PMID: 

Oxid Med Cell Longev. 2018 ;2018:4572893. Epub 2018 Oct 28. PMID: 30538801

Abstract Title: 

Procyanidins Extracted from Lotus Seedpod Ameliorate Amyloid–Induced Toxicity in Rat Pheochromocytoma Cells.

Abstract: 

Alzheimer's disease (AD) is a progressive neurodegenerative disease, which is characterized by extracellular senile plaque deposits, intracellular neurofibrillary tangles, and neuronal apoptosis. Amyloid-(A) plays a critical role in AD that may cause oxidative stress and downregulation of CREB/BDNF signaling. Anti-Aeffect has been discussed as a potential therapeutic strategy for AD. This study aimed to identify the amelioration of procyanidins extracted from lotus seedpod (LSPC) on A-induced damage with associated pathways for AD treatment. Rat pheochromocytoma (PC12) cells incubated with Aserve as an Adamage model to evaluate the effect of LSPC. Our findings illustrated that LSPC maintained the cellular morphology from deformation and reduced apoptosis rates of cells induced by A. The mechanisms of LSPC to protect cells from A-induced damage were based on its regulation of oxidation index and activation of CREB/BDNF signaling, including brain-derived neurotrophic factor (BDNF) and phosphorylation of cAMP-responsive element-binding (CREB), protein kinase B (also known as AKT), and the extracellular signal-regulated kinase (ERK). Of note, by high-performance liquid chromatography-tandem mass spectroscopy (LC-MS/MS), several metabolites were detected to accumulate, part of which could take primary responsibility for the amelioration of A-induced damage on PC12 cells. Taken together, our research elucidated the effect of LSPC on neuroprotection through anti-A, indicating it as a potential pretreatment for Alzheimer's disease.

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PMID: 

Ecotoxicol Environ Saf. 2019 Nov 15 ;183:109560. Epub 2019 Aug 14. PMID: 31421536

Abstract Title: 

Lotus seedpod proanthocyanidins protect against neurotoxicity after methyl-mercuric chloride injury.

Abstract: 

In the present study, to investigate the prevention mechanism of proanthocyanidins from lotus seedpod (LSPCs) on methyl mercuric chloride (MMC) induced neurotoxicity, neuron/astrocyte cells were co-cultured to simulate the microenvironment in vivo to the greatest extent. The results showed that, compared with MMC group, pretreatment with LSPCs not only improved cell survival rate, decreased the release of lactate dehydrogenase (LDH), decreased the intracellular reactive oxygen species (ROS) level, and prevented the increase of intracellular [Ca]i, but also significantly increased the total anti-oxidation capacity (T-AOC) (p＜0.05), the levels of glutathione peroxidase (GSH-Px) (p＜0.05), glutathione (GSH) (p＜0.05), and mitochondrial membrane potential (MMP) (p＜0.01). Besides, LSPCs up-regulated the expression of transcriptional factor Nrf2/HO-1 in a concentration-dependent manner. Moreover, LSPCs reduced the expression of Bax protein, significantly increased the expression of Bcl-xl, Bcl-2, β-Ⅲ-Tubulin, SYN, and Arc proteins. The expression of these proteins is mainly regulated by genes and reflects the changes of genes functions. Taken together, these results suggested that LSPCs could enhance cellularantioxidant defense capacity through regulating the activation of Nrf2/HO-1, and involving the inhibition of mitochondria-mediated apoptotic signaling pathway.

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PMID: 

Nutrients. 2019 Nov 28 ;11(12). Epub 2019 Nov 28. PMID: 31795130

Abstract Title: 

Lotus Seedpod Extracts Reduced Lipid Accumulation and Lipotoxicity in Hepatocytes.

Abstract: 

Non-alcoholic fatty liver disease (NAFLD) is closely associated with metabolic disorders, including hepatic lipid accumulation and lipotoxicity. Plant-derived polyphenols have attracted considerable attention in the prevention of NAFLD. Lotus seedpod, rich in polyphenols, is a traditional Chinese herbal medicine. Previous studies have showed that lotus seedpod possess radioprotective, antioxidant, anti-cancer, and anti-inflammatory activities. In this study, the in vitro hepatoprotective effect of lotus seedpod extract (LSE) and its main component epigallocatechin (EGC) was examined. Firstly, oleic acid (OA), an unsaturated fatty acid, was used to induce the phenotype of NAFLD in human hepatocytes, HepG2 cells. LSE dose-dependently improved the OA-induced viability loss of HepG2 cells. Non-cytotoxic concentrations of LSE or EGC abolished intracellular lipid accumulation and oxidative stress in the OA-treated cells. In addition, LSE and EGC showed a minor effect on autophagy, and potential in reducing OA-induced occurrence of apoptosis confirmed by morphological and biochemical features, including an increase in the formation of apoptotic bodies, the exposure of phosphatidylserine, and activation of caspases. Molecular data showed the anti-apoptotic effect of LSE might be mediated via downregulation of the mitochondrial pathway. Our data imply that EGC-enriched LSE potentially could be developed as an anti-NAFLD agent.

