Potential of Cannabidiol for the Treatment of Viral Hepatitis . In the HCV assay, CBD inhibited the virus with minimal toxicity against the Huh cells that  The benefit of CBD in alleviating liver fibrosis, which is one of the outcomes of. Using CBD oil as a way of treating hepatitis has several benefits. CBD protects the liver. A recent study is providing hope for people with the hepatitis C virus at least open up avenues for further research into the benefits of CBD.
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At this point, over 58k people die each month because of this virus and the disease triggered by it, called hepatitis C. Counseling and education are already a part of the program, but CBD Oil can be another piece of the puzzle. Given that the third world is such a central part of the Hep C story, its hardly surprising that a big factor is about economics. At this point, CBD Oil is still too expensive for widespread use in developing countries as a treatment for Hep C, but this curve will change over time, so relevant research is continuing.
In the case of the WHA, we are talking about members representing as many different nations. Hopefully, as more and more research emerges that supports this idea — that CBD oil is a viable and important treatment for this terrible health problem — we will see a ratification step taken by these delegates.
That step will incentivize greater production, which will help battle costs and make this a realistic process. However, even at that point, the issue of transportation will still have to be addressed. There is a striking problem of piracy en route as medical treatments are the Spanish gold of the 21 st century. However, three cross-sectional studies in patients with chronic hepatitis C suggest that daily cannabis use is associated with fibrosis and steatosis.
Talk to your doctor and watch for more studies. Fight for affordable healthcare for all. Newly-elected federal officials are threatening to fundamentally change a variety of healthcare insurance programs serving moderate- and low-income Americans and roll back protections, including mandated coverage of pre-existing conditions like hepatitis B.
Many of these programs and coverage mandates have helped people living with hepatitis B get the care and medications they need. There are more drugs in the works.
Keep checking the Drug Watch page and clinical trials page to learn the latest. There may not be a cure yet, but there are effective treatment options. Be brave, protect your health, and go to the lab for your blood test. Demand to be screened for liver cancer. So take charge of your health and ask for a liver cancer screen, which includes a semi-annual blood test and an ultrasound. Hepatitis B-infected Asian men or of Asian descent over age 40 years and Asian women over age 50 years, patients with a family history of liver cancer, patients with cirrhosis, and Africans over the age of 20 should all be screened.
If someone promises a new cure or treatment that sounds too good to be true…. In our search to be rid of hepatitis B, we may be tempted to yield to clever marketing and try a supplement that promises to cure us. When an effective amount of the cannabidiol is administered by intravenous or subcutaneous injection, the compositions can generally be in the form of a pyrogen-free, parenterally acceptable aqueous solution. The preparation of such parenterally acceptable solutions, having due regard to pH, isotonicity, stability, and the like, is within the skill in the art.
A preferred pharmaceutical composition for intravenous, cutaneous, or subcutaneous injection can contain, in addition to the phenolic compound of the present invention, an isotonic vehicle such as Sodium Chloride Injection, Ringer's Injection, Dextrose Injection, Dextrose and Sodium Chloride Injection, Lactated Ringer's Injection, or other vehicle as known in the art.
The treatment composition of the present invention may also contain stabilizers, preservatives, antioxidants, or other additives known to those of skill in the art.
Preliminary studies have shown that exposure to THC or CBD in mice induces apoptosis in thymocytes and peripheral T cells but not in bone marrow hematopoietic progenitors. These properties make the cannabinoids candidates for therapeutic modality against autoimmune diseases such as hepatitis. While THC, due to psychotropic effects, is not suitable for clinical use, CBD, being non-psychoactive, can constitute an excellent choice for clinical use.
However, because THC is psychoactive, it is not an appropriate candidate for clinical use. More recently, studies have focused on cannabidiol CBD which is yet another constituent of the Cannabis plant that is nonpsychoactive and thus has the potential for clinical applications.
The in vitro efficacy of CBD to induce apoptosis in thymocytes was tested. As shown in FIG. It should be noted that thymocytes when cultured in vitro for hr do undergo spontaneous apoptosis partially which was evident from data in vehicle-treated groups. Next, the effect of CBD on apoptosis induction in splenocytes was investigated. As seen from FIG. Concentrations of about 2.
Next it was determined whether administration of CBD into mice would trigger apoptosis and loss of cells. After 24 hr, the thymi and spleens were harvested and the cells were enumerated for viability using trypan blue dye exclusion.
The data shown in FIG. Forty eight hours later, cell proliferation was measured by thymidine incorporation assay. CBD has been shown to have little or no activity against cannabinoid receptor CB1, which is expressed in the central nervous system CNS and to some extent on immune cells, and moderate activity against CB2 that is exclusively expressed in immune cells. It should be noted that in this experiment, the CB1 and CB2 receptor antagonists when used in the absence of CBD, failed to exhibit a significant effect.
Next, the caspase-dependence of CBD-induced apoptosis in thymocytes was investigated, using inhibitors as described. The mediation of apoptosis induction through cannabinoid receptors, CB1 and CB2, was also investigated.
Interestingly, when these experiments using CBD were repeated, the involvement of caspases was noted. However, CB1 antagonist completely failed to block apoptosis while CB2 antagonist blocked it partially. These data demonstrate that THC-induced apoptosis was caspase-dependent involving both the intrinsic and extrinsic pathways of apoptosis. These data also demonstrate that CBD-induced apoptosis was caspase-dependent involving both the intrinsic and extrinsic pathways of apoptosis.
In addition, the possibility that CBD was acting through vanilloid receptors was investigated. Vanilloid receptors are expressed mainly by primary sensory neurons involved in nociception and neurogenic inflammation.
