Sagan Dalya - a Shamanic Adaptogen, Novel Canniboid Compounds, Natural Anti-Viral, Arbutin, Health Effects and Benefits, Research
Many people have heard of Labrador Tea, typically meaning northern Alaskan Labrador, or Rhododendron tomentosum. Sagan Dalya is Rhododendron Adamsii and doesn’t grow natively Alaska, but in Siberia.
Unfortunately, there is a severe lack of research in regards to sagan dalya itself. This isn’t all that surprising. Thankfully, there is fairly extensive research on some of the compounds found in sagan dalya, like arbutin and the novel cannibanoids that it contains.
The plant itself thee single most enchanting aroma I have ever encountered from any natural substance, hands down. It’s like smoky, sweet, fruity, Christmas, seductively acrid? Truly, nothing compares. I really enjoy adding sagan dalya to different tea blends to see how it can accentuate or transform other flavors in unique ways.
Overall, it is safe to say that using sagan dalya sparingly and mindfully is probably going to be your best and safest practice with such a plant, but at least trying it out here and then isn’t going to pose much of a problem, probably, for the overwhelming majority of people. If you have some sort of heath condition, you are perhaps a great candidate for simply avoiding it all together.
Plant Compounds Found in Sagan Dalya:
Lepalol
Caffeic Acid
Azelaic Acid
Calamenene
Germacron
Myristic Acid
Pentadecanoic Acid
Palmitoleic Acid
Stearic Acid
Kaempferol
Nonadecanoic Acid
Farrerol
Quercetin
Cannabigerorcinic acid
Cannabigerocinolic Acid
Cannabiorogerolic Acid
Arachic Acid
Azaleatin
Myricetin
Gossypetin
Ampelopsin
Heneicosanoic Acid
Esculin
Behenic Acid
Pentacosane
Chlorogenic Acid
Scopolin
Tricanoic Acid
Fraxin
Beta-Sitosterin
Cyanidin-3-alpha-l-arabinoside
Montanic Acid
Alpha Amyrin
Lupeol
Pentoside
Erithrodiol
Uvaol
Catechins
Alpha-Tocopherol-Beta-d-Mannoside
Some of these compounds are very well researched, and others you will have trouble even finding one or two papers documenting their qualities.
General, Alleged Benefits:
Lowers Blood Pressure.
Compounds found in sagan dalya are conclusively shown to induce hypotension, which may be useful, IF, there was a way to establish the safety of a daily or longterm sagan dalya regimen.
Is a Novel Central Nervous System Stimulant:
This is why sagan dalya is so appealing for those who either don’t want caffeine or want to experience the effects of relatively rare and unheard of adaptogen
Potential Risks:
Possibly Critically Disrupts Electrolyte Function:
Sagan Dalya contains compounds known as Cardenolides which are known to be toxic to animals through inhibition of the enzyme Na+/K+‐ATPase, which is responsible for maintaining the sodium and potassium ion gradients across the cell membranes.
Is shown to induce respiratory depression.
So like, if you have a respiratory disfunction or disease, maybe pass on the sagan dalya.
Another compound to be aware of is Andromedotoxin.
From Wikipedia: Grayanotoxins are a group of closely related neurotoxins named after Leucothoe grayana, a plant native to Japan originally named for 19th century American botanist Asa Gray. Grayanotoxin I (grayanotaxane-3,5,6,10,14,16-hexol 14-acetate) is also known as andromedotoxin, acetylandromedol, rhodotoxin and asebotoxin. Grayanotoxins are produced by Rhododendron species and other plants in the family Ericaceae. Honey made from the nectar and so containing pollen of these plants also contains grayanotoxins and is commonly referred to as mad honey.Consumption of the plant or any of its secondary products, including mad honey, can cause a rare poisonous reaction called grayanotoxin poisoning, mad honey disease, honey intoxication, or rhododendron poisoning. It is most frequently produced and consumed in regions of Nepal and Turkey as a recreational drug and traditional medicine.
