imalgen
06-30-2009, 04:12 PM
Heres some clips of interesting information i found regarding this interesting plant.
It is a herbaceous (http://en.wikipedia.org/wiki/Herbaceous) perennial (http://en.wikipedia.org/wiki/Perennial_plant) vines (http://en.wikipedia.org/wiki/Vine) growing to around 4 m tall, with a large, woody caudex (http://en.wikipedia.org/wiki/Caudex). The leaves (http://en.wikipedia.org/wiki/Leaf) are arranged spirally on the stem, and are peltate, with the leaf petiole attached near the centre of the leaf.Fen fang ji(S.tetrandra) is of low toxicity (standard dose is: 4.5 to 9g, overdose can occur at 30-100g) and is traditionally used to dispell wind and dampness to relieve pain and to promote diuresis. It is acrid, bitter and cold. The part used is the root. The main active alkaloids are: tetrandrine (12 to 23 grams / kg) and fangchinoline (0.3-3 mg/kg). Also present are: cyclanoline, menisine, menisidine, oxofangchirine, stephenanthrine, stepholidine and bisbenzylisoquinoline.
The effect of L-stepholidine, a novel extract of Chinese herb, on the acquisition, expression, maintenance, and re-acquisition of morphine conditioned place preference in rats.
hXXp://www.ncbi.nlm.nih.gov/pubmed/17027045?dopt=Abstract
The effect of L-stepholidine (SPD), a novel alkaloid extract of the Chinese herb Stephania with partial dopamine D1 receptor agonistic and D2 receptor antagonistic dual actions, on morphine conditioned place preference (CPP) was studied. Daily injection of morphine (10 mg/kg, i.p.) for 6 days induced CPP in rats, and daily treatment with SPD at 10 or 20 mg/kg before morphine injection dose-dependently attenuated morphine-induced CPP. On the day following acquisition of morphine CPP, a single administration of SPD at 10 or 20 mg/kg failed to block the expression of CPP. However, daily administration of SPD at 20 mg/kg for 7 days attenuated the maintenance of CPP. Morphine-induced CPP extinguished after a 21-day saline training and then a single injection of morphine (3 mg/kg, i.p.) induced re-acquisition of morphine CPP; however, pretreatment with SPD at 10 or 20 mg/kg 30 min before morphine injection dose-dependently blocked morphine (3 mg/kg, i.p.)-induced re-acquisition of morphine CPP. Furthermore, our data indicate that SPD had no effect on food-induced CPP or state-dependent learning, suggesting that the observed effect of SPD does not result from an inhibition of general learning ability. These results demonstrate that SPD can inhibit acquisition, maintenance, and re-acquisition of morphine conditioned place preference and suggest its potential for treatment of opioid addiction.
Effects of l-Stepholidine on Forebrain Fos Expression: Comparison with Clozapine and Haloperidol
hXXp://www.nature.com/npp/journal/v30/n2/abs/1300628a.html
l-Stepholidine (SPD) is a tetrahydroprotoberberine alkaloid and a mixed dopamine D1 agonist/D2 antagonist. Preliminary clinical trials suggest that SPD improves both positive and negative symptoms of schizophrenia without producing significant extrapyramidal side effects. Here, we report that SPD mimics the effect of the atypical antipsychotic drug clozapine, preferentially increasing Fos expression in corticolimbic areas. Thus, at 10 mg/kg (i.p.), SPD induced Fos expression in the medial prefrontal cortex (mPFC), nucleus accumbens (NAc), and lateral septal nucleus (LSN) without significantly affecting the dorsolateral striatum (DLSt). At higher doses (20–40 mg/kg), SPD also increased Fos expression in the DLSt. The increase, however, was less pronounced than the increase seen in the NAc. Within the NAc, SPD also induced more Fos expression in the shell than in the core. In all subcortical areas examined, the Fos expression induced by SPD was mimicked by the D2 antagonist sulpiride and reversed by the D2 agonist quinpirole, suggesting that the effect is due to blockade of D2-like receptors by SPD. In the mPFC, however, the effect was not mimicked by sulpride or reversed by quinpirole. It was also not mimicked by the D1 agonist SKF38393 or SKF38393 plus sulpride, and not reversed by the D1 antagonist SCH23390. These results suggest that, in the mPFC, SPD may induce Fos expression through a non-DA mechanism. Whether the mechanism involves an interaction of SPD with other neurotransmitters such as 5-HT and norepinephrine remains to be determined.
