PMID: 

J Cell Physiol. 2019 Aug ;234(10):17144-17158. Epub 2019 Mar 27. PMID: 30916403

Abstract Title: 

Impact of chrysin on the molecular mechanisms underlying diabetic complications.

Abstract: 

Diabetes mellitus is a chronic metabolic disorder, resulting in high morbidity and mortality worldwide. Neuropathy, ocular diseases, kidney diseases, and cardiovascular disease are common complications of diabetes that threats the patient's life. Chrysin (CH), a natural flavonoid, has several pharmacological effects, including antioxidant, antiapoptotic, anti-inflammatory, and anticancer. Strong scientific documents indicated that chrysin may be effective for preventing and treating complications of diabetes in experimental models. The present study was designed to review the association between chrysin administration and diabetes complications by focusing on the possible molecular pathway. The findings indicate that chrysin has protective effects against diabetes outcomes by modulating oxidative stress, inflammation, and apoptosis in animal models. However, more clinical trial study should be done to clear the protective effects of chrysin in diabetic patients.

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PMID: 

Life Sci. 2019 Jun 1 ;226:202-209. Epub 2019 Apr 13. PMID: 30991061

Abstract Title: 

Chrysin prevents cognitive and hippocampal long-term potentiation deficits and inflammation in rat with cerebral hypoperfusion and reperfusion injury.

Abstract: 

INTRODUCTION: Ischemic stroke is one of the leading causes of death worldwide, and extensive efforts have focused on the neuroprotective strategies to minimize complications due to ischemia. This study aimed to examine neuroprotective potential of chrysin, as a natural potent antioxidative and anti-inflammatory agent in an animal model of bilateral common carotid artery occlusion and reperfusion (BCCAO/R).METHODS: Adult male Wistar rats (250-300 g) were randomly divided into 6 groups and submitted to either sham surgery or BCCAO/R after pretreatment with chrysin (10, 30 and 100 mg/kg, once daily, for 21 consecutive days) or saline containing %5 DMSO. To make the animal model of BCCAO/R, bilateral common carotid arteries were occluded for 20 min, followed by reperfusion. Subsequently, spatial cognitive performance was evaluated in a Morris water maze (MWM), hippocampal long-term potentiation (LTP) was recorded from hippocampal dentate gyrus region, after then the hippocampal tissue content of IL-1β and TNF-α were assayed usingELISA kits.RESULTS: The results showed that pretreatment with chrysin significantly prevented BCCAO/R-induced cognitive and hippocampal LTP impairments (p 

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PMID: 

Dement Geriatr Cogn Disord. 2014 ;37(3-4):246-56. Epub 2013 Nov 15. PMID: 24247062

Abstract Title: 

Serum lycopene, lutein and zeaxanthin, and the risk of Alzheimer's disease mortality in older adults.

Abstract: 

BACKGROUND: Oxidative stress is implicated in the pathogenesis of Alzheimer's disease (AD). Accumulating evidence shows that antioxidant-rich food reduces the risk of AD by inhibiting oxidative stress. This study investigates whether serum levels of carotenoids were associated with the risk of AD mortality in a nationally representative sample of US adults.METHODS: We used data from the Third Nutrition and Health Examination Survey (NHANES III) database and the NHANES III Linked Mortality File. A total of 6,958 participants aged older than 50 years were included in this study.RESULTS: We found that high serum levels of lycopene and lutein+zeaxanthin at baseline were associated with a lower risk of AD mortality after adjustment for potential covariates. The reduction in the mortality risk was progressively raised by increasing serum lycopene (HR = 0.26, 95% CI 0.10-0.69) and lutein+zeaxanthin (HR = 0.43, 95% CI 0.22-0.85) levels. In contrast, no associations with AD mortality were observed for other serum carotenoids, including alpha-carotene, beta-carotene, and beta-cryptoxanthin.CONCLUSION: High serum levels of lycopene and lutein+zeaxanthin are associated with a lower risk of AD mortality in adults. Our findings suggest that a high intake of lycopene- or lutein+zeaxanthin-rich food may be important for reducing the AD mortality risk.

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PMID: 

Cell Physiol Biochem. 2019 ;52(5):1236-1250. PMID: 31001962

Abstract Title: 

Chrysin Inhibits Proinflammatory Factor-Induced EMT Phenotype and Cancer Stem Cell-Like Features in HeLa Cells by Blocking the NF-κB/Twist Axis.

