Big pharma is not the only answer to treating ailments. There is actually a plant that can be used to treat a wide variety of conditions, and until about 1979 it grew wild across the country. That plant is cannabis, and it can be used to make CBD oil, which can treat anything from anxiety to drug addiction. But how can one compound treat so many different ailments? The answer lies in human physiology.

CBD interacts with the serotonin in the human body, and this one neurotransmitter can control a whole host of bodily processes. It can inhibit fear and anxiety, control stress levels and response, and much more. When your serotonin levels get depleted your body can experience a whole host of different reactions, ranging from anxiety and depression to inflammatory disorders. Over time low serotonin can have a cumulative effect that leads to more and more problems, and CBD can help reverse that trend.

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PMID: 

Anticancer Agents Med Chem. 2019 Jul 4. Epub 2019 Jul 4. PMID: 31272361

Abstract Title: 

Cranberry as a Promising Natural Source of Potential Nutraceuticals with Anticancer Activity.

Abstract: 

Studies have shown that cranberry and its components may exert anticancer properties. The present study aims to critically summarise the existing experimental studies evaluating the potential effects of cranberry on cancer prevention and treatment. PubMed database was searched to identify rele-vant studies. Current in vitro studies have indicated that cranberry and/or its components may act as chemopreventive agents, diminishing the risk for cancer by inhibiting cells oxidation and inflammatory-related processes, while they may also exert chemotherapeutic effects by inhibiting cell proliferation and angiogenesis, inducing cell apoptosis and attenuating the ability of tumour cells to invade and metastasis. Limited in vivo studies have further documented potential anticancer activity. Cranberry could be considered as a conglomeration of potential effective anticancer drug-like compounds.

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PMID: 

Br J Pharmacol. 2019 Jul 19. Epub 2019 Jul 19. PMID: 31322286

Abstract Title: 

Ursolic Acid promotes apoptosis and mediates transcriptional suppression of CT45A2 gene expression in NSCLCs harboring EGFR T790M.

Abstract: 

BACKGROUND AND PURPOSE: In non-small-cell lung carcinoma (NSCLC) patients, the L858R/T790M mutation of the epithelial growth factor receptor (EGFR) is a major cause of acquired resistance to EGFR-TKIs treatment that limits the therapeutic efficacy. Identification of drugs that can preferentially kill the NSCLC harboring L858R/T790M mutation is therefore critical. In the present study, we evaluated the effects of ursolic acid (UA), an active component isolated from herbal medicine, on erlotinib-resistant H1975 cells that harbor the L858R/T790M mutation.EXPERIMENTAL APPROACH: Gene expression omnibus (GEO) profiles analyses was applied to detect differentially expressed genes in NSCLC cells harboring EGFR mutation. AnnexinV-FITC/PI, TUNEL staining, MTT, wound healing, RT-PCR, qRT-PCR, western blots, immunostaining, dual-luciferase reporters and ChIP-PCR were utilized to investigate the pharmacological effects of UA in vitro and in vivo.KEY RESULTS: The cancer/testis antigen family 45 member A2 (CT45A2) was highly expressed in H1975 cells. Ectopic expression of CT45A2 in H1975 cells significantly promotes cell proliferation and motility in vitro. Silencing the CT45A2 expression strongly attenuates H1975 cells motility and growth. The anti-cancer effect of UA is critically dependent on CT45A2 expression in H1975 cells. UA suppressed CT45A2 gene transcription that is mediated by transcriptional factor TCF4 andβ-catenin signaling.CONCLUSIONS AND IMPLICATIONS: CT45A2 is a novel oncogene for NSCLC with an EGFR T790 mutation. Moreover, UA significantly induces apoptosis and inhibits the proliferation of H1975 cells by negatively regulating theβ-catenin/TCF4/CT45A2 signaling pathway. Therefore, UA may be a potential candidate for NSCLC harboring EGFR-L858R/T790M mutation therapy.

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PMID: 

Oncol Lett. 2019 Sep ;18(3):2628-2638. Epub 2019 Jul 4. PMID: 31404298

Abstract Title: 

Ursolic acid suppresses the biological function of osteosarcoma cells.