The rest of the wikipedia article on andromedotoxin is……pretty scary sounding honestly.
It is also well known that with both Alaskan Labrador and Sagan Dalya, consuming too much of either can famously cause GI upset and headaches.
This paper seems to highlight some of the best simple take-aways for this plant.
Sagan Dalya Tea, a New "Old" Probable Adaptogenic Drug: Metabolic Characterization and Bioactivity Potentials of Rhododendron adamsii Leaves
https://pubmed.ncbi.nlm.nih.gov/34072186/
“Adams' rhododendron (Rhododendron adamsii Rehder) or Sagan Dalya tea is a famous Siberian evergreen medical plant of the Ericaceae family used in traditional medicines of Buryats, Yakuts, and Mongols as a tonic, stimulant, and adaptogenic drug. The high popularity of R. adamsii coupled with poor scientific knowledge prompted the addressing of gaps related to metabolic and biomedical data of Sagan Dalya tea. The application of solid-phase extraction and liquid chromatography-mass spectrometric techniques for the metabolomic study of R. adamsii leaf extracts resulted in the identification of more than 170 compounds, including carbohydrates, organic acids, simple phenol glycosides, triterpene glycosides, flavonoids, prenylated phenols, benzoic acid derivatives, hydroxycinnamates, dihydrochalcones, catechins, and procyanidins, most of which were identified for the first time in the plant. Extended surveys of the seasonal content of all detected compounds prove that specific metabolite variations reflect the bioactivity of R. adamsii extracts. Regarding in vitro methods, the expressed antioxidant potential of R. adamsii extracts was investigated via radical-scavenging, nitric oxide scavenging, and ferrous (II) ion chelating assays. The animal-based swimming to exhaustion test demonstrates the stimulating influence of R. adamsii extract on physical performance and endurance, concluding that the drug could act as an adaptogen. Thus, Sagan Dalya tea (R. adamsii) has confirmed its "old" application as a tonic remedy and requires further precise study as a novel adaptogenic plant.”
Now let’s check out some research about the individual compounds that are found inside sagan dalya.
Caffeic Acid:
Hybrid molecules based on caffeic acid as potential therapeutics: A focused review
https://www.sciencedirect.com/science/article/abs/pii/S022352342200647X
“Caffeic acid-based compounds possess a high degree of structural diversity and show a variety of pharmacological properties, providing a useful framework for the discovery of new therapeutic agents. They are well-known analogues of antioxidants found in many natural products and synthetic compounds. The present review surveys the recent developments in structure-activity relationships (SAR) and mechanism of action (MOA) of various caffeic acid-containing compounds that play important roles in the design and synthesis of new bioactive molecules with antioxidant, antidiabetic, antiviral, antibacterial, anticancer, anti-inflammatory, and other properties. This review should provide inspiration to scientists in the research fields of organic synthesis and medicinal chemistry related to the development of new antioxidants with versatile therapeutic potential.”
Kaempferol:
Kaempferol is a plant compound (also found in blue lotus flower) that has been EXTENSIVELY studied.
Therapeutic potential of kaempferol on Streptococcus pneumoniae infection
https://www.sciencedirect.com/science/article/pii/S1286457922001289
“Co-infections with pathogens and secondary bacterial infections play significant roles during the pandemic coronavirus disease 2019 (COVID-19) pathogenetic process, caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2). Notably, co-infections with Streptococcus pneumoniae (S. pneumoniae), as a major Gram-positive pathogen causing pneumonia or meningitis, severely threaten the diagnosis, therapy, and prognosis of COVID-19 worldwide. Accumulating evidences have emerged indicating that S. pneumoniae evolves multiple virulence factors, including pneumolysin (PLY) and sortase A (SrtA), which have been extensively explored as alternative anti-infection targets. In our study, natural flavonoid kaempferol was identified as a potential candidate drug for infection therapeutics via anti-virulence mechanisms. We found that kaempferol could interfere with the pore-forming activity of PLY by engaging with catalytic active sites and consequently inhibit PLY-mediated cytotoxicity. Additionally, exposed to kaempferol significantly reduced the SrtA peptidase activity by occupying the active sites of SrtA. Further, the biofilms formation and bacterial adhesion to the host cells could be significantly thwarted by kaempferol incubation. In vivo infection model by S. pneumoniae highlighted that kaempferol oral administration exhibited notable treatment benefits, as evidenced by decreased bacterial burden, suggesting that kaempferol has tremendous potential to attenuate S. pneumoniae pathogenicity. Scientifically, our study implies that kaempferol is a promising therapeutic option by targeting bacterial virulence factors.”
