Is Healthy Green CBD For Inflammation?

Inflammation is the body’s natural response to injury, illness or infection that helps it heal itself. But prolonged inflammation can lead to a variety of issues like joint pain, autoimmune disease, high blood pressure, cardiovascular disease and cancer cells – just to name a few!

CBD can reduce inflammation by blocking inflammatory messengers that cause pain and discomfort. It also reduces oxidative stress and shields the immune system from inflammatory responses.

Anti-Inflammatory Effects

Inflammation is an entirely normal part of the immune system’s response, but it can also cause pain and other issues. Anti-inflammatory medications like NSAIDs and steroids are usually prescribed to combat inflammation; however, some people prefer taking a more natural approach with less risks associated with these drugs.

CBD has been scientifically demonstrated to be an effective anti-inflammatory in multiple studies. It could potentially reduce chronic inflammation associated with diseases like cancer, heart disease and rheumatoid arthritis.

CBD’s anti-inflammatory effects are caused by its ability to inhibit certain inflammatory enzymes and cytokines. Cytokines are small proteins released by immune cells when the body experiences stress or injury.

By inhibiting COX2, CBD helps prevent the production of these inflammatory proteins and thus helps prevent inflammation from taking hold. Furthermore, it reduces oxidative stress by suppressing free radical production and can lower levels of IL-6 and TNF-alpha as well.

Another way CBD helps combat inflammation is by inhibiting cellular apoptosis. Apoptosis is the process by which your body purges unwanted cells that are no longer needed, leaving behind damaged DNA that can lead to inflammation and other health issues.

Though CBD’s anti-inflammatory effects have been demonstrated in various research models, more human trials are necessary to fully comprehend how it functions and how it can benefit those suffering from pain and inflammation. One animal study suggests that applying CBD directly onto the skin may reduce pain associated with arthritis.

CBD appears to have anti-inflammatory effects in rheumatoid arthritis synovial fibroblasts, which play a significant role in the disease process. These cells produce pro-inflammatory cytokines like IL-8 and MMP-3 which can wreak havoc on joints and worsen symptoms associated with Rheumatoid Arthritis.

CBD can inhibit these pro-inflammatory cytokines by activating TRPA1 protein located within intracellular compartments. This action causes Ca2+ release into the cytosol and uptake into mitochondria, increasing activity of organic cation transporters (OCT). Ultimately, this increases CBD uptake for enhanced therapeutic effects.

Inhibition of COX2

Inflammation occurs due to increased levels of prostaglandins (PGs), produced by the COX-2 enzyme. Nonsteroidal anti-inflammatory drugs (NSAIDs) like Celebrex and Motrin are frequently prescribed in order to reduce inflammation and pain associated with chronic inflammatory diseases like rheumatoid arthritis or osteoarthritis, among others.

COX2 is an important inflammatory mediator, with overexpression linked to various disorders and cancers. Furthermore, COX2 plays a significant role in gastric toxicities and bleeding diathesis that are commonly observed when taking NSAIDs.

Therefore, developing drugs that inhibit COX-2 while sparing COX-1 is an attractive therapeutic target. This could potentially mark a breakthrough in treating both inflammatory and non-inflammatory disorders as well as various cardiovascular and neurodegenerative illnesses.

Though many NSAIDs exhibit inhibitory effects against COX1 and COX2, the degree of this inhibition varies among drugs. This could explain why different NSAIDs have differing toxicity profiles. It’s essential to note that COX-2 inhibition is only one mechanism of action for NSAIDs.

COX2 is an inflammatory enzyme found in various tissues such as the gastrointestinal tract and joints. It metabolizes free arachidonic acid to produce proinflammatory messengers like prostacyclin and thromboxanes, and plays an integral role in producing proinflammatory and anti-inflammatory resolvins [6, 10].

CBD has been shown to exert concentration-dependent effects on ATP-dependent substrate transporters such as FABPs and P-glycoprotein, with the highest Kis reported at concentrations as low as 1.5-1.9 mM. Furthermore, AEA is transported by FABPs which could explain why CBD causes an increase in AEA levels. Unfortunately, the in vivo effects of these receptors remain poorly understood; further investigation is necessary to pinpoint their involvement.

Additionally, the pentameric glycine ionotropic receptors a1 and a1b (GlyR), which are key players in mediating neuropathic pain and inflammation, have been demonstrated to respond to CBD both in vitro and on HEK293 cells expressing the a1 GlyR subtype [21, 22]. Furthermore, glycine-induced currents are significantly enhanced by CBD in HEK293 cells expressing a3 GlyR (Table 1) which could indicate that CBD exerts its anti-inflammatory effect through direct action on these receptors.

