New Zealand Salvia divinorum - Our Current Wordpress Web Page: HERE
Facebook @ New Zealand Salvia Divinorum NorthlandSalvia
Our Current Wordpress Web Page: HERE
New Zealand - Our Current Wordpress Web Page: HERE
Facebook @ New Zealand Salvia Divinorum NorthlandSalvia
**Increase in N.Z Post Delivery Rates** July 2023
Due to inflationary pressures, new Rates are as follows:
Economy Rate, tracked @ $8.
Courier Rate, tracked @ $10. (*Fastest Delivery)
Rural Delivery Rate @ plus+ $5.50
Due to N.Z Post price increases, you might like to consider *Parcel Collect to avoid the extra Rural Delivery Costs for some Customers.
Due to ongoing cost increases, ALL Salvia Specials, *Excluding our 5x Extract Deals & 5x Combo Specials, are Suspended until further Notice.
*R.18 N.Z Customers Only. Proof of Age Required.
If you do not Verify Age, we will not process your Order.
Payment via Online Banking. N.Z Post track & trace.
*Price List & Specials - HERE
*NorthlandSalvia Lite: view Previews of all our Primary content: HERE
Contact: northlandsalvia@gmail.com
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Salvia divinorum - bioactive for/in:
*antinociceptive = the action or process of blocking the detection of a painful or injurious stimulus by sensory neurons.
*R.18 N.Z Customers Only.
Therapeutic Potential of Salvia divinorum.
K.O.R agonists - Kappa Opioid Receptor Agonists such as SA (Salvia divinorum) have applications for multiple
ailments, and SA is extremely affine, potent, and precise when it comes
to binding to these brain receptors. Some of the valuable medications
that could be developed from S.divinorum are:
Safe analgesics without addictive properties:
The efficacy of SA as an analgesic has been demonstrated in animal studies (Guida et al., 2012).
In current medical practice, sometimes very powerful analgesics like morphine are used, which are habit forming and produce dependence. This is not the case with SA. In fact, research has shown that SA has anti-addictive properties (Serra et al., 2015).
Anti-inflammatories:
It has been demonstrated in animal studies that SA has
ultra-potent
effects on macrophages via the KOR and CB1 receptors and exerts an
important attenuation of inflammation and antipruritic effects.
SA inhibits intestinal motility and reduces abdominal pain in the irritable bowel syndrome. In recent studies with mice, SA has been shown to inhibit the leukotriene-mediated inflammatory response.
Leukotrienes are crucial in various autoimmune and inflammatory conditions such as urticaria, bronchial asthma, allergic rhinitis, and cardiovascular problems (Aviello et al., 2011; Rossi et al., 2016).
Medication to treat Psychostimulant abuse:
Animal research has revealed that SA (Salvinorin A) reduces dopamine levels in parts of the basal ganglia, disrupting many of the effects of cocaine and the addiction cycle.
In the experiments with rats, SA does not seem to suppress their movement, the action of pushing the lever to drink, or their motivation before stimuli.
In contrast, SA appears to specifically suppress cocaine-related behaviors and motivations (Dos Santos, Crippa, Machado-de-Sousa, & Hallak, 2015).
Western medicine has developed—with questionable success—pharmacological treatments for the abuse of opiates, alcohol, and tobacco, but there is currently no treatment for the abuse of psychostimulants, so research with SA hold the promise to help millions of addicts.
Medications to treat different types of cancer:
When there are tumors in the brain, one of the difficulties of therapeutics is to get the drugs through the blood-brain barrier and reach the tumor.
The terpene SA is able to cross the blood-brain barrier and reach the brain and structures of the CNS in less than a minute.
SA
analogs have demonstrated antiproliferative properties, inhibiting the
growth of 77–86% of tumor cells in breast cancer (Vasiljevik, Groer,
Lehner, Navarro, & Prisinzano, 2014).
Source: The Use of Salvia divinorum from a Mazatec Perspective. Ana Elda Maqueda
Salvia divinorum: analgesic and anti-inflammatory action without addiction:
Today, we are facing a crisis in relation to the use and abuse of opiates and related molecules.
The experimental evidence supports the fact that S. divinorum, SA, and their analogues decrease the pain induced by neuropathy and inflammation.
Moreover, the fact that S divinorum administration does not increase the release of dopamine in the Nacc suggests that salvinorins and their analogues can be a suitable therapeutic alternative without the risk of producing addiction.
Long-lasting pain has been among the major therapeutic challenges of the 21st century due to its disabling effects, especially with the growing population of the elderly. In this regard, finding new molecules or associations to decrease or alleviate pain is of utmost importance.
Source: Salvia divinorum: analgesic and anti-inflammatory action. HERE
Therapeutic Potential of CB2R.A Cannabinoid Oil:
C.B 2 R.A - Cannabinoid Oil DOES NOT activate the CB1 Receptors, which are
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More information on the E.C.S - Endocannabinoid System & phyto-cannabinoids HERE
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Novel pharmacological strategies involving the use of CB2 receptor agonists may be much more useful than CB1 ligands:
Although, their role in the treatment of alcohol dependence is still under investigation and a development of a drug that possesses the same activity both in animals and human is greatly needed, novel pharmacological strategies involving the use of CB2 receptor agonists (particularly highly selective ones) may be much more useful than CB1 ligands due to the lack of psychotropic effects mediated by cannabinoid 1 receptors. Kleczkowska et al, 2015.
