Cannaderm Croatia

Što kaže Chatgpt o delta9THC

Delta-9-tetrahidrokanabinol (Δ⁹-THC), glavni psihoaktivni sastojak kanabisa, pokazuje antitumorska svojstva u laboratorijskim uvjetima, i to kroz više mehanizama. Iako su istraživanja još uvijek u fazama pretkliničkih i ranih kliničkih ispitivanja, u nastavku su načini na koje Δ⁹-THC može djelovati protiv stanica raka:

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🔬 1. Indukcija apoptoze (programirane stanične smrti)

THC aktivira CB1 i CB2 kanabinoidne receptore, koji su prisutni i na mnogim stanicama raka.

Aktivacija ovih receptora pokreće signalne puteve (npr. ceramidna sinteza, stres endoplazmatskog retikuluma) koji uzrokuju samouništenje stanica tumora, bez oštećenja zdravih stanica.

> Npr. u gliomima (vrsta tumora mozga), THC povećava razinu ceramida, što pokreće apoptozu.

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🔬 2. Inhibicija proliferacije stanica raka

THC može zaustaviti rast tumorskih stanica inhibicijom signalnih puteva poput:

PI3K/Akt/mTOR

MAPK/ERK

Ovi putevi su često pretjerano aktivirani u raku, potičući rast i preživljavanje tumora.

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🔬 3. Smanjenje angiogeneze (stvaranja krvnih žila za tumor)

THC smanjuje ekspresiju VEGF-a (vaskularnog endotelnog faktora rasta), koji je ključan za stvaranje novih krvnih žila koje hrane tumor.

Bez nove opskrbe krvlju, tumor usporava rast ili propada.

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🔬 4. Inhibicija metastaziranja (širenja raka)

THC može smanjiti invazivnost tumorskih stanica utječući na enzime kao što su matriks metaloproteinaze (MMPs), koje pomažu tumoru da probije tkiva i širi se.

Također može utjecati na citokine i adhezijske molekule, smanjujući sposobnost tumora da kolonizira nova područja.

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🔬 5. Imunomodulacija

Iako THC može imati imunosupresivne učinke, u kontekstu raka to može biti korisno jer:

Neke stanice raka izbjegavaju imunološki nadzor induciranjem kronične upale.

THC može smiriti tu štetnu upalu i omogućiti tijelu bolju imunološku kontrolu nad tumorom.

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🧪 U kojim vrstama raka je to istraženo?

Najviše podataka imamo za:

Gliome (tumori mozga)

Rak dojke

Rak prostate

Rak pluća

Rak gušterače

Leukemije i limfomi

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⚠️ VAŽNO: Ograničenja i status istraživanja

Većina ovih podataka dolazi iz in vitro (u epruveti) ili in vivo (na životinjama) istraživanja.

Nema još dovoljno kliničkih dokaza da THC sam po sebi liječi rak kod ljudi.

U nekim slučajevima, THC može čak poticati rast raka, ovisno o vrsti stanica i dozi.

Potrebna su dodatna istraživanja prije nego što THC postane standardna antikancerogena terapija.

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✅ Zaključak

Delta-9 THC može:

Ubiti stanice raka putem apoptoze

Zaustaviti njihov rast i širenje

Smanjiti razvoj krvnih žila koje hrane tumor

Ali trenutno se ne koristi kao primarna terapija za rak, već u nekim slučajevima kao dopuna (npr. protiv mučnine kod kemoterapije ili za poboljšanje apetita).

Ako želiš, mogu ti pronaći najnovije studije o utjecaju THC-a na točno određeni tip raka.

