose incorporation into lipids.

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