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PMID: 

BMC Complement Altern Med. 2019 Dec 11 ;19(1):361. Epub 2019 Dec 11. PMID: 31829185

Abstract Title: 

In vitro anti-allergic activity of Moringa oleifera Lam. extracts and their isolated compounds.

Abstract: 

BACKGROUND: Moringa oleifera Lam. is a commonly used plant in herbal medicine and has various reported bioactivities such as antioxidant, antimicrobial, anticancer and antidiabetes. It is rich in nutrients and polyphenols. The plant also has been traditionally used for alleviating allergic conditions. This study was aimed to examine the anti-allergic activity of M. oleifera extracts and its isolated compounds.METHOD: M. oleifera leaves, seeds and pods were extracted with 80% of ethanol. Individual compounds were isolated using a column chromatographic technique and elucidated based on the nuclear magnetic resonance (NMR) and electrospray ionisation mass spectrometry (ESIMS) spectral data. The anti-allergic activity of the extracts, isolated compounds and ketotifen fumarate as a positive control was evaluated using rat basophilic leukaemia (RBL-2H3) cells for early and late phases of allergic reactions. The early phase was determined based on the inhibition of beta-hexosaminidase and histamine release; while the late phase was based on the inhibition of interleukin (IL-4) and tumour necrosis factor (TNF-α) release.RESULTS: Two new compounds; ethyl-(E)-undec-6-enoate (1) and 3,5,6-trihydroxy-2-(2,3,4,5,6-pentahydroxyphenyl)-4H-chromen-4-one (2) together with six known compounds; quercetin (3), kaempferol (4),β-sitosterol-3-O-glucoside (5), oleic acid (6), glucomoringin (7), 2,3,4-trihydroxybenzaldehyde (8) and stigmasterol (9) were isolated from M. oleifera extracts. All extracts and the isolated compounds inhibited mast cell degranulation by inhibiting beta-hexosaminidase and histamine release, as well as the release of IL-4 and TNF-α at varying levels compared with ketotifen fumarate.CONCLUSION: The study suggested that M. oleifera and its isolated compounds potentially have an anti-allergic activity by inhibiting both early and late phases of allergic reactions.

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PMID: 

Environ Toxicol Pharmacol. 2019 Nov 23 ;74:103306. Epub 2019 Nov 23. PMID: 31812117

Abstract Title: 

Allicin modulates diclofenac sodium induced hepatonephro toxicity in rats via reducing oxidative stress and caspase 3 protein expression.

Abstract: 

PURPOSE: This study was designed to evaluate the protective effects of allicin against diclofenac sodium induced hepatonephro toxicity in rats.METHODS: Sixty male Wister albino rats were assigned into six groups. The control group received calcium carbonate and corn starch. 2group received diclofenac sodium (2 mg/kg bw orally) for 30 days. 3group received allicin (45 mg/kg bw orally) for 30 days. 4group administrated diclofenac sodium as in the 2group and allicin (15 mg/kg bw orally) for 30 days. 5group received diclofenac sodium as in the 2group and allicin (30 mg/kg bw orally) for 30 days. 6group received diclofenac sodium as 2and allicin (45 mg/kg bw orally) for 30 days.RESULTS: Diclofenac sodium significantly elevated activities of serum aspartate aminotransferase and alanine aminotransferase and serum levels of creatinine and urea. In addition, it induced hyperglycemia, lipid peroxidation, pathological alteration and caspase 3 protein expression in hepatic and renal tissues. However, it decreased reduced glutathione concentration and proliferating cell nuclear antigen protein expression in hepatic tissues. In contrast, allicin modulated the diclofenac sodium induced alteration in liver and kidney functions and structures dose dependently.CONCLUSION: This study indicated that allicin had potential preventive effects against diclofenac sodium induced hepatonephro toxicity in rats.

