PMID: 

Prog Mol Biol Transl Sci. 2019 ;167:25-75. Epub 2019 Aug 28. PMID: 31601406

Abstract Title: 

Effects of cannabidiol (CBD) in neuropsychiatric disorders: A review of pre-clinical and clinical findings.

Abstract: 

Cannabis sativa (cannabis) is one of the oldest plants cultivated by men. Cannabidiol (CBD) is the major non-psychomimetic compound derived from cannabis. It has been proposed to have a therapeutic potential over a wide range of neuropsychiatric disorders. In this narrative review, we have summarized a selected number of pre-clinical and clinical studies, examining the effects of CBD in neuropsychiatric disorders. In some pre-clinical studies, CBD was demonstrated to potentially exhibit anti-epileptic, anti-oxidant, anti-inflammatory anti-psychotic, anxiolytic and anti-depressant properties. Moreover, CBD was shown to reduce addictive effects of some drugs of abuse. In clinical studies, CBD was shown to be safe, well-tolerated and efficacious in mitigating the symptoms associated with several types of seizure disorders and childhood epilepsies. Given that treatment with CBD alone was insufficient at managing choreic movements in patients with Huntington's disease, other cannabis-derived treatments are currently being investigated. Patients with Parkinson's disease (PD) have reported improvements in sleep and better quality of life with CBD; however, to fully elucidate the therapeutic potential of CBD on the symptoms of PD-associated movement disorders, larger scale, randomized, placebo-controlled studies still need to be conducted in the future. Currently, there are no human studies that investigated the effects of CBD in either Alzheimer's disease or unipolar depression, warranting further investigation in this area, considering that CBD was shown to have effects in pre-clinical studies. Although, anxiolytic properties of CBD were reported in the Social Anxiety Disorder, antipsychotic effects in schizophrenia and anti-addictive qualities in alcohol and drug addictions, here too, larger, randomized, placebo-controlled trials are needed to evaluate the therapeutic potential of CBD.

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PMID: 

Pharmacol Rep. 2019 May 7 ;71(5):855-861. Epub 2019 May 7. PMID: 31408784

Abstract Title: 

Puerarin protects pulmonary arteries from hypoxic injury through the BMPRII and PPARγ signaling pathways in endothelial cells.

Abstract: 

BACKGROUND: Recent evidence indicates that Puerarin has a protective effect on pulmonary arteries. In the present study, we aimed to investigate whether Puerarin could protect pulmonary arterial endothelial cells from hypoxic injury and determine its potential targets.METHODS: In our study, human pulmonary arterial endothelial cells (HPAECs) were injured by hypoxic (1% O) incubation. Cell viability was detected by a cell counting kit (CCK8). The production of nitric oxide (NO) was detected by Griess reagent and endothelin-1 (ET-1) was detected by the ELISA method. Oxidative stress was measured by a fluorescence microscope via the fluorescent probe DCFH-DA. Western blotting was employed for studying the mechanism.RESULTS: The results show that Puerarin protects HPAECs from hypoxia-induced apoptosis and slightly improves cell viability. Puerarin increases NO and decreases ET-1 to prevent the imbalance between vasoactive substances induced by hypoxia in HPAECs. Puerarin also inhibits the oxidative stress induced by hypoxia. The results from the Western blot show that Puerarin activates the BMPRII/Smad and PPARγ/PI3K/Akt signaling pathways.CONCLUSION: In conclusion, Puerarin protects HPAECs from hypoxic injury through the inhibition of oxidative stress and the activation of the BMPRII and PPARγ signaling pathways. This work provides insight into the development of Puerarin as a treatment for hypoxic pulmonary hypertension.

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PMID: 

Int J Biol Sci. 2019 ;15(10):2211-2223. Epub 2019 Aug 19. PMID: 31592236

Abstract Title: 

Tanshinone IIA attenuates demyelination and promotes remyelination in-infected BALB/c mice.

