cureme
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- Joined
- Jan 28, 2021
- Messages
- 33
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Effects of Evodia rutaecarpa Acupoint Sticking Therapy on Rats with Insomnia Induced by Para-Chlorophenylalanine in 5-HT1Aand 5-HT2A Gene Expressions
Abstract
The main feature of insomnia is difficulty in starting or maintaining sleep. 5-HT1A receptor and 5-HT2A receptor are two subtypes of the classic central 5-HT neurotransmitter closely related to sleep and wakefulness. To observe the effects of Evodia rutaecarpa acupoint sticking therapy on the mRNA expressions of 5-HT1A and 5-HT2A in the hypothalamus, brainstem, and hippocampus of insomnia rats induced by para-chlorophenylalanine (PCPA). Ten rats were randomly selected as the normal group, and 80 PCPA insomnia model rats were randomly divided into eight groups, including a model group, a positive control group (diazepam group), a low-dose E. rutaecarpa acupoint sticking therapy group (Yongquan acupoint group and Shenque acupoint group; the same applied below), a middle-dose E. rutaecarpa acupoint sticking therapy group, and a high-dose E. rutaecarpa acupoint sticking therapy group. The normal group and the model group did not receive treatment. The positive control group was given diazepam through intragastric administration, and the three-dose E. rutaecarpa acupoint sticking therapy groups were divided into the Yongquan acupoint group and the Shenque acupoint group. After seven days of administration, the rat hypothalamus, brainstem, and hippocampus tissues were taken, and a real-time polymerase chain reaction method was used to detect the mRNA expressions of 5-HT1A and 5-HT2A. E.rutaecarpa acupoint sticking therapy significantly upregulated 5-HT1A mRNA expression and downregulated 5-HT2A mRNA expression in rats with insomnia caused by PCPA. No significant differences were found in the expression between the two acupoints and the expression among the three brain tissues. E. rutaecarpa acupoint sticking therapy can improve insomnia. The mechanism may be related to the upregulation of 5-HT1A mRNA expression and the downregulation of 5-HT2A mRNA expression in brain tissue.
Im using it right now from an acupunture vendor in Amsterdam (Green Nature Co Ltd Hong Kong). Be careful to apply a low dosage and take with some aspirin to prevent liver issues.I want to try this herb. Anyone found a good vendor?
Discussion
... It has been reported that the acute toxicity of EF is dose-dependent (Huang et al., 2012; Sun et al., 2012). In this work, the hepatotoxicity of EF was found to be dose-dependent on various approaches and toxicology indexes. For an adult, the range of clinical dose of EF is very wide with 1–70 g/day, and the pharmacopeial dose is 2–5 g/day. The low dose in this work was set at 1.05 g/kg/day, and equivalent to 10 g/day for an adult. Fortunately, no significant hepatotoxicity was observed for the low dose of CEF and LPEF, which indicates that the pharmacopoeia dose may be a safe one during short-term ingestion of CEF or LPEF. It can be inferred that most cases of toxic and side effects of EF may be generally caused by long-term use of large doses.
Chinese medicine has noted the toxicity of EF since ancient time, and EF is marked with “mild toxic” and “toxic” in TCM books. Drug processing and compatibility are often used to reduce or eliminate its toxic and side effects. Licorice processing is one of the commonly used processing techniques for CEF. After processing with licorice, a series of physical, chemical, and biological changes occurred in EF, in which the contents of organic acids significantly decreased and quinolone alkaloids increased a little. As interpreted above, caffeoyl gluconic acids and quinolone alkaloids are potential hepatotoxic components in EF. The increase and decrease of toxic components are closely related to the detoxification mechanism of drug processing. In addition, licorice is good at moderating all kinds of toxic herbs probably through antagonism. Liquiritin and glycyrrhizic acid in licorice have been reported to have detoxification effect (Wu et al., 2020; Xiao et al., 2021). Accordingly, the hepatotoxicity of LPEF is significantly lower than that of CEF. We speculate that licorice processing combines the effects of drug processing and compatibility, and further studies on the material basis and mechanism of detoxification are underway.
I believe inositol reverses desensitization of certain receptors. For me, it created strong anxiety and depersonalization.Great share. That Sensory Processing Sensitivity study is very interesting too.
Are PSSD and post-SSRI anhedonia things you deal with? Let us know if you see results with these herbs.
There was a report of a person with PSSD and blunted perception after SSRIs who profoundly improved with high-dose inositol. He said it made his vision have depth again, colors saturated again, butterflies in stomach again, plus the relief of PSSD.
Berberine seems to have great benefits alone, so this combination is intriguing.
Im using it right now from an acupunture vendor in Amsterdam (Green Nature Co Ltd Hong Kong). Be careful to apply a low dosage and take with some aspirin to prevent liver issues.
Here is a study about it's potential liver damaging effects in medium and high dosages. Unless it is prepared in licorice. See here: Hepatotoxicity Comparison of Crude and Licorice-Processed Euodiae Fructus in Rats With Stomach Excess-Cold Syndrome
Aspirin attenuates liver fibrosis by suppressing TGF‑β1/Smad signaling - PubMed
Aspirin alleviates hepatic fibrosis by suppressing hepatic stellate cells activation via the TLR4/NF-κB pathway - PubMed
Yeah that’s the same with me, I also responded very poorly to inositol it gave me some really weird anxiety.I believe inositol reverses desensitization of certain receptors. For me, it created strong anxiety and depersonalization.
I wonder what the most likely pathway responsible for causing that reaction could be. It has been linked to the 5HT2A receptor, and acetylcholine.Yeah that’s the same with me, I also responded very poorly to inositol it gave me some really weird anxiety.
Palmitoylethanolamide increases serotonergic neurotrans-
mission through the serotonin receptor 5HT1 and downregu-
lates 5HT2A/C receptors. CB1 agonists are reported to reduce
the reuptake of dopamine and serotonin.
103,104
Deletions of CB1 receptors in animals reduce synaptic serotonin caused
by selective serotonin reuptake inhibitors. [105]
I believe inositol reverses desensitization of certain receptors. For me, it created strong anxiety and depersonalization.
I wonder what the most likely pathway responsible for causing that reaction could be. It has been linked to the 5HT2A receptor, and acetylcholine.
It’s been mentioned whenever I look up what exactly it does in the brain, but seems rather vague. It is definitely a second messenger system. It has been linked to 5HT2A (nasty anxiety receptor) and D2 receptors. Not sure if it unregulated both. Some trials used grams upon grams for OCD. Personally, I do not like the effects, but perhaps my anxiety from it came via acetylcholine. Too much will do that to me, especially fish oil.This is what led me to take myo inositol. I already had depersonalization but I got terrible cognitive problems and muscle twitching/spasms after taking it which haven't abated.
Could you elaborate on the acetylcholine part please?