Capsaicin, the pungent compound of red pepper, mediates its effect primarily through vanilloid receptors that can act as voltage-independent channels. Recent studies have shown that Vanilloid receptor 1 VR1 is not only expressed on primary neurons of the CNS but also on immune cells, including thymocytes. Furthermore, VR1 has been shown to be involved in apoptosis. To this end, the thymocytes with THC or CBD as described in the previous figure were cultured in the presence or absence of vanilloid receptor antagonist, capsazepine.
These data demonstrate the exciting possibility that CBD mediates apoptosis in normal T cells through vanilloid receptors. It has been shown that normal and transformed T cells may differ in their sensitivity and signaling pathways of apoptosis.
It has also been shown that CBD can induce apoptosis in a wide range of transformed T cells, including Jurkat cells. However, if the Jurkat cells were pre-exposed to the CB2-selective antagonist, SR, the level of CBD-induced apoptosis was significantly reduced to Similar results were seen using the Wright-Giemsa assay, where it was shown that following exposure to about 5.
In contrast, Jurkat cells pretreated with SR displayed significantly fewer signs of apoptosis following CBD exposure. Treatment with either the CB1 antagonist was unable to prevent cannabidiol-induced apoptosis.
Together, these results demonstrate that cannabidiol-induced apoptosis of Jurkat cells was mediated, at least in part, through CB2. To further investigate the mechanism of cannabidiol-induced apoptosis, the activation pattern of caspases following CBD exposure was examined.
To this end, Jurkat cells were exposed to various concentrations of cannabidiol about 2. More specifically, cleavage of caspase-8, and reduction in procaspase-2, 9, and 10, which are thought to be involved in initiating the caspase cascade were observed. The results showed that the CB2 antagonist was able to significantly prevent CBD-mediated induction of the caspase cascade.
Interestingly, CBD-induced cleavage of Bad was observed in Jurkat cells suggesting possible cross-talk between the intrinsic and extrinsic apoptotic pathways. Together, the studies using transformed T cells suggest that CB2 receptors clearly play a critical role in CBD-mediated apoptosis. Because of its ability to induce a strong immune response, and to trigger autoimmune hepatitis, we used this model to address whether CBD administration in vivo would suppress the immune response against SEB.
Following SEB immunization, there was almost a five-fold increase in lymph node cellularity. Together, these data demonstrate that CBD is very effective at down regulating the robust immune response generated by SEB. Extensive studies have been performed to identify the signaling pathways that trigger apoptosis induced by cannabis plant-derived cannabinoids.
Interestingly, whereas exposure of the Jurkat cells to the cannabinoid antagonists alone had little effect on Raf-1 expression FIG. Also, no changes were observed in levels of total p38 or JNK. Western analysis revealed that cells cultured in the absence of doxycycline displayed minimal expression of a HA-tag and modest basal expression of phospho-MEK FIG.
However, when cells were cultured in the presence of doxycycline, a pronounced increase in expression of the HA tag was noted, along with substantial increases in expression of both phospho-MEK and -ERK.
Analogous to results obtained with the inducible MEK system, in the absence of doxycycline, THC treatment alone resulted in the unequivocal induction of DNA fragmentation. When cells were cultured in the presence of doxycycline, DNA degradation was completely blocked in all treated-conditions. Recently, RSK was demonstrated to promote cell survival through phosphorylation and inactivation of the proapoptotic Bcl-2 family member, Bad.
Bad resides in the cytosol but translocates to the mitochondria following death signaling. Double-immunofluorescence analysis with anti-Bad Abs and mitochondria-specific dye MitoTracker Deep Red showed a strong association of Bad with mitochondria in THC-treated cells, when compared to vehicle-treated cells. Currently, similar studies are being performed to identify the molecular pathways of apoptosis induced by CBD which is acting through VR-1 receptors.
A single injection of concanavalin-A Con A has been shown to induce hepatitis in mice and has been shown to represent human autoimmune hepatitis. ConA can directly induce hepatitis and within h, clinical and histological evidence of hepatitis occurs, with elevation of transaminase activities in the plasma and hepatic lesions characterized by massive leukocyte accumulation and hepatic necrosis. ConA injected mice were administered i.
Next, blood was collected at 6, 12, 24 and 48 h by retro-orbital bleeding. Increased AST levels were seen as early as 6 h after Con A injection, reaching a peak at 12 h and declining thereafter. At 48 h, the plasma AST reached normal levels. Hematoxylin-eosin staining of liver section was conducted 48 h after Con A challenge because of significant liver damage seen at this time point.
Damage to hepatocytes and presence of mixed inflammatory infiltrate consisting of lymphocytes, macrophages, and neutrophils was observed in mice injected with Con A alone.
In summary, these studies demonstrate that:. The foregoing description of the invention and examples along with other modifications and variations to the present invention may be practiced by those of ordinary skill in the art, without departing from the spirit and scope of the present invention. In addition, it should be understood that aspects of the various embodiments may be interchanged both in whole and in part.
Furthermore, those of ordinary skill in the art will appreciate that the foregoing description is by way of example only, and is not intended to limit the invention. Year of fee payment:
CBD Application: Hepatitis C
It won't treat your hep C, but it can help relieve stress and help overcome Living with hepatitis C can often leave you feeling overwhelmed and anxious. not much research has been done to show that CBD helps with hep C or if it's safe. There's no evidence that they can benefit people with hep C. Hepatitis is the best known liver-damaging virus. Cannabis can help with not only treating these conditions, but other common comorbidities. Cannabidiol (CBD) oil has become the hot new product in states that have But experts say the evidence is scant for most of these touted benefits. Only one purported use for cannabidiol, to treat epilepsy, has significant.