Influence of mao-inhibitors, neuroleptics, morphine, mescaline, divascan, aconitine, and pyrogenes on prostaglandin-biosynthesis

Bekemeier, H; Giessler, A. J.; Vogel, E.

doi:10.1016/s0031-6989(77)80087-8

Cited by 17 publications

(2 citation statements)

References 22 publications

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“…COX-2 inhibitors inhibited the PGE 2 synthesis, suggesting a potential positive role in depression [17][18]. Several studies have reported that antidepressant drugs could inhibit PGE 2 synthesis including MAO inhibitors [19][20][21][22] and Tricyclic antidepressants [23].…”

Section: Introductionmentioning

confidence: 99%

Possible Influence of Loxoprofen in Lipopolysaccharide Induced Alterations in Sucrose Intake in Chronic Mild Stress Model in Mice

Rana

2021

Asian J Pharm Clin Res

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Objective: The objective of the present study was to evaluate the influence of Loxoprofen in sucrose intake in the absence and presence of Lipopolysaccharide in chronic mild stress model of depression in mice. Methods: There was a measurement of sucrose intake in chronic mild stress model (CMS), consisting of 21 days stress schedule in which mice were subjected to the treatment of Loxoprofen (16.8 mg/kg, p.o.) with or without treatment of lipopolysaccharide (LPS) (0.5 mg/kg i.p.) for the past 14 days. Results: The result of the present study indicated that mice treated with Venlafaxine and Loxoprofen showed a significant increase in the sucrose intake in stressed mice in chronic mild stress model. LPS-treated mice presented a decrease in sucrose intake when compared to controls. Similarly, Venlafaxine and Loxoprofen in the presence of LPS could increase the sucrose intake as compared to LPS treated stressed mice. Conclusion: The results of the present study showed that Loxoprofen could influence LPS induced alterations in sucrose intake in mice in chronic mild stress model. It can also indicate the possible anti-depressant effect of Loxoprofen in mice subjected to chronic mild stress model of depression, having its possible implication in future treatment of depression.

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Section: Introductionmentioning

confidence: 99%

Possible Influence of Loxoprofen in Lipopolysaccharide Induced Alterations in Sucrose Intake in Chronic Mild Stress Model in Mice

Rana

2021

Asian J Pharm Clin Res

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“…Since then the problem has been much studied, and many investigators have amassed a convincing body of evidence that opioid ligands influence the effects of prostaglandins, a cyclooxygenase metabolite of AA [2-51. Morphine has been shown to inhibit, in many tissues, the effects of prostaglandins [2,3] but stimulate their synthesis [4,5]. The relationship between opioid ligands and prostaglandins, however, has not been studied in cells of the immune system.…”

Section: Introductionmentioning

confidence: 99%

Direct influence of morphine on the release of arachidonic acid and its metabolites

et al. 1993

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The influence of 10−10–10−6 M morphine on the release of [3H]arachidonic acid and its metabolites ([3H]AAM) from prelabeled resident peritoneal murine macrophages was investigated. Morphine enhanced [3H]AAM release from A23187‐ and LPS‐stimulated macrophages, as well as the basal release of [3H]AAM. Dose‐response curves showed a maximum at 10−8 M morphine. Naloxone had no effect on morphine enhancement of [3H]AAM release. These results are in agreement with the hypothesis that [3H]AAM may be involved in the effects of morphine.

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Biochemical Effects of Alkaloids

Robinson

1981

Molecular Biology Biochemistry and Biophysics

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Influence of mao-inhibitors, neuroleptics, morphine, mescaline, divascan, aconitine, and pyrogenes on prostaglandin-biosynthesis

Cited by 17 publications

References 22 publications

Possible Influence of Loxoprofen in Lipopolysaccharide Induced Alterations in Sucrose Intake in Chronic Mild Stress Model in Mice

Possible Influence of Loxoprofen in Lipopolysaccharide Induced Alterations in Sucrose Intake in Chronic Mild Stress Model in Mice

Direct influence of morphine on the release of arachidonic acid and its metabolites

Biochemical Effects of Alkaloids

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