tagonist
08-20-2009, 07:06 PM
Since our fungus friends can blast us into outer space, why not into nod land? During one of my daily browsing through science and medical journals, this research article caught my eye:
Activity-Directed Fractionation of Pleurotus ostreatus. in the Search for Analgesics
Pharmaceutical Biology 2008, Vol. 46, No. 5, Pages 295-301 , DOI 10.1080/13880200801887047
N. S. Vasudewahttp://www.informahealthcare.com/entityImage/?code=200B*, D. T. U. Abeytungahttp://www.informahealthcare.com/entityImage/?code=200B* and W. D. Ratnasooriyahttp://www.informahealthcare.com/entityImage/?code=200B*Department of Chemistry, University of Colombo, Colombo, Sri Lanka
Department of Zoology, University of Colombo, Colombo, Sri Lanka
Department of Chemistry, University of Colombo, Colombo 3, Sri Lanka
Abstract
Pleurotus ostreatus. (Jacquin: Fries) P. Kummer (Tricholomataceae) was subjected to an antinociceptive activity-guided fractionation procedure in order to identify the fraction having highest activity. Three extracts, namely, acetone, dichloromethane, and hexane, were prepared at room temperature using fresh P. ostreatus., and 500 mg/kg was orally administered to male rats. The acetone extract showed significant antinociceptive activity with the hot-plate assay (male, 68%; p < 0.05), whereas dichloromethane and hexane extracts did not show significant activity. The same dose of acetone extract with female rats in the diestrous stage also showed prolongation of reaction time using the hot-plate test (female, 54%; p < 0.05). None of the extracts showed a significant increase in reaction time with the tail-flick test. The acetone extract was further fractionated by solvent partition to obtain four fractions (hexane, dichloromethane, ethyl acetate, and aqueous). Of these extracts, only the aqueous fraction showed marked prolongation in reaction time with the hot-plate test (500 mg/kg dose) on both male rats and on female rats in the diestrous stage (male, 37%; female, 26%). The aqueous fraction, following purification on a reverse phase column, yielded AqFrA-1, AqFrA-2, and AqFrA-3. Oral administration of a 500 mg/kg dose of these three fractions also showed marked prolongation in reaction time with the hot-plate test after 1 h of treatment (AqFrA-1, 26%; AqFrA-2, 69%; AqFrA-3, 101%). The effect was highest in AqFrA-3 at 1 h of treatment, and the effect lasted for 3 h. Hence, we can conclude that the compounds responsible for the activity have very high polarity. The acetone extract of P. ostreatus. did not induce a membrane-stabilizing effect and did not cause prostaglandin inhibition. Naloxone blocked the antinociceptive activity in the hot-plate test upon feeding of 500 mg/kg of acetone extract of P. ostreatus., indicating the mechanism of action is via opioid receptor mediation.
Folks, this is the common oyster mushroom. More research must be done to determine the receptor in which the extract binds to. Why didn't they use selective opioid antagonists?? :confused:
Erinacine E as a kappa opioid receptor agonist and its new analogs from a basidiomycete, Hericium ramosum.
A kappa opioid receptor binding inhibitor was isolated from the fermentation broth of a basidiomycete, Hericium ramosum CL24240 and identified as erinacine E (1). Three analogs of 1 were produced by fermentation in other media and by microbial biotransformation. Of these compounds, 1 was shown to be the most potent binding inhibitor. Preliminary SAR studies of these compounds indicated that all functional groups and side chains were required for the activity. Compound 1 was a highly-selective binding inhibitor for the kappa opioid receptor: 0.8 microM (IC50) for kappa, >200 microM for mu, and >200 microM for delta opioid receptor. Compound 1 suppressed electrically-stimulated twitch responses of rabbit vas deferens with an ED50 of 14 microM. The suppression was recovered by adding a selective kappa opioid receptor antagonist nor-binaltorphimine, indicating that 1 is a kappa opioid receptor agonist.hxxp://www.journalarchive.jst.go.jp/jnlpdf.php?cdjournal=antibiotics1968&cdvol=51&noissue=11&startpage=983&lang=en&from=jnlabstract
I currently have no use for kappa agonists, not really my thing. This was added for anyone that is.