A review of the dietary flavonoid, kaempferol on human health and cancer chemoprevention
https://www.sciencedirect.com/science/article/abs/pii/S0308814612019176
“Kaempferol is a polyphenol antioxidant found in fruits and vegetables. Many studies have described the beneficial effects of dietary kaempferol in reducing the risk of chronic diseases, especially cancer. Epidemiological studies have shown an inverse relationship between kaempferol intake and cancer. Kaempferol may help by augmenting the body’s antioxidant defence against free radicals, which promote the development of cancer. At the molecular level, kaempferol has been reported to modulate a number of key elements in cellular signal transduction pathways linked to apoptosis, angiogenesis, inflammation, and metastasis. Significantly, kaempferol inhibits cancer cell growth and angiogenesis and induces cancer cell apoptosis, but on the other hand, kaempferol appears to preserve normal cell viability, in some cases exerting a protective effect. The aim of this review is to synthesize information concerning the extraction of kaempferol, as well as to provide insights into the molecular basis of its potential chemo-preventative activities, with an emphasis on its ability to control intracellular signaling cascades that regulate the aforementioned processes. Chemoprevention using nanotechnology to improve the bioavailability of kaempferol is also discussed.”
Novel Cannibanoids:
Cannabigerorcynic acid & cannabigerorcynic acid methylester are the two main canniboids that are found sagan dalya.
These two compounds are structurally related to Cannabigerol and Cannabichromene which have been EXTENSIVELY researched. This doesn’t necessarily mean that sagan dalya’s canniboids will also have similar health benefits, but the trend has definitely been established that identically structured compounds often each possess distinct benefits.
Affinity selection-mass spectrometry in the discovery of anti-SARS-CoV-2 compounds
https://analyticalsciencejournals.onlinelibrary.wiley.com/doi/10.1002/mas.21800
“Small molecule therapeutic agents are needed to treat or prevent infections by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), which is the cause of the COVID-19 pandemic. To expedite the discovery of lead compounds for development, assays have been developed based on affinity selection-mass spectrometry (AS-MS), which enables the rapid screening of mixtures such as combinatorial libraries and extracts of botanicals or other sources of natural products. AS-MS assays have been used to find ligands to the SARS-CoV-2 spike protein for inhibition of cell entry as well as to the 3-chymotrypsin-like cysteine protease (3CLpro) and the RNA-dependent RNA polymerase complex constituent Nsp9, which are targets for inhibition of viral replication. The AS-MS approach of magnetic microbead affinity selection screening has been used to discover high-affinity peptide ligands to the spike protein as well as the hemp cannabinoids cannabidiolic acid and cannabigerolic acid, which can prevent cell infection by SARS-CoV-2. Another AS-MS method, native mass spectrometry, has been used to discover that the flavonoids baicalein, scutellarein, and ganhuangenin, can inhibit the SARS-CoV-2 protease 3CLpro. Native mass spectrometry has also been used to find an ent-kaurane natural product, oridonin, that can bind to the viral protein Nsp9 and interfere with RNA replication. These natural lead compounds are under investigation for the development of therapeutic agents to prevent or treat SARS-CoV-2 infection.”
