Salvia Sage: A Review of its Potential Cognitive-Enhancing and Protective Effects PMC
There are several actions that could trigger this block including submitting a certain word or phrase, a SQL command or malformed data. Since salvia impairs your thoughts and emotions and causes you to lose contact with external reality, it can lead to impaired judgement and risk-taking 58 best rehab centers in california 2023 free and private options behaviour, leading to traumatic injuries and even death. Salvia is controlled under Schedule IV of the Controlled Drugs and Substances Act. Activities such as sale, possession and production of salvia are illegal unless authorized for medical, scientific or industrial purposes.
Long-term health effects of salvia
Get professional help from an online addiction and mental health counselor from BetterHelp. In taxonomy, Salvia divinorum belongs to the sage genus of the mint family. As such, Salvia as a recreational drug is often called “Sage Of The Diviners” or “Seer’s Sage.” Magic Mint, Sally-D, and María Pastora are other street names for Salvia. In the United States, the legal status of Salvia varies by jurisdiction. At the federal level, Salvia is not a controlled substance, but it is illegal to use or possess in the majority of states.
Salvia miltiorrhiza: A Potential Red Light to the Development of Cardiovascular Diseases
- Its main pathological features include degradation of articular cartilage, thickening of subchondral bone, formation of osteophytes, synovial inflammation, degradation of knee ligament and meniscus as well as hypertrophy of joint capsule (Pountos and Giannoudis, 2017).
- Miltiorrhiza and its active components (Danshensu and salvianolic acid B) inhibited TNF-α induced hyper-permeability by inhibiting VEGF expression [133] in HUVECs.
- Miltiorrhiza significantly inhibited the mRNA and protein expression of TNF-α, IL-1β, and IL-8 in LPS-stimulated macrophages [65].
It is accepted that increased expression and activation of ICAM-1 and VCAM-1 as well as E-selectin contribute to the attachment of circulating monocytes/leukocytes to the surface of endothelial cells, which initials atherosclerosis [132]. Treatment with salvianolic acid B (8 m/kg/d) and tanshinone IIA (24 mg/kg/d) for 8 weeks were demonstrated to inhibit atherogenesis of HFD-fed rabbits by increasing NO release [9]. Although the influence of plants of different species of Salvia on cognition has been reviewed, differences in the active constituents across each species are likely to affect their influence on biological processes and therefore their therapeutic efficacy. Currently, the relative efficacy of different Salvia species on cognitive function is unknown. The influence of individual constituents also requires further investigation.
4. Effects of Salvia miltiorrhiza on Endothelial Cells, Smooth Muscle Cells and Myocardial Cells
Fracture healing is a complex pathophysiological process, typically divided into 4 phases of inflammatory response, cartilage formation, woven bone formation, and bone remodeling (Annamalai et al., 2018; Tian et al., 2019). SM had been used as one of the bioactive ingredients in the clinical fracture treatment of traditional Chinese medicine for many years. In a study of He and Shen (2014), salvianolic acid B was found to increase the activity of ALP and the secretion of osteocalcin in a time-and dose-dependent manner, thus accelerating the early fracture healing of tibia. In Liu’s study (Liu et al., 2018), tanshinol bone-targeted liposomes were formulated using pyrophosphorylated cholesterol as a bone targeting ligand for the treatment of delayed fracture. Nitric oxide (NO) is a free radical that exerts significant effects on osteoblast function. Studies have demonstrated that NO inhibits both bone resorption and bone formation, leading to reduced bone turnover in severe inflammatory conditions (van’t Hof and Ralston, 2001).
Salvianolic acid B treatment (0.001, 0.01 and 0.1 mg/mL for 2 h) decreased Ca2+ and cAMP, and inhibited PKA in H9C2 cell (a myogenic cell line derived from embryonic rat heart ventricle) [79]. TRPC proteins may act as molecualr components of store-operated Ca2+ channels which mediate Ca2+ influx [135]. Elevation famous alcoholics you never knew about of intracellular Ca2+ concentration ([Ca2+]i) contributes to cell growth and contraction [136]. Administration of sodium tanshinone IIA sulfonate (10 mg/kg) reduced SOCE and inhibited elevation of basal [Ca2+]i through supressing TRPC1 and TRPC6 expression in distal PASMCs from chronical hypoxic rats [84].
Part of the reason for the scientific establishment’s neglect of salvinorin A may have to do with how many people find its effects deeply unpleasant. Compared to LSD and psilocybin, which became emblematic of the 1960s feel-good mindset, salvinorin A comes on fast and can make a person feel like they’ve left their body, which has probably turned many people off from using it recreationally. Indeed, it’s one of the few well-known psychedelics that isn’t a federally controlled substance under Drug Enforcement Administration regulations, although its use is outlawed in several states. Salvia’s active ingredient, salvinorin A, is considered one of the most potent naturally occurring psychoactive drugs. The effects of this drug include hallucinations, dizziness, visual disturbances, and more. Officinalis and a mix of Salvia adopt a 30% of spatial strategy, whereas control and S.