Reduction of oxidative stress

Inhibiting oxidative stress is an essential aspect of CBD’s anti-inflammatory effects. When cells are under oxidative strain, ROS (reactive oxygen species) are produced which can have numerous negative consequences on the body such as increased inflammation, DNA damage and cell death. Thankfully, the endocannabinoid system (ECS) and its receptors help to combat the production of these harmful molecules.

CBD inhibits the degradation of lipids and proteins by blocking oxidative modifications to these macromolecules. Furthermore, it blocks MDA- and 4-HNE-protein adducts – which are largely responsible for oxidative stress and apoptosis – from forming.

Another protective effect of CBD is its capacity to enhance the activity of antioxidant enzymes like glutathione peroxidase and glutathione reductase, which help protect cells from ROS damage. This explains why CBD has such remarkable effectiveness in fighting inflammatory conditions like asthma and psoriasis, where inflammation levels tend to be high.

These effects of CBD are caused by an interaction between the ECS and CB2 receptor [62]. CBD inhibits inflammatory proteins like tumor necrosis factor-a (TNF-a) and cytokines while increasing levels of antioxidant enzymes like superoxide dismutase and glutathione peroxidase. Furthermore, CBD activates Nrf2 gene transcriptional activation which then leads to expression of antioxidant enzymes like thioredoxin or glutathione reductase.

Keratinocytes exposed to CBD experienced an uptick in both glutathione peroxidase (GSHPx) and glutathione (GSH) activity following UVB irradiation, along with a dose-dependent decrease of malonaldehyde (MDA) levels. This led to an impressive boost in keratinocyte antioxidant capacity – essential for maintaining healthy skin while protecting it from UV-induced damage.

Studies have demonstrated that CBD can reduce oxidative stress and inflammation, as well as improve skin health. These results are especially pertinent to those suffering from psoriasis or other skin diseases where oxidative stress is often high. Therefore, CBD could potentially serve as a treatment for these conditions as well as many others; however, further research is necessary to confirm its efficacy in doing so. Try Healthy Green CBD Oil Today

Inhibition of TRPV2

CBD’s anti-inflammatory effects are thought to be due to its ability to decrease the production of pro-inflammatory mediators. This includes inhibiting COX2 and decreasing intracellular and mitochondrial oxidative stress – an element involved in many human diseases like chronic obstructive pulmonary disease and obesity [3, 4].

Though the exact mechanism by which CBD modulates inflammation remains uncertain, this compound appears to do so through inhibition of TRPV2 channels. Indeed, reports have demonstrated that CBD antagonizes both human and rat TRPV2 receptors when overexpressed in HEK293 cells; additionally, patch clamp electrophysiology revealed significant desensitization of ruthenium red-sensitive TRPA1 neurons.

CBD’s inhibition of TRPV2 was also demonstrated in other cell types, including mouse brain and rat basophilic leukemia cells (RBL-2H3). Scintillation counting the membrane transporter for anandamide (AEA) showed that CBD inhibited AEA uptake at concentrations ranging from 5-50 mM in these cell lines; these findings were replicated using another cell line.

This inhibition is likely the result of CBD’s actions at the ABCC1 transporter, which has a broad substrate specificity and important therapeutic applications. In vitro experiments using Fluo3 and vincristine revealed that CBD was an “effective” inhibitor of ABCC1-mediated transport when present at 10 and 50 mM CBD concentrations (Table 3).

Additionally, CBD was observed to inhibit nicotinic acetylcholine receptors in Xenopus oocytes at an IC50 of 1-30 mM. Similar results were also seen with rat hippocampal slices where CBD inhibited acetylcholine-induced ion currents at an IC50 value of 12.7 mM.

Finally, CBD was demonstrated to significantly decrease cell viability, proliferation and cytokine production of rat airway smooth muscle cells (RASF) when exposed to 20 uM CBD. This effect was further amplified after pretreatment with TNF through the mPTP protein. Furthermore, IL-6/IL-8 and MMP-3 levels were altered by 20 uM CBD treatment as well.

CBD also inhibited intracellular calcium and uptake of the cationic viability dye PoPo3 in RASF by 20 uM, which was correlated to inhibition of cell growth caused by cyclosporin A pre-treatment. These effects were further amplified with TNF pre-treatment, suggesting that CBD’s cytokine reducing properties may be due to its apoptotic effects on immune cells. Start Feeling Better Today Click HERE To Order