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cbd strains for cervical cancer

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Cbd strains for cervical cancer

Cervical cancer used to be the leading cause of cancer death among women in the United States, but those rates have gone down by almost 50 percent due to the widespread use of the Pap test for cervical cancer. In South Africa, however, over 80 percent of the population still relies on medicinal plants, which begs the question: do these women have the same access to the Pap test as American women do? Not likely.

In the absence of a solid medical infrastructure capable of administering Pap smears to its entire female population, rural regions of the world need a cheap and easily accessible treatment for the disease that won’t have them riddled with toxic side effects.

Oregon Breeders Group

Recent research from South Africa has highlighted the potential cannabis has to treat cervical cancer, a disease that kills over a quarter of a million women annually. This latest study was not conducted on humans, but is the first of it’s kind and shows promising results.

Researchers from the Department of Biochemistry at North-West University in Potchefstroom, South Africa used in vitro analyses to assess the efficacy of cannabis in killing cervical cancer cells. They used herbal extracts and pure CBD, and they found that CBD is most likely the compound responsible for the anti-cancer effects of the Cannabis sativa extract. However, they did not perform the analysis with pure THC (the psychoactive component), meaning this compound is not off the hook for having any anti-cancer effects similar to CBD. Cannabis killed cervical cancer cells by inducing apoptosis; literally forcing cancer cells—and only cancer cells—to kill themselves.

Research in this field has a long way to progress before cannabis can become part of an official treatment program for cervical cancer. If regulatory agencies do one day approve cannabis as a treatment option, this could spell great news for the rural populations of Sub-Saharan Africa and around the world. Growers contracted by local pharmacies could grow the same indigenous varieties of cannabis used in this study and send them to extraction labs for processing into medicinal formulations.

Cannabis sativa is a dioecious plant that belongs to the Cannabaceae family and it originates from Central and Eastern Asia [11, 28]. It is widely distributed in countries including Morocco, South Africa, United States of America, Brazil, India, and parts of Europe [14, 28]. Cannabis sativa grows annually in tropical and warm regions around the world [11]. Different ethnic groups around the world use Cannabis sativa for smoking, preparing concoctions to treat diseases, and for various cultural purposes [17]. According to [28], it is composed of chemical constituents including cannabinoids, nitrogenous compounds, flavonoid glycosides, steroids, terpenes, hydrocarbons, non-cannabinoid phenols, vitamins, amino acids, proteins, sugars and other related compounds. Cannabinoids are a family of naturally occurring compounds highly abundant in Cannabis sativa plant [1, 6, 14, 24]. Screening of Cannabis sativa has led to isolation of at least 66 types of cannabinoid compounds [1, 14, 30]. These compounds are almost structurally similar or possess identical pharmacological activities and offer various potential applications including the ability to inhibit cell growth, proliferation and inflammation [22]. One such compound is cannabidiol (CBD), which is among the top three most widely studied compounds, following delta-9-tetrahydrocannabinol (Δ 9 -THC) [14]. It has been found to be effective against a variety of disorders including neurodegerative disorders, autoimmune diseases, and cancer [24, 25]. In a research study conducted by [26], it was found that CBD inhibited cell proliferation and induces apoptosis in a series of human breast cancer cell lines including MCF-10A, MDA-MB-231, MCF-7, SK-BR- 3, and ZR-7-1 and further studies found it to possess similar characteristics in PC-3 prostate cancer cell line [25]. However, to allow us to further our studies in clinical trials a range of cancers in vitro should be tested to give us a clear mechanism before we can proceed. Cannabis sativa in particular cannabidiol, we propose it plays important role in helping the body fight cancer through inhibition of pain and cell growth. Therefore, the aim of this study was to evaluate the cytotoxic and anti-proliferative properties of Cannabis sativa and its isolate, cannabidiol in cervical cancer cell lines.

Conclusions

Five hundred microliter of 1×10 4 cells was added onto a 6-well plate containing coverslips. The plate was incubated overnight to allow the cells to attach. Following attachment, media was removed and cells were washed twice with PBS, prior to incubation with IC50 of Cannabis sativa extracts for 24 h. After 24 h, media was removed and cells were washed twice with PBS. Four percent (4 %) was added into each well and the plate incubated for 20 min at room temperature, to allow efficient fixation of cells. Cells were washed twice with PBS and once with 0.1 % BSA wash buffer and further stained with DAPI and Annexin V/FITC for 5 min. BX-63 Olympus microscope (Germany) was used to visualize the cells.

Cell culture

Apoptosis is known to occur via two pathways, the death receptor pathway and the mitochondrial pathway [30]. Cannabis sativa isolates including cannabidiol have been implicated in apoptosis induction via the death receptor pathway, by binding to Fas receptor or through an activated of Bax triggered by the synthesis of ceramide in the cells [4]. However, not much has been reported on the induction of apoptosis via activation of p53 by Cannabis sativa. Our focus in this study was also to identify downstream molecular effect of extracts. One such important gene is p53 which acts as a transcription factor for a number of target genes [29]. Under normal conditions, p53 levels are maintained through constant degradation MDM2 and its monomers [29]. RBBP6 is one of the monomers that helps degrade p53, due the presence of Ring finger domain that promotes the interaction of both proteins [14]. In response to stress stimuli such as DNA damage, hypoxia, UV light, and radiation light, p53 becomes activated and causes MDM2 expression to decrease [10]. Mutation of p53, implicated to be associated with 50 % of all human cancers, promote the tumorigenesis. Bax and Bcl-2 form part of the proteins that regulate apoptosis via the mitochondria [21]. Following activation, p53 translocates into the cytosol and triggers the oligomerization of Bcl-2 with BAD, resulting in the inhibition of Bcl-2 activity [17]. This in turn allows Bax protein to be translocated to the mitochondria and participate in the release of cytochrome c through poration of the outer mitochondrial membrane [9, 17]. An imbalance between Bax and Bcl-2 has been linked to the development and progression of tumours through the resistance of apoptosis [17]. It is therefore crucial to design drugs that would effectively target these genes involved in the execution of apoptosis via the mitochondrial pathway. Camptothecin, hexane extract, and cannabidiol effectively up-modulated the expression of p53 in all three cell lines, leading to a decrease in RBBP6 protein expression. Apart from SiHa and HeLa, butanol extract failed to up-modulate p53 in ME-180 cells. Interesting to note is that butanol extract reduced the expression of RBBP6 protein in ME-180 cells. The mechanism behind failure of butanol to up-modulate p53 while down-modulating RBBP6 is unclear. However, we came to a conclusion that butanol induces apoptosis independently of p53. We further demonstrated that Cannabis sativa extracts, cannabidiol, and camptothecin were able to down-modulate the expression of Bcl-2 protein and up-modulate Bax expression.