Abstract: 

BACKGROUND: infection can cause demyelination in the central nervous system, and there is no effective treatment.METHODS: We used dexamethasone, Tanshinone IIA (TSIIA) and Cryptotanshinone(Two traditional Chinese medicine monomers) in combination with albendazole (AB, a standard anti-helminthic compound) to observe their therapeutic effect on demyelination in-infected mice. Luxol fast blue staining and electron microscope of myelin sheath, Oligodendrocyte (OL) number and myelin basic protein (MBP) expression in brain was detected in above groups.RESULTS: TSIIA+AB facilitated OL proliferation and significantly increased both myelin sheath thickness and the population of small-diameter axons. In addition, TSIIA treatment inhibited the expression of inflammation-related factors (interleukin [IL]-6, IL-1β, tumor necrosis factor [TNF]-α, inducible nitric oxide synthase [iNOS]) rather than inhibiting eosinophil infiltration in brain. TSIIA also decreased microglial activation and shifted their phenotype from M1 to M2.CONCLUSIONS: Taken together, these results provide evidence that TSIIA combined with AB may be an effective treatment for demyelination caused byinfection and other demyelinating diseases.

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PMID: 

Exp Ther Med. 2019 Nov ;18(5):3347-3356. Epub 2019 Sep 6. PMID: 31602208

Abstract Title: 

Puerarin inhibits apoptosis and inflammation in myocardial cells via PPARα expression in rats with chronic heart failure.

Abstract: 

Chronic heart failure affects myocardial energy metabolism and cardiac function. Puerarin has been reported to improve cardiac function through regulation of energy metabolism in mice with myocardial infarction. The aim of the current study was to determine whether puerarin can improve body weight and reduce inflammation and apoptosis in rats with chronic heart failure. Rats were divided into three groups: Puerarin, PBS and sham group. Transverse aortic constriction was performed to induce chronic heart failure in the puerarin an PBS groups. Cardiac function, apoptosis and inflammation were evaluated following a 4-week treatment in rats with chronic heart failure. The results demonstrated that puerarin significantly increased the survival rate of rats and improved cardiac function compared with the PBS group. In addition, puerarin decreased lactate dehydrogenase and succinate dehydrogenase activity compared with the PBS group. Puerarin treatment increased the expression levels of glucose transporter type 4 and decreased the expression levels of CD36. Additionally, puerarin decreased the levels inflammatory factors, including tumor necrosis factorα, interleukin (IL)-1β and IL-6 in serum and myocardial tissue compared with the PBS group. Puerarin upregulated peroxisome proliferator-activated receptor α (PPARα) and its downstream target genes nuclear respiratory factor 1, FOS proto-oncogene, YY1 transcription factor, acetyl-coenzyme A carboxylase a, Fas cell surface death receptor, L-type pyruvate kinase and acetyl-coenzyme A dehydrogenase medium chain in myocardial cells from rats with chronic heart failure. These results demonstrated that puerarin inhibited apoptosis and inflammation in myocardial cells via the PPARα pathway. In conclusion, the present study indicated that puerarin may exhibit antiapoptotic and anti-inflammatory activity through the PPARα pathway in rats with chronic heart failure.

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PMID: 

Int J Biol Macromol. 2019 Aug 21 ;140:1006-1017. Epub 2019 Aug 21. PMID: 31445146

Abstract Title: 

COX-2/iNOS regulation during experimental hepatic injury and its mitigation by cloudy apple juice.

Abstract: 

A number of enzymes and transcription factors have been correlated with disease etiology. In this study, involvement of cyclooxygenase-2 and inducible-nitric oxide synthase is examined during diethylnitrosamine (DEN)-induced hepatic injury and cloudy apple juice (CAJ) supplementation. Liver injury was administered in rats by single dose of DEN (10 ml/kg bwt of 1% DEN), while 10 ml/kg bwt CAJ daily was given after 2 h of latency in DEN-treated animals for two weeks. CAJ was characterized by HPLC and subsequently examined for antioxidant power. During the course of treatment liver function, collagen (hydroxyproline), malondialdehyde, protein oxidation, antioxidant enzymes, ATPases, nitrite levels were investigated along with liver histopathology and electron microscopy. COX-2 and iNOS proteins were also localized in liver specimens. The results demonstrated rich polyphenols and antioxidant activity in CAJ. CAJ supplementation significantly restored liver biochemistry and anatomy as revealed by the refurbished investigated parameters. CAJ treatment also declined COX-2 and iNOS activities in injured animals. Electron microscopy demonstrated rejuvenated hepatocytes, Kupffer cells, RER, mitochondria and nucleus in CAJ supplemented animals. The novel outcomes of this study suggest that CAJ potentiates hepatoprotection by stimulating antioxidant power and regulating the COX-2 and iNOS proteins in the liver during experimental liver injury.