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Researchers investigated the effects of CB2 agonists on cocaine self-administration in mice. Systemic administration of CB2 agonists reduced the number of self-infusions of cocaine in mice, as well as reducing locomotor activity and the break point (maximum amount of level presses to obtain cocaine). Local injection of CB2 agonists into the nucleus accumbens was found to produce the same effects as systemic administration. Systemic administration of CB2 agonists also reduced basal and cocaine-induced elevations of extracellular dopamine in the nucleus accumbens. Xeng Xiong Xi et al, 2011.
findings indicate that BCP beta Caryophyllene may be useful for the treatment of CUD, (Cocaine Use Disorder) likely by stimulation of PPARα and PPARγ in the mesolimbic system.
BCP (beta Caryophyllene) is a major component in the essential oils of cannabis and other spice and food plants (Sharma et al., 2016; Galaj and Xi, 2019).
In the present study, we demonstrate that systemic administration of BCP is highly effective in attenuating METH-taking and METH-seeking in rodents via both CB2- and non-CB2-dependent mechanisms.
BCP is an FDA-approved food additive with good oral bioavailability, favorable pharmacokinetics, and low toxicity, BCP deserves further research as a promising repurposed drug in translational studies for the treatment of METH use disorder.
BCP beta Caryophyllene - direct action on CB2R (Receptors) without creating tolerance.
BCP beta Caryophyllene is an attractive compound for chronic pain (both inflammatory and neurogenic) due to its direct action on CB2R without creating a tolerance, as demonstrated in an animal model of neuropathic pain [30]. Remarkably, the researchers concluded that the effect of BCP became stronger during the treatment period.
This is significant considering drug tolerance after prolonged use is observed with other analgesic therapies and may require increased dosage, which may accelerate tolerance and further reduce the effects of a therapeutic substance.
BCP exerts potent anti-inflammatory effects when taken orally, which may be explained by its ability to simultaneously inhibit pathways (toll-like receptor complex CD14/TLR4/MD2) that increase the production of proinflammatory cytokines (IL-1β, IL-6, IL-8, and TNF-⍺), reduce immune-related inflammation, and synergize the µ-opioid receptor pathways.
Preclinical models demonstrate that BCP can reduce inflammation in a variety of bacterial-caused, eosinophil-related, and neuropathic inflammatory conditions [32].
It can also enhance the effects of other pain medications like morphine, making it a promising candidate to reduce effective drug dose and therefore potential drug dependence and tolerance.
In this way, it modulates pain signaling pathways in a manner that may enhance, and not compete with, the benefits of other pain-or inflammation-relieving substances.
BCP shows promise for treating depression and stress related mental illnesses due to its direct binding to CB2R, which modulates ECS activity]. The ECS controls cognitive and emotional responses to stressors through CBR interactions.
In addition, preclinical research suggests BCP is helpful for substance abuse disorders, and protects against nonalcoholic fatty liver disease. Scott A. Johnson et al, 2020.
The Cannabinoid BCP beta Caryophyllene, an attractive compound for chronic pain (both inflammatory and neurogenic)
The Cannabinoid BCP beta Caryophyllene is an attractive compound for chronic pain (both inflammatory and neurogenic) due to its direct action on CB2R without creating a tolerance, as demonstrated in an animal model of neuropathic pain [30].
Remarkably, the researchers concluded that the effect of BCP became stronger during the treatment period.
This is significant considering drug tolerance after prolonged use is observed with other analgesic therapies and may require increased dosage, which may accelerate tolerance and further reduce the effects of a therapeutic substance.
BCP exerts potent anti-inflammatory effects when taken orally, which may be explained by its ability to simultaneously inhibit pathways (toll-like receptor complex CD14/TLR4/MD2) that increase the production of proinflammatory cytokines (IL-1β, IL-6, IL-8, and TNF-⍺), reduce immune-related inflammation, and synergize the µ-opioid receptor pathways.
Preclinical models demonstrate that BCP can reduce inflammation in a variety of bacterial-caused, eosinophil-related, and neuropathic inflammatory conditions [32].
It can also enhance the effects of other pain medications like morphine, making it a promising candidate to reduce effective drug dose and therefore potential drug dependence and tolerance.
In this way, it modulates pain signaling pathways in a manner that may enhance, and not compete with, the benefits of other pain-or inflammation-relieving substances. Scott A. Johnson et al, 2020.
" while all attempts are being focused on control of viral replication through development of vaccines, it is also critical to ensure that the vaccines do not trigger hyperactivation of immune response.
It is equally important to develop new anti-inflammatory therapies that can effectively block the cytokine storm seen in patients with severe form of COVID-19.
We believe that cannabinoids hold significant promise as potent anti-inflammatory agents."
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