We just need to make sure the identification of the plant is correct, as you dont want any aristolochic acid!
It is a herbaceous (http://en.wikipedia.org/wiki/Herbaceous) perennial (http://en.wikipedia.org/wiki/Perennial_plant) vines (http://en.wikipedia.org/wiki/Vine) growing to around 4 m tall, with a large, woody caudex (http://en.wikipedia.org/wiki/Caudex). The leaves (http://en.wikipedia.org/wiki/Leaf) are arranged spirally on the stem, and are peltate, with the leaf petiole attached near the centre of the leaf.Fen fang ji(S.tetrandra) is of low toxicity (standard dose is: 4.5 to 9g, overdose can occur at 30-100g) and is traditionally used to dispell wind and dampness to relieve pain and to promote diuresis. It is acrid, bitter and cold. The part used is the root. The main active alkaloids are: tetrandrine (12 to 23 grams / kg) and fangchinoline (0.3-3 mg/kg). Also present are: cyclanoline, menisine, menisidine, oxofangchirine, stephenanthrine, stepholidine and bisbenzylisoquinoline.
The effect of L-stepholidine, a novel extract of Chinese herb, on the acquisition, expression, maintenance, and re-acquisition of morphine conditioned place preference in rats.
hXXp://www.ncbi.nlm.nih.gov/pubmed/17027045?dopt=Abstract
The effect of L-stepholidine (SPD), a novel alkaloid extract of the Chinese herb Stephania with partial dopamine D1 receptor agonistic and D2 receptor antagonistic dual actions, on morphine conditioned place preference (CPP) was studied. Daily injection of morphine (10 mg/kg, i.p.) for 6 days induced CPP in rats, and daily treatment with SPD at 10 or 20 mg/kg before morphine injection dose-dependently attenuated morphine-induced CPP. On the day following acquisition of morphine CPP, a single administration of SPD at 10 or 20 mg/kg failed to block the expression of CPP. However, daily administration of SPD at 20 mg/kg for 7 days attenuated the maintenance of CPP. Morphine-induced CPP extinguished after a 21-day saline training and then a single injection of morphine (3 mg/kg, i.p.) induced re-acquisition of morphine CPP; however, pretreatment with SPD at 10 or 20 mg/kg 30 min before morphine injection dose-dependently blocked morphine (3 mg/kg, i.p.)-induced re-acquisition of morphine CPP. Furthermore, our data indicate that SPD had no effect on food-induced CPP or state-dependent learning, suggesting that the observed effect of SPD does not result from an inhibition of general learning ability. These results demonstrate that SPD can inhibit acquisition, maintenance, and re-acquisition of morphine conditioned place preference and suggest its potential for treatment of opioid addiction.
Effects of l-Stepholidine on Forebrain Fos Expression: Comparison with Clozapine and Haloperidol
hXXp://www.nature.com/npp/journal/v30/n2/abs/1300628a.html
l-Stepholidine (SPD) is a tetrahydroprotoberberine alkaloid and a mixed dopamine D1 agonist/D2 antagonist. Preliminary clinical trials suggest that SPD improves both positive and negative symptoms of schizophrenia without producing significant extrapyramidal side effects. Here, we report that SPD mimics the effect of the atypical antipsychotic drug clozapine, preferentially increasing Fos expression in corticolimbic areas. Thus, at 10 mg/kg (i.p.), SPD induced Fos expression in the medial prefrontal cortex (mPFC), nucleus accumbens (NAc), and lateral septal nucleus (LSN) without significantly affecting the dorsolateral striatum (DLSt). At higher doses (20–40 mg/kg), SPD also increased Fos expression in the DLSt. The increase, however, was less pronounced than the increase seen in the NAc. Within the NAc, SPD also induced more Fos expression in the shell than in the core. In all subcortical areas examined, the Fos expression induced by SPD was mimicked by the D2 antagonist sulpiride and reversed by the D2 agonist quinpirole, suggesting that the effect is due to blockade of D2-like receptors by SPD. In the mPFC, however, the effect was not mimicked by sulpride or reversed by quinpirole. It was also not mimicked by the D1 agonist SKF38393 or SKF38393 plus sulpride, and not reversed by the D1 antagonist SCH23390. These results suggest that, in the mPFC, SPD may induce Fos expression through a non-DA mechanism. Whether the mechanism involves an interaction of SPD with other neurotransmitters such as 5-HT and norepinephrine remains to be determined.
We just need to make sure the identification of the plant is correct, as you dont want any aristolochic acid!