Abstract: 

BACKGROUND/AIMS: TNF-α and TGF-β associated epithelial-mesenchymal transition (EMT) occurs via NF-κB-dependent transcriptional upregulation of Twist1.Chrysin (ChR) is a major active ingredient ofpropolis, which inhibits various cancer cells and possesses anti-inflammatory activities. This study aimed to assess whether and how ChR inhibits proinflammatory cytokine-induced EMT phenotype and cancer stem-like cell (CSLC) features in the HeLa cell line.METHODS: HeLa cells were co-administered TNF-α (10.0 ng/mL) and TGF-β (5.0 ng/mL) for 24h following TGF-β (5.0 ng/mL) alone for 6 d in the presence or absence of ChR (5.0, 10.0 and 20.0μM). Then, the levels of EMT-related factors, multi-potential transcription factors, and stem cell markers were analyzed by immunoblot. Wound healing and tumor sphere formation assays were performed to assess the migration and self-renewal capabilities of cells, respectively. Overexpression and/or knockdown of NF-κBp65 and/or Twsit1 were used to explore the molecular mechanisms.RESULTS: The results showed that ChR inhibited EMT and CSLC properties in HeLa cells administered TNF-α after prolonged TGF-β treatment, in a concentration-dependent fashion. NF-κBp65 knockdown and ChR(10.0μM) cooperatively enhanced the inhibition of NF-κBp65 and Twist1 expression, EMT, and CSLC properties. Conversely, overexpression of NF-κBp65 combined with ChR(10.0μM) antagonized such activities. Meanwhile, Twist1silencing or overexpression combined with ChR treatment did not affect NF-κBp65 levels, but also reduced or enhanced EMT and CSLC properties. Importantly, overexpressing Twist1 combined with ChR reversed the effects of NF-κBp65 knockdown and ChR.CONCLUSION: ChR inhibits proinflammatory cytokine-induced EMT and CSLC features in HeLa cells by blocking the NF-κB/Twist axis.

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Research has found CBD may help ease symptoms of GI disorders. As doctors have recently discovered the importance of gut health to your overall health, many patients have turned to CBD to control symptoms of GI illnesses like IBS, Chron’s Disease, Ulcerative Colitis, and Gastritis.

CBD’s natural anti-inflammatory properties have been proven to help with the often debilitating symptoms of GI conditions. These conditions cause some inflammation to a part of the digestive system. For example, Chron’s disease causes inflammation in the digestive tract, and gastritis is the inflammation of the stomach lining.

CBD supplements help the body’s endocannabinoid system(ECS) with healing responses and functions like sleep, anxiety, and immune response. For those with GI health issues, CBD reacts with the endocannabinoid receptors and helps ease symptoms. Some researchers believe the (ECS) connects to the brain that allows the gut and brain to “speak” to one another.” 

The ECS plays a major role in gut health by helping with key functions.

• Modulates inflammation

Both CB1 and CB2 receptors help modulate inflammatory responses in the gut when stimulated by certain cannabinoids like CBD.

• Regulates digestive action

Gut motility is the contraction of muscles in the gastrointestinal tract. This contracting movement enables food to move through the digestive tract and ensures that nutrients are absorbed. Several cannabinoids stimulate the CB1 receptor. This calms nausea, slows emptying of the stomach, and reduces stomach acid.

• Regulates communication with your brain

Changes in the brain related to stress or pain can alter gastrointestinal function. In addition, changes in your gut from inflammation or infection are communicated back to the brain via the ECS. This is important in maintaining bowel health and can even influence conditions like irritable bowel syndrome.

Along with helping ease pain associated with common GI conditions, CBD may also help with additional symptoms like promoting appetite and relieving nausea.

PMID: 

Life Sci. 2019 Jul 1 ;228:285-294. Epub 2019 May 4. PMID: 31063733

Abstract Title: 

Therapeutic effects of chrysin in a rat model of traumatic brain injury: A behavioral, biochemical, and histological study.

Abstract: 

AIMS: Oxidative stress and apoptosis have major roles in the progression of traumatic brain injury (TBI)-associated motor and cognitive deficits. The present study was aimed to elucidate the putative effects of chrysin, a natural flavonoid compound, against TBI-induced motor and cognitive dysfunctions and possible involved mechanisms.MAIN METHODS: Chrysin (25, 50 or 100 mg/kg) was orally administered to rats starting immediately following TBI induction by Marmarou's weight-drop technique and continuously for 3 or 14 days. Neurological functions, motor coordination, learning and memory performances, histological changes, cell apoptosis, expression of pro- and anti-apoptotic proteins, and oxidative status were assayed at scheduled time points after experimental TBI.KEY FINDINGS: The results indicated that treatment with chrysin improved learning and memory disabilities in passive avoidance task, and ameliorated motor coordination impairment in rotarod test after TBI. These beneficial effects were accompanied by increased the concentrations of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione (GSH), decreased malondialdehyde (MDA) content, prevented neuronal loss, diminished apoptotic index, elevated the expression of anti-apoptotic Bcl-2 protein, and reduced the expression of pro-apoptotic Bax protein in the cerebral cortex and hippocampus tissues.SIGNIFICANCE: Our findings suggest that both anti-oxidative and anti-apoptotic properties of chrysin (especially in the dose of 100 mg/kg) are possible mechanisms that improve cognitive/motor deficits and prevent neuronal cell death after TBI.