This gem of a few paragraphs was also found from:
hxxp://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1193547
Screening investigations of selected basidiomycetes indicate inhibitory effects of P. betulinus, G. applanatum, H. annosum, Fomitopsis pinicola (Sowerby: Fr.) P. Karst and Daedaleopsis confragosa (Bolton: Fr.) J. Schröt. on neutral endopeptidase (enkephalinase, EC 3.4.24.11) (IC 50 values between 40 and 55 μg ml−1). Selective inhibitors of this metalloendopeptidase could be useful in the treatment of pain with a spectrum of activity similar to that of opioids.
Scutigeral (25), isolated from fruiting bodies of Scutiger ovinus (Schaeff.: Fr.) Murrill [syn. Albatrellus ovinus (Schaeff.: Fr.) Kotl. & Pouzar], has affinity to the brain dopamine D1 receptors and may act as an orally active pain killer targeting vanilloid receptors [VR1,]. Albaconol (26) from the fruiting bodies of Scutiger confluens (Alb. & Schwein.: Fr.) Bondartsev & Singer [syn. Albatrellus confluens (Alb. & Schwein.: Fr.) Kotl. & Pouzar is an antagonist at the VR1 receptor with an IC 50 value of 5 μM.
Enkephalinase inhibitors have medicinal values as antinociceptives and antidepressants, because they inhibit the breakdown of endogenous opioids that act primarily on the delta receptor and also on the mu :).
Now I could retrieve all but the first paper, could anyone help me out? This thread was started specifically for discussing possible opioid-active fungi.
-begin rant-
OBVIOUSLY do not look up a picture of one of the above mushrooms, go behind your parents house and begin eating anything that looks like it. These things might have activity, but they also might be toxic somehow. None of the studies reported any toxic activity because they were not studying the species toxicity. If one of the species isnt toxic, there are three others that look exactly like it that are deadly is a good rule of thumb to go by when dealing with mushroom IDing. Also eating a handful of oyster mushrooms will not get you high, if it did it would more than likely be illegal in USA, notice how they worked with an extract and used 500mg per kg of the shit.
If ranting like this is frowned upon here, I will refrain from doing so in the future as this is my first post. I just do not want anyone harming themselves because I scour pubmed too much!
-end rant-
Activity-Directed Fractionation of Pleurotus ostreatus. in the Search for Analgesics
Pharmaceutical Biology 2008, Vol. 46, No. 5, Pages 295-301 , DOI 10.1080/13880200801887047
N. S. Vasudewahttp://www.informahealthcare.com/entityImage/?code=200B*, D. T. U. Abeytungahttp://www.informahealthcare.com/entityImage/?code=200B* and W. D. Ratnasooriyahttp://www.informahealthcare.com/entityImage/?code=200B*Department of Chemistry, University of Colombo, Colombo, Sri Lanka
Department of Zoology, University of Colombo, Colombo, Sri Lanka
Department of Chemistry, University of Colombo, Colombo 3, Sri Lanka
Abstract
Pleurotus ostreatus. (Jacquin: Fries) P. Kummer (Tricholomataceae) was subjected to an antinociceptive activity-guided fractionation procedure in order to identify the fraction having highest activity. Three extracts, namely, acetone, dichloromethane, and hexane, were prepared at room temperature using fresh P. ostreatus., and 500 mg/kg was orally administered to male rats. The acetone extract showed significant antinociceptive activity with the hot-plate assay (male, 68%; p < 0.05), whereas dichloromethane and hexane extracts did not show significant activity. The same dose of acetone extract with female rats in the diestrous stage also showed prolongation of reaction time using the hot-plate test (female, 54%; p < 0.05). None of the extracts showed a significant increase in reaction time with the tail-flick test. The acetone extract was further fractionated by solvent partition to obtain four fractions (hexane, dichloromethane, ethyl acetate, and aqueous). Of these extracts, only the aqueous fraction showed marked prolongation in reaction time with the hot-plate test (500 mg/kg dose) on both male rats and on female rats in the diestrous stage (male, 37%; female, 26%). The aqueous fraction, following purification on a reverse phase column, yielded AqFrA-1, AqFrA-2, and AqFrA-3. Oral administration of a 500 mg/kg dose of these three fractions also showed marked prolongation in reaction time with the hot-plate test after 1 h of treatment (AqFrA-1, 26%; AqFrA-2, 69%; AqFrA-3, 101%). The effect was highest in AqFrA-3 at 1 h of treatment, and the effect lasted for 3 h. Hence, we can conclude that the compounds responsible for the activity have very high polarity. The acetone extract of P. ostreatus. did not induce a membrane-stabilizing effect and did not cause prostaglandin inhibition. Naloxone blocked the antinociceptive activity in the hot-plate test upon feeding of 500 mg/kg of acetone extract of P. ostreatus., indicating the mechanism of action is via opioid receptor mediation.