Abstract: 

Osteosarcoma is a highly malignant tumour that occurs in adolescents. Upregulation or the constitutive activation of epidermal growth factor receptor (EGFR) is a hallmark of osteosarcoma. To investigate the effect of ursolic acid on the biological function of osteosarcoma, MTT assay was used to detect the effect of ursolic acid on the proliferation of HOS and MG63 cells, while flow cytometry was used to analyse the effect on the cell cycle and apoptosis. Transwell and Matrigel assays were used to detect the effect of ursolic acid on cell migration and invasion, respectively. Western blot analysis and reverse transcription-quantitative polymerase chain reaction were used to detect the effects of different concentrations of ursolic acid on EGFR signaling pathway-related proteins, cell cycle, apoptosis and cell migration-related proteins. After overexpression or silencing of EGFR, the effects of ursolic acid on EGFR pathway and cell biological function were subsequently detected, using the same methods. The present study identified that ursolic acid had inhibitory effects on the growth and metastatic ability of osteosarcoma cells by suppressing EGFR.

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PMID: 

Front Physiol. 2019 ;10:956. Epub 2019 Jul 30. PMID: 31417419

Abstract Title: 

Protective Effect of Ursolic Acid on the Intestinal Mucosal Barrier in a Rat Model of Liver Fibrosis.

Abstract: 

Oxidative stress mediated by nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX) plays an important role in intestinal mucosal barrier damage in various disease states. Recent evidence suggests that intestinal mucosal barrier damage and intestinal dysbiosis occur in mice with hepatic fibrosis induced by CCl4 or bile duct ligation. Another study showed that ursolic acid (UA) attenuates experimental colitis via its anti-inflammatory and antioxidant activities. The goal of this study was to investigate the effects of UA on the intestinal mucosal barrier in CCl4-induced hepatic fibrosis in rats and identify its associated mechanisms. Male Sprague-Dawley rats were randomly divided into the following 3 groups (= 10/group): the control, CCl4 model and UA treatment groups. Rats were sacrificed at 72 h after the hepatic fibrosis model was established and assessed for liver fibrosis, intestinal injury, enterocyte apoptosis, bacterial translocation, system inflammation, intestinal oxidative stress, and tight junction protein and NOX protein expression. The results demonstrated that UA attenuated the following: (i) liver and intestinal pathological injury; (ii) cleaved caspase-3 expression in the ileal epithelial cells; (iii) serum lipopolysaccharide and procalcitonin levels; (iv) intestinal malondialdehyde levels; and (v) the expression of the NOX protein components NOX2 and P67phox in ileal tissues. Furthermore, our results suggested that UA improved intestinal dysbiosis and the expression of the tight junction proteins Claudin 1 and Occludin in the ileum of rats. These results indicate that UA has protective effects on the intestinal mucosal barrier in rats with CCl4-induced liver fibrosis by inhibiting intestinal NOX-mediated oxidative stress. Our findings may provide a basis for further clinical studies of UA as a novel and adjuvant treatment to cure liver fibrosis.

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PMID: 

Biomol Ther (Seoul). 2017 Sep 1 ;25(5):535-544. PMID: 28655070

Abstract Title: 

Inhibitory Effect of Carnosol on Phthalic Anhydride-Induced Atopic Dermatitis via Inhibition of STAT3.

Abstract: 

Carnosol is a phenolic antioxidant present in rosemary (). It is known for anti-inflammatory effects, analgesic activity and anti-cancer effects. However, no study has been dedicated yet to its effect on atopic dermatitis (AD). Here, we show that carnosol effectively inhibited LPS-induced nitric oxide (NO) generation and expression of inflammatory marker proteins (iNOS and COX-2) in RAW 264.7 cells. In addition, carnosol effectively inhibits the phosphorylation of STAT3 and DNA binding activity in RAW 264.7 cells. Pull down assay and docking model analysis showed that carnosol directly binds to the DNA binding domain (DBD) of STAT3. We next examined the anti-atopic activity of carnosol (0.05µg/cm) using 5% Phthalic anhydride (PA)-induced AD model in HR1 mice. Carnosol treatment significantly reduced 5% PA-induced AD like skin inflammation in skin tissues compared with control mice. Moreover, carnosol treatment inhibits the expression of iNOS and COX-2 in skin tissue. In addition, the levels of TNF-α, IL-1β, and Immunoglobulin-E in blood serum was significantly decreased in carnosol treated mice compared with those of 5% PA treated group. Furthermore, the activation of STAT3 in skin tissue was decreased in carnosol treated mice compared with control mice. In conclusion, these findings suggest that carnosol exhibited a potential anti-AD activity by inhibiting pro-inflammatory mediators through suppression of STAT3 activation via direct binding to DBD of STAT3.

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PMID: 

Life Sci. 2019 Aug 11 ;233:116748. Epub 2019 Aug 11. PMID: 31412263

Abstract Title: 

Resveratrol prevents chronic intermittent hypoxia-induced cardiac hypertrophy by targeting the PI3K/AKT/mTOR pathway.