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PMID: 

Neurosci Lett. 2019 07 27 ;706:158-163. Epub 2019 May 20. PMID: 31121284

Abstract Title: 

Chrysin protects against behavioral, cognitive and neurochemical alterations in a 6-hydroxydopamine model of Parkinson's disease.

Abstract: 

Parkinson's disease (PD) is an age-related neurodegenerative disorder that severely affects quality of life of patients and their families. The flavonoid chrysin (5,7-dihydroxylflavone) is a naturally occurring flavone with several pharmacological activities, including anti-inflammatory and anti-oxidative. We investigated the effects of a 28-day chrysin treatment (10 mg/kg/day, i.g.) on a model of PD induced by 6-OHDA in aged (20-month old) mice. We found a protective effect of chrysin on behavioral and cognitive alterations (rotational behavior, passive avoidance and Barnes maze tests), nitric oxide synthesis (NOx), lipid peroxidation (HNE), glutathione levels (GSH), reactive species levels (RS), neuroinflammation (interleukin-1 beta – IL-1β and tumor necrosis factor alpha – TNF-α), Na, K-ATPase and nicotinamide adenine dinucleotide phosphate oxidase activity (NADPH oxidase) activities. In addition, chrysin protected against changes in striatal dopamine (DA), 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) levels. In conclusion, chrysin improved several behavioral, cognitive and neurochemical parameters in a relevant preclinical model of PD in aged mice.

PMID: 

Cancer Manag Res. 2019 ;11:2977-2985. Epub 2019 Apr 10. PMID: 31114345

Abstract Title: 

Chrysin inhibits sphere formation in SMMC-7721 cells via modulation of SHP-1/STAT3 signaling pathway.

Abstract: 

Chrysin is a natural flavonoid which has been identified as a candidate anti-cancer agent due to its inhibitory effect on a variety of cancer cells, including targeted inhibition of sphere formation in hepatocellular carcinoma (HCC) cell lines. However, the mechanism by which chrysin modulates HCC spheres remains unclear.In this study, we investigate the effect of chrysin on the regulation of SHP-1 and its downstream signal molecule STAT3 to explain the mechanism by which chrysin inhibits sphere formation of HCC cell lines.Here, we found that SHP-1 protein expression was markedly down-regulated in the spheres from both SMMC-7721 and MHCC97H cells. Chrysin significantly inhibited sphere formation and upregulated the expression of SHP-1 protein in both SMMC-7721 and MHCC97H cells, as well as reduced p-STAT3 and Twist1 expressions in SMMC-7721 cells. Furthermore, knockdown of SHP-1 in SMMC-7721 cells resulted in the induction of p-STAT3 and Twist1 protein expression and antagonizing the inhibitory effect of chrysin on sphere formation in SMMC-7721 cells.Overall, the study findings demonstrated that chrysin acts as a candidate for the treatment of HCC through modulating SHP-1/STAT3 signaling pathway.

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PMID: 

Chest. 2020 Feb ;157(2):e21-e23. PMID: 32033656

Abstract Title: 

Vitamin C Deficiency-Induced Pulmonary Arterial Hypertension.

Abstract: 

We report a case of a man in his 60s who developed pulmonary arterial hypertension (PAH) in association with profound vitamin C deficiency. Decreased availability of endothelial nitric oxide and activation of the hypoxia-inducible family of transcription factors, both consequences of vitamin C deficiency, are believed to be mechanisms contributing to the pathogenesis of the pulmonary hypertension. The PAH resolved following vitamin C supplementation. The current case highlights the importance of testing for vitamin C deficiency in patients with PAH in the proper clinical setting.

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PMID: 

Food Chem Toxicol. 2018 Nov ;121:131-139. Epub 2018 Aug 24. PMID: 30149109

Abstract Title: 

Protective effects of p-coumaric acid against acetaminophen-induced hepatotoxicity in mice.

Abstract: 

Acetaminophen (N-acetyl-p-aminophenol, AAP) is an effective analgesic and antipyretic drug with minimal toxicity when used at therapeutic doses. However, AAP overdose is the most common cause of drug-induced acute liver failure and one of the main causes of morbidity and mortality. p-Coumaric acid (PCA) is the most abundant isomer of hydroxycinnamic acid in nature, and it can be widely found in fruits, vegetables, and plants products. PCA has strong antioxidant activity and exhibits protective effects in numerous disease models associated with reactive oxygen species (ROS) generation. In this study, we investigated the protective effects of PCA on AAP-induced hepatotoxicity and the underlying mechanisms using an in vivo model. We found that PCA ameliorates AAP-induced hepatotoxicity as well as the reduced serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activity. Furthermore, we observed that PCA suppressed hepatic apoptosis via ROS-mediated DNA damage responses and inflammation by modulating the mitogen-activated protein kinase (MAPK) signaling axis in an ROS-dependent manner. These findings indicate that the administration of PCA protects against AAP-induced hepatotoxicity, suggesting it could be a novel therapeutic strategy for AAP-induced liver injury.

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