The effects of delta-9-THC. One study in mice and rats suggested that cannabinoids may have a protective effect against the development of certain types of tumors.3 During this 2-year study, groups of mice and rats were given various doses of THC by gavage. A dose-related decrease in the incidence of hepatic adenoma tumors and hepatocellular carcinoma (HCC) was observed in the mice.

Decreased incidences of benign tumors (polyps and adenomas) in other organs (mammary gland, uterus, pituitary, testis, and pancreas) were also noted in the rats.

In another study, delta-9-THC, delta-8-THC, and cannabinol were found to inhibit the growth of Lewis lung adenocarcinoma cells in vitro and in vivo.4 In addition, other tumors have been shown to be sensitive to cannabinoid-induced growth inhibition.

The effects of delta-9-THC in mice and rats

Cannabinoids may cause antitumor effects by various mechanisms, including induction of cell death, inhibition of cell growth, and inhibition of tumor angiogenesis invasion and metastasis.9–12 Two reviews summarize the molecular mechanisms of action of cannabinoids as antitumor agents. Cannabinoids appear to kill tumor cells but do not affect their nontransformed counterparts and may even protect them from cell death.

For example, these compounds have been shown to induce apoptosis in glioma cells in culture and induce regression of glioma tumors in mice and rats, while they protect normal glial cells of astroglial and oligodendroglial lineages from apoptosis mediated by the CB1 receptor.

The effects of delta-9-THC and a synthetic agonist of the CB2 receptor were investigated in HCC.15 Both agents reduced the viability of HCC cells in vitro and demonstrated antitumor effects in HCC subcutaneous xenografts in nude mice. The investigations documented that the anti-HCC effects are mediated by way of the CB2 receptor. Similar to findings in glioma cells, the cannabinoids were shown to trigger cell death through stimulation of an endoplasmic reticulum stress pathway that activates autophagy and promotes apoptosis.

Other investigations have confirmed that CB1 and CB2 receptors may be potential targets in non-small cell lung carcinoma16 and breast cancer.

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An in vitro study of the effect of CBD on programmed cell death in breast cancer cell lines found that CBD induced programmed cell death, independent of the CB1, CB2, or vanilloid receptors. CBD inhibited the survival of both estrogen receptor-positive and estrogen receptor-negative breast cancer cell lines, inducing apoptosis in a concentration-dependent manner while having little effect on nontumorigenic mammary cells.18 Other studies have also shown the antitumor effect of cannabinoids (i.e., CBD and THC) in preclinical models of breast cancer.

CBD has also been demonstrated to exert a chemopreventive effect in a mouse model of colon cancer. In this experimental system, azoxymethane increased premalignant and malignant lesions in the mouse colon. Animals treated with azoxymethane and CBD concurrently were protected from developing premalignant and malignant lesions. In in vitro experiments involving colorectal cancer cell lines, the investigators found that CBD protected DNA from oxidative damage, increased endocannabinoid levels, and reduced cell proliferation.

In a subsequent study, the investigators found that the antiproliferative effect of CBD was counteracted by selective CB1 but not CB2 receptor antagonists, suggesting an involvement of CB1 receptors.

Another investigation into the antitumor effects of CBD examined the role of intercellular adhesion molecule-1 (ICAM-1). CAM-1 expression has been reported to be negatively correlated with cancer metastasis. In lung cancer cell lines, CBD upregulated ICAM-1, leading to decreased cancer cell invasiveness.

In an in vivo model using severe combined immunodeficient mice, subcutaneous tumors were generated by inoculating the animals with cells from human non-small cell lung carcinoma cell lines.23 Tumor growth was inhibited by 60% in THC-treated mice compared with vehicle-treated control mice. Tumor specimens revealed that THC had antiangiogenic and antiproliferative effects. However, research with immunocompetent murine tumor models has demonstrated immunosuppression and enhanced tumor growth in mice treated with THC.

When choosing a cannabis product, you should choose one that is made specifically for pets. Dogs and cats have a lower tolerance for THC and may be more sensitive to miniscule amounts a human would not notice.

Several companies now offer cannabis products for pets. As these are marketed as supplements, not drugs, there’s not as much oversight as might otherwise be desirable. Buyers should be cautious of upstart companies.

The pioneer is the field is a Seattle company, Canna-Pet. They claim to be (and that claim appears to be true) the only provider with a multi-year product track record, established research connections with major veterinary universities, third-party published data on their products, and acceptance by major pet insurers like Trupanion and Petplan (with proper riders for herbal therapy).

They remain the only company to have achieved formal registration for their cannabinoid pet products with the United States Patent and Trademark Office (USPTO).

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The company assures that its products meet the recommendations for manufacture outlined, using industrial hemp, full-spectrum CO2 extraction, high-performance liquid chromatography (HPLC) testing, phytochemical diversity, and oral-mucosal delivery for best bioavailability. The products contain over two dozen cannabinoids, terpenes, and flavonoids, including CBD, ß-caryophyllene, CBC, CBG, limonene, α-pinene, and linalool. All production occurs in the United States.