In silico discovery of non-psychoactive scaffolds in Cannabis halting SARS-CoV-2 host entry and replication machinery
https://www.futuremedicine.com/doi/10.2217/fvl-2021-0309
“Coronavirus disease still poses a global health threat which advocates continuous research efforts to develop effective therapeutics. Materials & methods: We screened out an array of 29 Cannabis phytoligands for their viral spike-ACE2 complex and main protease (Mpro) inhibitory actions by in silico modeling to explore their possible dual viral entry and replication machinery inhibition. Physicochemical and pharmacokinetic parameters (ADMET) formulating drug-likeness were computed. Results: Among the studied phytoligands, cannabigerolic acid (2), cannabigerol (8), and its acid methyl ether (3) possessed the highest binding affinities to SARS-CoV-hACE2 complex essential for viral entry. Canniprene (24), cannabigerolic methyl ether (3) and cannabichromene (9) were the most promising Mpro inhibitors. Conclusion: These non-psychoactive cannabinoids could represent plausible therapeutics with added-prophylactic value as they halt both viral entry and replication machinery.”
Neuroprotection with the cannabigerol quinone derivative VCE-003.2 and its analogs CBGA-Q and CBGA-Q-Salt in Parkinson's disease using 6-hydroxydopamine-lesioned mice
https://www.mdpi.com/1422-0067/23/8/4170
“The quinone derivative of the non-psychotropic cannabinoid cannabigerol (CBG), so-called VCE-003.2, has been recently investigated for its neuroprotective properties in inflammatory models of Parkinson's disease (PD) in mice. Such potential derives from its activity at the peroxisome proliferator-activated receptor-γ (PPAR-γ). In the present study, we investigated the neuroprotective properties of VCE-003.2 against the parkinsonian neurotoxin 6-hydroxydopamine (6-OHDA), in comparison with two new CBG-related derivatives, the cannabigerolic acid quinone (CBGA-Q) and its sodium salt CBGA-Q-Salt, which, similarly to VCE-003.2, were found to be active at the PPAR-γ receptor, but not at the cannabinoid CB1 and CB2 receptors. First, we investigated their cytoprotective properties in vitro by analyzing cell survival in cultured SH-SY5Y cells exposed to 6-OHDA. We found an important cytoprotective effect of VCE-003.2 at a concentration of 20 μM, which was not reversed by the blockade of PPAR-γ receptors with GW9662, supporting its activity at an alternative site (non-sensitive to classic antagonists) in this receptor. We also found CBGA-Q and CBGA-Q-Salt being cytoprotective in this cell assay, but their effects were completely eliminated by GW9662, thus indicating that they are active at the canonical site in the PPAR-γ receptor. Then, we moved to in vivo testing using mice unilaterally lesioned with 6-OHDA. Our data confirmed that VCE-003.2 administered orally (20 mg/kg) preserved tyrosine hydroxylase (TH)-positive nigral neurons against 6-OHDA-induced damage, whereas it completely attenuated the astroglial (GFAP) and microglial (CD68) reactivity found in the substantia nigra of lesioned mice. Such neuroprotective effects caused an important recovery in the motor deficiencies displayed by 6-OHDA-lesioned mice in the pole test and the cylinder rearing test. We also investigated CBGA-Q, given orally (20 mg/kg) or intraperitoneally (10 mg/kg, i.p.), having similar benefits compared to VCE-003.2 against the loss of TH-positive nigral neurons, glial reactivity and motor defects caused by 6-OHDA. Lastly, the sodium salt of CBGA-Q, given orally (40 mg/kg) to 6-OHDA-lesioned mice, also showed benefits at behavioral and histopathological levels, but to a lower extent compared to the other two compounds. In contrast, when given i.p., CBGA-Q-Salt (10 mg/kg) was poorly active. We also analyzed the concentrations of dopamine and its metabolite DOPAC in the striatum of 6-OHDA-lesioned mice after the treatment with the different compounds, but recovery in the contents of both dopamine and DOPAC was only found after the treatment with VCE-003.2. In summary, our data confirmed the neuroprotective potential of VCE-003.2 in 6-OHDA-lesioned mice, which adds to its previous activity found in an inflammatory model of PD (LPS-lesioned mice). Additional phytocannabinoid derivatives, CBGA-Q and CBGA-Q-Salt, also afforded neuroprotection in 6-OHDA-lesioned mice, but their effects were lower compared to VCE-003.2, in particular in the case of CBGA-Q-Salt. In vitro studies confirmed the relevance of PPAR-γ receptors for these effects.”