Abstract: 

AIMS: Resveratrol is a polyphenolic compound that has received much attention for its use in ameliorating various systemic pathological conditions. The present study was performed to investigate whether the resveratrol alleviated cardiac hypertrophy and functional remodelling by regulating autophagy.MATERIALS AND METHODS: Male rats were exposed to CIH 8 h/day for five weeks and/or intragastric administration of resveratrol daily. The morphological and echocardiography were used to evaluate the cardiac protective effects. The apoptosis was detected by TUNEL staining. The biochemical assessments were used to evaluate oxidative stress. Further, theeffect of resveratrol on autophagy and PI3K/AKT/mTOR pathway was investigated.KEY FINDINGS: The CIH group exhibited increased heart weight/body weight and left ventricle weight/body weight ratios, which was accompanied by left ventricular remodelling. Echocardiography analysis showed that CIH-treated rats had significantly higher left ventricular posterior wall thickness, ejection fraction and fractional shortening than those of controls. In addition, the apoptosis index and oxidative markers were significantly elevated in the CIH group versus the control. The autophagy marker Beclin-1 was elevated, while p62 was decreased by CIH treatment. Resveratrol treatment significantly improved cardiac function and alleviated cardiac hypertrophy, oxidative stress, and apoptosis in CIH rats. Further results indicated that PI3K/AKT pathway-mediated inhibition of the mammalian target of rapamycin (mTOR) pathway played a role in the activation of autophagy by resveratrol after CIH stimulation.SIGNIFICANCE: In conclusion, resveratrol supplementation during CIH upregulates autophagy by targeting the PI3K/AKT/mTOR pathway, which appears to be beneficial for resisting cardiac hypertrophy.

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Brain regeneration: long considered a feat impossible to accomplish, compelling research now reveals how a simple spice might contribute to stimulating the stem-cell mediated repair of the damaged brain.

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PMID: 

Phytother Res. 2019 Jul 25. Epub 2019 Jul 25. PMID: 31342604

Abstract Title: 

β-Elemene inhibits peritoneal metastasis of gastric cancer cells by modulating FAK/Claudin-1 signaling.

Abstract: 

Peritoneal metastasis is common in advanced gastric cancer patients and is typically associated with a worse prognosis.β-Elemene is a natural compound that can be isolated from the Curcuma wenyujin plant and has been widely used in China to treat a variety of cancers. However, the anti-metastatic impacts of β-elemene on gastric cancer remain unknown. In our study, we found that β-elemene significantly inhibited the migration and invasive capacity of gastric cells in vitro and inhibited the capacity of gastric cancer cells to peritoneally diffuse and metastasize in vivo. Mechanistically, we demonstrated that the anti-metastatic effects of β-elemene were exerted by downregulating the expression of Claudin-1.Furthermore, β-elemene was found to inhibit the metastatic capacity of cells by downregulating FAK phosphorylation, which regulated Claudin-1. Overall, our result revealed that β-elemene inhibited peritoneal metastases from gastric cancer by modulating the FAK/Claudin-1 pathway.

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PMID: 

J Cell Mol Med. 2019 Jul 25. Epub 2019 Jul 25. PMID: 31343107

Abstract Title: 

Beta-elemene inhibits breast cancer metastasis through blocking pyruvate kinase M2 dimerization and nuclear translocation.

Abstract: 

Pyruvate kinase M2 (PKM2), playing a central role in regulating aerobic glycolysis, was considered as a promising target for cancer therapy. However, its role in cancer metastasis is rarely known. Here, we found a tight relationship between PKM2 and breast cancer metastasis, demonstrated by the findings that beta-elemene (β-elemene), an approved drug for complementary cancer therapy, exerted distinct anti-metastatic activity dependent on PKM2. The results indicated that β-elemene inhibited breast cancer cell migration, invasion in vitro as well as metastases in vivo. β-Elemene further inhibited the process of aerobic glycolysis and decreased the utilization of glucose and the production of pyruvate and lactate through suppressing pyruvate kinase activity by modulating the transformation of dimeric and tetrameric forms of PKM2. Further analysis revealed that β-elemene suppressed aerobic glycolysis by blocking PKM2 nuclear translocation and the expression of EGFR, GLUT1 and LDHA by influencing the expression of importin α5. Furthermore, the effect of β-elemene on migration, invasion, PKM2 transformation, and nuclear translocation could be reversed in part by fructose-1,6-bisphosphate (FBP) and L-cysteine. Taken together, tetrameric transformation and nuclear translocation of PKM2 are essential for cancer metastasis, and β-elemene inhibited breast cancer metastasis via blocking aerobic glycolysis mediated by dimeric PKM2 transformation and nuclear translocation, being a promising anti-metastaticagent from natural compounds.

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