An agonist attaches to and activates specific central nervous system receptors that are mainly in the brain. Mazatec Indians have used salvia for centuries for spiritual divination, shamanism, and medical practices. Also, it has a low addiction potential, people can easily obtain it, and they do not consider it highly toxic. In this article, we find out what salvia is, how it works, and explain the effects and risks of taking it as a recreational drug.
They may differ from person to person and include both mental and physical effects. Salvia is a general name for plants of the sage family (genus). One type of salvia, salvia divinorum has hallucinogenic properties. There is also no evidence that Salvia causes violent behavior, withdrawal, or dependence, but a person with an addiction to other Hallucinogens may be more likely to use Salvia repeatedly. Scientists continue to study the effects of Salvia on the human brain. The basic chemical structure of the water soluble phenolic acids of S.
In this review, the active constituents in plants belonging to the genus Salvia are summarised, and their influence on pharmacodynamic activity pertinent to cognition are detailed. Their potential effects in dementia, including Alzheimer’s disease, are also reviewed. To investigate the effect of Salvia supplementation on oxidative stress, we evaluated the impact of Salvia supplementation on lipid peroxidation and superoxide dismutase activity.
The marijuana and salvia similarities have led to adolescents and young adults abusing the drug. Both produce a similar high, but salvia provides potential hallucinogenic effects, although they are not as strong as LSD or psilocybin. If you or someone you love is addicted to salvia, The Recovery Village Columbus in Ohio can help. Our trained medical professionals can provide you with the support you need to regain control of your life. Looking for addiction treatment in Columbus, Ohio or the surrounding areas? We have inpatient and outpatient facilities nearby and across the country ready to help.
Wang W demonstrated that cryptotanshinone inhibited RANKL-induced osteoclastogenesis and NFATc1 expression in bone marrow macrophages (BMM) by regulating ERK and NF-κB signaling pathways (Wang W. et al., 2019). Miltiorrhiza is one of the most frequently used herbs in formulations prescribed for the clinical treatment of CVD in China. Although most studies reported promising efficacy in improving clinical symptoms, their significance is still need to be improved through well designed clinical trials in order to provide sufficient evidence to fully demonstrate the effects of S. The investigators are also needed to pay more attention to potential adverse effects and drug-drug interactions of this herb. Currently, there have been more than 200 compounds have been identified from S. Most of these compounds exhibit multipotent pharmacological activities.
Further, magnesium tanshinoate B (MTB, 0.7–175 mg/kg via the jugular vein) was evidenced to exhibit hypotensive effect on phenylephrine induced elevated blood pressure in male SD rats [86]. Miltiorrhiza (0.125 g/mouse) and salvianolic acid B (0.5 mg/mouse) decreased the average blood flow velocity in liver in endothelin (ET)-1 induced portal hypertension mice evaluated by laser-Doppler flow instrument [87]. Matrix metalloproteinases and tissue inhibitors of metalloproteinases (MMPs/TIMPs) impact vascular relaxation/contraction via regulating ion channels in the endothelium and vascular smooth muscle during vascular remodeling [96, 97].
Monocyte chemotactic protein (MCP)-1 is upregulated in the development of MI both in clincal trial [115] and animal model [116], which facilliates infiltration, activation and cytokine secretion of inflammatory cells. MCP-1 null mice exhibited decreased macrophage recruitment in the infarcted heart, delayed phagocytosis of dead cardiomyocytes, diminished fibroblast infiltration and attenuated left ventricular remodeling [117]. Meanwhile, Ang II and TNF-α stimulate MCP-1 production [118] and amplify the pro-inflammatory response through NF-κB and mitogen activated protein kinase (MAPK) p38 5 types of alcoholics characteristics of each alcoholic type signaling pathway [119, 120]. Tanshinone IIA (60 mg/kg/day for 7 days) treatment decreased infarct sizes and collagen deposition and improved heart recovery in permanent left anterior descending coronary artery (LAD) ligation induced MI rats [81]. The cardioprotective effect of tanshinone IIA could be attributed to its abilty of inhibiting inflammatory responses by reducing expressions of MCP-1, transforming growth factor (TGF)-β1, TNF-α and NF-κB [81]. In addition, tanshinone IIA (2-8 μM) treatment also reduced MCP-1 and TGF-β1 secretion in TNF-α stimulated cardiac fibroblasts [81].