Folks, this is the common oyster mushroom. More research must be done to determine the receptor in which the extract binds to. Why didn't they use selective opioid antagonists?? :confused:
Erinacine E as a kappa opioid receptor agonist and its new analogs from a basidiomycete, Hericium ramosum.
A kappa opioid receptor binding inhibitor was isolated from the fermentation broth of a basidiomycete, Hericium ramosum CL24240 and identified as erinacine E (1). Three analogs of 1 were produced by fermentation in other media and by microbial biotransformation. Of these compounds, 1 was shown to be the most potent binding inhibitor. Preliminary SAR studies of these compounds indicated that all functional groups and side chains were required for the activity. Compound 1 was a highly-selective binding inhibitor for the kappa opioid receptor: 0.8 microM (IC50) for kappa, >200 microM for mu, and >200 microM for delta opioid receptor. Compound 1 suppressed electrically-stimulated twitch responses of rabbit vas deferens with an ED50 of 14 microM. The suppression was recovered by adding a selective kappa opioid receptor antagonist nor-binaltorphimine, indicating that 1 is a kappa opioid receptor agonist.hxxp://www.journalarchive.jst.go.jp/jnlpdf.php?cdjournal=antibiotics1968&cdvol=51&noissue=11&startpage=983&lang=en&from=jnlabstract
I currently have no use for kappa agonists, not really my thing. This was added for anyone that is.
This gem of a few paragraphs was also found from:
hxxp://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1193547
Screening investigations of selected basidiomycetes indicate inhibitory effects of P. betulinus, G. applanatum, H. annosum, Fomitopsis pinicola (Sowerby: Fr.) P. Karst and Daedaleopsis confragosa (Bolton: Fr.) J. Schröt. on neutral endopeptidase (enkephalinase, EC 3.4.24.11) (IC 50 values between 40 and 55 μg ml−1). Selective inhibitors of this metalloendopeptidase could be useful in the treatment of pain with a spectrum of activity similar to that of opioids.
Scutigeral (25), isolated from fruiting bodies of Scutiger ovinus (Schaeff.: Fr.) Murrill [syn. Albatrellus ovinus (Schaeff.: Fr.) Kotl. & Pouzar], has affinity to the brain dopamine D1 receptors and may act as an orally active pain killer targeting vanilloid receptors [VR1,]. Albaconol (26) from the fruiting bodies of Scutiger confluens (Alb. & Schwein.: Fr.) Bondartsev & Singer [syn. Albatrellus confluens (Alb. & Schwein.: Fr.) Kotl. & Pouzar is an antagonist at the VR1 receptor with an IC 50 value of 5 μM.
Enkephalinase inhibitors have medicinal values as antinociceptives and antidepressants, because they inhibit the breakdown of endogenous opioids that act primarily on the delta receptor and also on the mu :).
Now I could retrieve all but the first paper, could anyone help me out? This thread was started specifically for discussing possible opioid-active fungi.
-begin rant-
OBVIOUSLY do not look up a picture of one of the above mushrooms, go behind your parents house and begin eating anything that looks like it. These things might have activity, but they also might be toxic somehow. None of the studies reported any toxic activity because they were not studying the species toxicity. If one of the species isnt toxic, there are three others that look exactly like it that are deadly is a good rule of thumb to go by when dealing with mushroom IDing. Also eating a handful of oyster mushrooms will not get you high, if it did it would more than likely be illegal in USA, notice how they worked with an extract and used 500mg per kg of the shit.
If ranting like this is frowned upon here, I will refrain from doing so in the future as this is my first post. I just do not want anyone harming themselves because I scour pubmed too much!
-end rant-