Comparative Analysis of Far East Sikhotinsky Rhododendron (Rh. sichotense) and East Siberian Rhododendron (Rh. adamsii) Using Supercritical CO2-Extraction and HPLC-ESI-MS/MS Spectrometry
https://pdfs.semanticscholar.org/6953/6321413722f0471b61d27fbc6ba0e41160a0.pdf?_ga=2.203472656.1857470788.1668037375-1623449422.1665100195
“Rhododendron sichotense Pojark. and Rhododendron adamsii Rheder have been actively used in ethnomedicine in Mongolia, China and Buryatia (Russia) for centuries, as an antioxidant, immunomodulating, anti-inflammatory, vitality-restoring agent. These plants contain various phenolic compounds and fatty acids with valuable biological activity. “
ARBUTIN:
Investigation of the pro-apoptotic effects of arbutin and its acetylated derivative on murine melanoma cells
https://www.spandidos-publications.com/10.3892/ijmm.2017.3256
“Arbutin, a natural polyphenol isolated from the bearberry plant Arctostaphylos uvaursi, possesses whitening and anticancer properties. The effects of arbutin on melanogenesis and its pro-apoptotic effect on B16 murine melanoma cells have not yet been reported. In the present study, acetylated arbutin was prepared in order to improve the biological effects of arbutin, and it was found to significantly inhibit the biosynthesis of melanin and tyrosinase activity compared with parent arbutin in B16 murine melanoma cells. Interestingly, only acetylated arbutin strongly inhibited B16 murine melanoma cell migration in a dose-dependent manner. Both arbutin and acetylated arbutin significantly reduced cell viability, promoted cell apoptosis, caused G1 cell cycle arrest and induced mitochondrial disruption in B16 murine melanoma cells. Furthermore, reduced expression of B-cell lymphoma‑extra large (Bcl-xL) and Bcl-2 were observed in arbutin- and acetylated arbutin-treated cells. Therefore, arbutin and acetylated arbutin were found to exert pro-apoptotic effects on B16 murine melanoma cells, mediated through the mitochondrial pathway. The findings of the present study also support the use of acetylated arbutin as a new potential candidate agent for skin whitening and melanoma treatment.”
Anticancer Effect of Arbutin on Diethylnitrosamine-Induced Liver Carcinoma in Rats via the GRP and GADD Pathway
https://pubmed.ncbi.nlm.nih.gov/35378001/
“Liver cancer is the third most common cancer, with increasing morbidity and mortality rates worldwide. Despite the increasing occurrence of liver cancer, it has a poor prognosis and potential treatment options are still lacking. The current study aimed to explore the anticancer potential of arbutin against diethylnitrosamine (DEN)-triggered liver carcinogenesis in rats. Liver cancer was initiated in rats via the administration of DEN (200 mg/kg) and then treated with 30 mg/kg of arbutin. Albumin, globulin, and total protein were quantified using kits. Antioxidant, liver injury marker, and tumor biomarker contents were quantified using marker-specific assay kits. The inflammatory markers c-JNK, TRAIL, caspase-8, and p53 contents were also detected using kits. Reverse transcription PCR analysis was used to study the expression of chaperones GRP78, GRP94, and PDIA4 as well as ERDJ4, ATF4, and GADD34. Liver histology was studied microscopically. The arbutin treatment effectively improved body weight and reduced liver weight in animals with DEN-provoked liver cancer. The treatment also improved the albumin, globulin, and total protein contents and antioxidants. In addition, arbutin reduced liver injury marker enzyme function and improved c-JNK, TRAIL, caspase-8, and p53 contents. Arbutin supplementation also decreased the expression of GRP78, PDIA4, GRP94, ERDJ4, ATF4, and GADD34 in the liver tissues of DEN-provoked animals. Arbutin effectively ameliorated the DEN-provoked histological alterations. Altogether, our findings show that arbutin has anti-inflammatory, antioxidant, and anticarcinogenic activities against DEN-provoked liver cancer in rats.”