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PMID: 

Front Immunol. 2019 ;10:1895. Epub 2019 Aug 7. PMID: 31440258

Abstract Title: 

Procyanidin B2 Activates PPARγ to Induce M2 Polarization in Mouse Macrophages.

Abstract: 

Procyanidins, a subclass of flavonoids found in commonly consumed foods, possess potential anti-inflammatory activity. Manipulation of M1/M2 macrophage homeostasis is an effective strategy for the treatment of metabolic inflammatory diseases. The objective of this study was to determine the effect of procyanidins on macrophage polarization. Procyanidin B2 (PCB2), the most widely distributed natural procyanidins, enhanced the expressions of M2 macrophage markers (Arg1, Ym1, and Fizz1). PCB2 activated peroxisome proliferator-activated receptorγ (PPARγ) activity and increased the expressions of PPARγ target genes (CD36 and ABCG1) in macrophages. Inhibition of PPARγ using siRNA or antagonist GW9662 attenuated the PCB2-induced expressions of M2 macrophage markers. In addition, we identified cognate PPAR-responsive elements (PPREs) within the 5'-flanking regions of the mouse Arg1, Ym1, and Fizz1 genes. Furthermore, macrophages isolated from db/db diabetic mice showed lower expressions of M2 markers. PCB2 effectively restored the Arg1, Ym1, and Fizz1 expressions in a PPARγ-dependent manner. These findings support the notion that PCB2 regulated macrophage M2 polarizationthe activation of PPARγ. Our results provide a new mechanism by which procyanidins exert their beneficial anti-inflammatory effects.

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PMID: 

Cell Biol Int. 2019 Sep 9. Epub 2019 Sep 9. PMID: 31498521

Abstract Title: 

The protective effects of grape seed procyanidin B2 against asporin mediates glycated low-density lipoprotein induced-cardiomyocyte apoptosis and fibrosis.

Abstract: 

The progression of diabetic cardiomyopathy is related to cardiomyocyte dysfunction and apoptosis. Our previous studies showed that asporin (ASPN) was significantly increased in the myocardium of db/db mice through proteomics, and grape seed procyanidin B2 (GSPB2) significantly inhibited the expression of ASPN in the heart of db/db mice. We report here that ASPN played a critical role in glycated low-density lipoproteins (gly-LDL) induced-cardiomyocyte apoptosis. We found that gly-LDL upregulated ASPN expression. ASPN increased H9C2 cardiomyocyte apoptosis with down-regulation of Bcl-2, upregulation of transforming growth factor-β1, Bax,collagen III, fibronectin, and phosphorylation of smad2 and smad3. However, GSPB2 treatment reversed ASPN-induced impairments in H9C2 cardiomyocytes. These results provide evidence for the cardioprotective action of GSPB2 against ASPN injury, and thus suggest a new target for fighting against diabetic cardiomyopathy.

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PMID: 

J Interferon Cytokine Res. 2019 Oct 11. Epub 2019 Oct 11. PMID: 31603717

Abstract Title: 

Procyanidin B2 Suppresses Lipopolysaccharides-Induced Inflammation and Apoptosis in Human Type II Alveolar Epithelial Cells and Lung Fibroblasts.