SKIN AND SKIN DISEASE:
The skin is the largest organ in the human body. One of its main functions is to protect the body from external factors and is the first defensive obstacle for the innate immune system. Other important functions of the skin include controlling body temperature, maintaining hydro-electrolyte balance and detecting painful or pleasant irritations. Any change in the function or appearance of our skin can have significant consequences for our physical and mental health. Many of the problems present in the skin are confined to it. In some cases the skin can reveal a disturbance that hurts the whole body.
Cannabinoids in dermatology
The local use of Cannabis sativa L dates back to ancient China, where cannabis was used for external use to treat skin rashes, sores, wounds and hair loss.
There is also archeological evidence to show that the ancient Egyptians used cannabis topical remedies to treat eye diseases and also in bandages on injuries/wounds.
Cannabis leaves were used in medieval Arabian medicine to treat skin diseases such as pityriasis and lichen planus (a type of psoriasis). Not long ago, in the beginning of the twentieth century before the prohibition, pharmacies often sold cannabis tinctures. Among other things, they have been used to treat blisters, irritable bladder, menstrual pain and to help break opioid addiction.
The skin has all the elements of the endocannabinoid system, namely Endocannabinoids compounds (AEA and 2-AG), metabotropic (CB1R and CB2R) and ionotropic (TRPV-1) cannabinoid receptors and enzymes that work together in the synthesis and metabolism of endocannabinoids. (e.g. FAAH in MAGL).
Various elements of the endocannabinoid system are involved in key mechanisms of skin regulation, such as control of growth of the surface and skin adhesives, cell survival, immune and inflammatory response, transfer of sensory stimulus to the central nervous system (pain, itching) and lipid synthesis, among other activities.
Despite its long history of local cannabis use and advances in our understanding of the endocannabinoid skin system, research on cannabinoid use in skin pathologies is one of the youngest areas of research in this field and clinical data on cannabis use in dermatological practice remains very limited.
Nevertheless, there is growing evidence of the potential of cannabinoids to treat inflammatory skin diseases, including psoriasis and atopic dermatitis, and for the treatment of autoimmune diseases such as scleroderma, characterized by inflammation and fibrosis.
Scorpion
Psoriasis is one of the most common chronic inflammatory skin diseases. It is characterized by hyperproliferation and excretion of keratinocytes, which result from the infiltration of T-cells and neutrophilics and activation of dendritic cells and macrophages. Although psoriasis pathogenesis is not fully understood, there is solid evidence that deregulation of immune cells in the skin, especially cells Th1 and Th17, plays a key role in the development of psoriasis.
Atopic dermatitis
Atopic dermatitis (AD) is the most common chronic inflammatory skin disease. The onset and progression of diseases are caused by interactions of genetic, environmental and immune factors. Clinical characteristics of AD include skin dryness due to loss of surface, erythema, excretion, scabies and lihenification. In addition, AD is characterized by severe itching that leads to frequent scratches and staph infection. There is no cure for AD, the main goals of the treatment are the reduction of symptoms (itching and dermatitis), preventing worsening and reducing the risk of skin infection. Standard forms of treatment for patients with AD focus on the use of anti-inflammatory topical preparations with corticoids and skin hydration, but in serious cases patients may need a systematic treatment with strong immunosuppressants for example cyclosporin A or tachrolimus and antibiotics, to prevent infection with staphylococcus bacteria.
Cannabinoids and fibrootic skin diseases
Systemic sclerodermia (or sclerosis) (SSc) is a rare autoimmune disease that has three main characteristics: fibroblast dysfunction, which leads to increased release of proteins from the outside-cell matrix, small vessel vasculopathy that causes tissue hypoxia, and an immune response by the production of inflammatory cytokines and antibodies. SSc is characterized by gradual thickening and fibrosis of the skin, which is the result of excessive accumulation of collagen and can be confined to the skin (localized - or limited - skin SSc) or spread to the internal body (scattered SSc). SSc begins with microvascular damage and inflammation. Following is the activation of fibroblasts, which is a key event in the development of fibrosis.
Recent evidence shows that genetic and pharmacological manipulation with the endocannabinoid system modulates the fibrotic response. CB1 and CB2 receptors also showed different patterns in experimental models of dermal fibrosis. Blockage CB1R prevents fibroblasts activation and has a strong antifibrotic effect (Marquart and sod. , 2010). The role of CB1R as a proibrotic receptor has also been confirmed in mice isolated for FAAH, where high levels of endocannabinoids can cause fibrosis along the CB1R-dependent pathway. On the other hand, activation CB2R prevents skin fibrosis and infiltration of leucocytes of tissue in models of experimental dermal fibrosis (Akhmetshina et al. , 2009). As a result, JWH-133, a synthetic CB2R agonist, invalidates experimental dermal fibrosis in mice. This agrees with the fact, that mice with CB2R excretion are more susceptible to the development of fibrosis (Balistreri et al. , 2011). It was also proven that the PPAR Prav agonists inhibit the proibrotic response by inhibiting the TGF , signal path. PPAR aktiv / CB2R double agonists have also been proven to exhibit strong anti-inflammatory and antifibrotic activity in experimental models of SSc (Del Río et al. , 2016).

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