Potential radioprotective properties of arbutin against ionising radiation on human leukocytes in vitro
https://www.sciencedirect.com/science/article/abs/pii/S1383571821001042
“Arbutin is a simple phenolic glucoside biosynthesised in many plant families. Some of the everyday foods that contain arbutin are species of the genus Origanum, peaches, cereal products, coffee and tea and Arctostaphyllos uva ursi L. leaves. Arbutin possesses various beneficial effects in the organism, and was confirmed effective in the treatment of urinary tract infections as well as in preventing skin hyperpigmentation. It shows antioxidant and anti-inflammatory properties, and antitumor activity. The aim of this study was to explore potential radioprotective properties of arbutin in concentrations of 11.4 μg/mL, 57 μg/mL, 200 μg/mL and 400 μg/mL administered as a pre-treatment for one hour before exposing human leukocytes to ionising radiation at a therapeutic dose of 2 Gy. The alkaline comet assay was used to establish the levels of primary DNA damage, and cytokinesis-block micronucleus (CBMN) cytome assay to determine the level of cytogenetic damage. None of the tested concentrations of single arbutin showed genotoxic and cytotoxic effects. Even at the lowest tested concentration, 11.4 μg/mL, arbutin demonstrated remarkable potential for radioprotection in vitro, observed both at the level of primary DNA damage, and using CBMN cytome assay. The best dose reduction compared with amifostine was observed after pre-treatment with the highest concentration of arbutin, corresponding to 400 μg/mL. Promising results obtained on the leukocyte model speak in favour of extending similar experiments on other cell and animal models.”
Arbutin attenuates monosodium L-glutamate induced neurotoxicity and cognitive dysfunction in rats
https://www.sciencedirect.com/science/article/abs/pii/S0197018621002631
“Excitotoxicity, oxidative stress, and neuro-inflammation underlie the pathogenesis of neurodegenerative brain disorders. Although L-glutamate is the prime excitatory neurotransmitter involved in diverse brain functions, however, overabundance at synapse can activate cell death mechanisms. Previous studies indicate that arbutin affords relief in metabolic, cardiovascular, and gastrointestinal disorders. Recently, arbutin showed benefits in animal models of epilepsy, Parkinson's disease, and Alzheimer's disease that further expanded its therapeutic potential against brain disorders. In the present study, we aimed to evaluate the potential of arbutin against monosodium L-glutamate (MSG) neurotoxicity in rats. Wistar rats (male, 180–200 g) were administered MSG (4 mg/kg) and arbutin (50 and 100 mg/kg) intraperitoneally for 21 days. Cognitive functions were assessed using elevated plus maze and novel object recognition task. Biochemical parameters of oxidative stress, tumour necrosis factor-α (TNF-α), γ-amino butyric acid (GABA), acetylcholinesterase (AChE) activity, lactate dehydrogenase (LDH), and intracellular cation-levels (Na+, Ca2+, K+) were determined using whole brain. Administration of MSG augmented cation-levels, oxidative stress, inflammation, AChE, and LDH activities, and decreased GABA levels in the brain. Arbutin (50 and 100 mg/kg, i.p.) significantly decreased these biochemical disturbances in the brain of MSG administered rats. Behavioural results showed that MSG triggered cognitive deficits in rats that were significantly attenuated by arbutin. Histopathological findings in hippocampus and cortex revealed neuroprotective outcome of arbutin treatments against MSG. MK-801 and N(G)-nitro-L-arginine methyl ester (L-NAME) enhanced memory and neuroprotective effects in rats treated with arbutin and MSG. Arbutin may afford therapeutic advantages in neurodegenerative brain disorders by suppressing the excitotoxic pathways.”