Abstract: 

Acute lung injury (ALI) is characterized by acute lung inflammation and apoptosis of alveolar epithelial cells (AECs) with a high morbidity and mortality. Procyanidin B2 (PCB2) is a naturally occurring flavonoid with anti-inflammatory activity. Our previous study demonstrated that PCB2 inhibited NLRP3 inflammasome signaling and ameliorated paraquat-induced ALI in rat, indicating the protective role of PCB2. As lipopolysaccharide (LPS) induced acute cell injury and dysfunction, we continued to evaluate the protective effects of PCB2 using LPS-treated human AECs and lung fibroblasts (LFs) model. We tested the effects of PCB2 on cell permeability, viability, apoptosis, nuclear factor-kappaB (NF-κB) activation, NLRP3 inflammasome activation, and proinflammatory cytokines production in LPS-treated human AECs and LFs. PCB2 prevented LPS-induced cell apoptosis, and increased the cell viability in LPS-treated human AECs and LFs. PCB2 inhibited LPS-induced Bax and active caspase-3 expression, and promoted Bcl-2 expression. PCB2 prevented LPS-induced tumor necrosis factor-α, interleukin-1β expression, NF-κB activation, and NLRP3 inflammasome activation. PCB2 suppressed LPS-induced inflammation and apoptosis in human AECs and LFs by inhibiting NF-κB and NLRP3 inflammasome.

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PMID: 

Int J Yoga Therap. 2019 May 30. Epub 2019 May 30. PMID: 31145028

Abstract Title: 

A 5-Week Seminar on the Biopsychosocial-Spiritual Model of Self-Care Improves Anxiety, Self-Compassion, Mindfulness, Depression, and Stress in Graduate Healthcare Students.

Abstract: 

Graduate healthcare students can experience stress that affects their ability to perform academically and clinically, decreases empathy, and affects their well-being and clinical competence. The purpose of the current study was to determine the effects of a seminar on a yoga-inspired biopsychosocial-spiritual model of self-care on perceived levels of anxiety, self-compassion, mindfulness, depression, and stress in graduate healthcare students. We used a within-group repeated-measure design with baseline followed by intervention. The intervention was a 5-week seminar with 60-minute sessions that incorporated breathing, mindful movement, meditation, and education for self-care in five areas of a biopsychosocial-spiritual model (spiritual, physical, intellectual, energetic, and psychoemotional-social). The following outcomes measures assessed perceived changes in anxiety, self-compassion, mindfulness, depression, and stress: Beck Anxiety Inventory (BAI), Self-Compassion Scale-Short Form (SCS-SF), Freiburg Mindfulness Inventory (FMI), Kentucky Inventory of Mindfulness Skills (KIMS), Mindfulness Attention Awareness Scale (MAAS), Beck Depression Inventory (BDI), and Perceived Stress Scale (PSS). The Freidman test with Dunn's test post hoc pairwise comparisons was used for the BAI, SCS-SF, FMI, KIMS, and MAAS. A Wilcoxon signed-rank test was used for BDI and PSS. Twenty doctor of physical therapy students and one doctor of dental medicine student participated in the study. Significant improvements (all

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PMID: 

J Evid Based Integr Med. 2019 Jan-Dec;24:2515690X19855941. PMID: 31215234

Abstract Title: 

Mindfulness Meditation Effects on Poststroke Spasticity: A Feasibility Study.

Abstract: 

This study examined the feasibility of an adapted 2-week mindfulness meditation protocol for chronic stroke survivors. In addition, preliminary effects of this adapted intervention on spasticity and quality of life in individuals after stroke were explored. Ten chronic stroke survivors with spasticity listened to 2 weeks of short mindfulness meditation recordings, adapted from Jon Kabat-Zinn's Mindfulness-Based Stress Reduction course, in a pre/post repeated measures design. Measures of spasticity, quality of life, mindfulness, and anxiety, along with qualitative data from participants' daily journals, were assessed. On average, participants reported meditating 12.5 days of the full 15 days (mean 12.5 days, SD 0.94, range 8-15 days). Seven of the 10 participants wrote comments in their journals. In addition, there were no adverse effects due to the intervention. Exploratory preliminary analyses also showed statistically significant improvements in spasticity in both the elbow (= .032) and wrist (= .023) after 2 weeks of meditation, along with improvements in quality of life measures for Energy (= .013), Personality (= .026), and Work/Productivity (= .032). This feasibility study suggests that individuals with spasticity following stroke are able to adhere to a 2-week home-based mindfulness meditation program. In addition, preliminary results also suggest that this adapted, short mindfulness meditation program might be a promising approach for individuals with spasticity following stroke. Future research should expand on these preliminary findings with a larger sample size and control group.

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