Arbutin protects brain against middle cerebral artery occlusion-reperfusion (MCAo/R) injury
https://www.sciencedirect.com/science/article/abs/pii/S0006291X21012948
“Focal ischemia causes irreversible brain damage if cerebral blood flow is not restored promptly. Acute phase excitotoxicity and pro-oxidant and inflammatory events in the sub-chronic phase elicit coagulative necrosis, vascular injury, cerebral oedema, and neurobehavioral deficits. Earlier, in pre-clinical studies arbutin protected behavioral functions and improved therapeutic outcomes in different models of brain and metabolic disorders. Arbutin is natural hydroquinone that might protect against ischemia-reperfusion (I/R) injury. In this study, cerebro-protective effects of arbutin were evaluated in the middle cerebral artery occlusion-reperfusion (MCAo/R) mouse model. Mice were administered arbutin (50, 100 mg/kg, i.p.) for 21 days, and subjected to MCAo/R or sham surgery on day 14. Results showed brain infarction, blood-brain barrier dysfunction, oedema, and neurological deficits 24 h post-MCAo/R injury that were prevented by arbutin. Behavioral evaluations over the sub-chronic phase revealed MCAo/R triggered spatial and working memory deficits. Arbutin protected the memory against MCAo/R injury and decreased hydroxy-2′-deoxyguanosine, protein carbonyls, inflammatory cytokines (tumor necrosis factor-α, myeloperoxidase, matrix metalloproteinase-9, inducible nitric oxide synthase), and enhanced glutathione levels in the ischemia ipsilateral hemisphere. Arbutin decreased brain acetylcholinesterase activity, glutamate, and enhanced GABA levels against MCAo/R. Arbutin can alleviate I/R pathogenesis and protects neurobehavioral functions in the MCAo/R mouse model.”
TAKE NOTE with this study. It being shown to increase Glutathione levels, decrease acetylcholinesterase activity and to decrease glutamate, while it enhanced GABAL levels. These might prove to be significant findings for these extremely important biomarkers.
Arbutin improves gut development and serum lipids via Lactobacillus intestinalis
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9502005/
“Arbutin has been widely studied in whitening, anti-inflammatory, and antioxidant. However, the interaction between arbutin and intestinal microbes has been rarely studied. Thus, mice were treated with arbutin concentrations of 0, 0.1, 0.2, 0.4, and 1 mg/ml. We found that arbutin promoted gut development such as villus length, villus areas, and villus length/crypt depth (L/D). Total cholesterol (TC), high-density lipoprotein (HDL), and low-density lipoprotein (LDL) were significantly reduced by low concentrations of arbutin. Importantly, we analyzed the microbial composition in the control and 0.4 mg/ml arbutin group and found that the abundance of Lactobacillus intestinalis (L. intestinalis) was highest and enhanced in arbutin. Further, mice were fed with oral antibiotics and antibiotics + 0.4 mg/ml arbutin and then we transplanted fecal microbes from oral 0.4 mg/ml arbutin mice to mice pretreated with antibiotics. Our results showed that arbutin improves gut development, such as villus width, villus length, L/D, and villus areas. In addition, L. intestinalis monocolonization was carried out after a week of oral antibiotics and increased villus length, crypt depth, and villus areas. Finally, in vitro arbutin and L. intestinalis co-culture showed that arbutin promoted the growth and proliferation of L. intestinalis. Taken together, our results suggest that arbutin improves gut development and health of L. intestinalis. Future studies are needed to explore the function and mechanism of L. intestinalis affecting gut development.”
We’re going to stop right here. Hopefully this article has provided you with a generous introduction to the various qualities of this relatively unknown Siberian adaptogen.
The above is for informational purposes only.
We are not suggesting you consume sagan dalya, and we are claiming that this product cures, prevents, or treats any disease. The above statements have not been evaluated by the FDA.
You can find our sagan dalya here: https://www.hyperborealherbs.com/shop/p/dried-sagan-dalya-arctic-witch-herbs-medicinal-loose-leaf-tea