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PMID: 

Nutrients. 2019 Dec 2 ;11(12). Epub 2019 Dec 2. PMID: 31810206

Abstract Title: 

Allicin Improves Metabolism in High-Fat Diet-Induced Obese Mice by Modulating the Gut Microbiota.

Abstract: 

Allicin, naturally present in the bulbs of the lily family, has anticancer, blood pressure lowering, blood fat lowering and diabetes improving effects. Recent studies have shown that allicin promotes the browning of white adipocytes and reduces the weight gain of mice induced by high-fat diet. While the gut microbiota has a strong relationship with obesity and energy metabolism, the effect of allicin on weight loss via gut microorganisms is still unclear. In this study, we treated obese mice induced by high-fat diet with allicin to determine its effects on fat deposition, blood metabolic parameters and intestinal morphology. Furthermore, we used high-throughput sequencing on a MiSeq Illumina platform to determine the gut microorganisms' species. We found that allicin significantly reduced the weight gain of obese mice by promoting lipolysis and thermogenesis, as well as blood metabolism and intestinal morphology, and suppressing hepatic lipid synthesis and transport. In addition, allicin changed the composition of the intestinal microbiota and increased the proportion of beneficial bacteria. In conclusion, our study showed that allicin improves metabolism in high-fat induced obese mice by modulating the gut microbiota. Our findings provide a theoretical basis for further elucidation of the weight loss mechanism of allicin.

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PMID: 

Nutrients. 2019 Dec 6 ;11(12). Epub 2019 Dec 6. PMID: 31817589

Abstract Title: 

Grape Seed Proanthocyanidins Induce Autophagy and Modulate Survivin in HepG2 Cells and Inhibit Xenograft Tumor Growth in Vivo.

Abstract: 

Liver cancer is one of the leading causes of death worldwide. Although radiotherapy and chemotherapy are effective in general, they present various side effects, significantly limiting the curative effect. Increasing evidence has shown that the dietary intake of phytochemicals plays an essential role in the chemoprevention or chemotherapy of tumors. In this work, HepG2 cells and nude mice with HepG2-derived xenografts were treated with grape seed proanthocyanidins (GSPs). The results showed that GSPs induced autophagy, and inhibition of autophagy increased apoptosis in HepG2 cells. In addition, GSPs also reduced the expression of survivin. Moreover, survivin was involved in GSPs-induced apoptosis. GSPs at 100 mg/kg and 200 mg/kg significantly inhibited the growth of HepG2 cells in nude mice without causing observable toxicity and autophagy, while inducing the phosphorylation of mitogen-activated protein kinase (MAPK) pathway-associated proteins, p-JNK, p-ERK and p-p38 MAPK and reducing the expression of survivin. These results suggested that GSPs might be promising phytochemicals against liver cancer.

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PMID: 

Antioxidants (Basel). 2019 Dec 6 ;8(12). Epub 2019 Dec 6. PMID: 31817734

Abstract Title: 

Melatonin Plus Folic Acid Treatment Ameliorates Reserpine-Induced Fibromyalgia: An Evaluation of Pain, Oxidative Stress, and Inflammation.

Abstract: 

BACKGROUND: Fibromyalgia is a chronic condition characterized by increased sensory perception of pain, neuropathic/neurodegenerative modifications, oxidative, and nitrosative stress. An appropriate therapy is hard to find, and the currently used treatments are able to target only one of these aspects.METHODS: The aim of this study is to investigate the beneficial effects of melatonin plus folic acid administration in a rat model of reserpine-induced fibromyalgia. Sprague-Dawley male rats were injected with 1 mg/kg of reserpine for three consecutive days and later administered with melatonin, folic acid, or both for twenty-one days.RESULTS: Administration of reserpine led to a significant decrease in the nociceptive threshold as well as a significant increase in depressive-like symptoms. These behavioral changes were accompanied by increased oxidative and nitrosative stress. Lipid peroxidation was significantly increased, as well as nitrotyrosine and PARP expression, while superoxide dismutase, nonprotein thiols, and catalase were significantly decreased. Endogenously produced oxidants species are responsible for mast cell infiltration, increased expression pro-inflammatory mediators, and microglia activation.CONCLUSION: Melatonin plus acid folic administration is able to ameliorate the behavioral defects, oxidative and nitrosative stress, mast cell infiltration, inflammatory mediators overexpression, and microglia activation induced by reserpine injection with more efficacy than their separate administration.

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PMID: 

Food Funct. 2019 Dec 11 ;10(12):7926-7939. PMID: 31773121

Abstract Title: 

Cocoa ameliorates renal injury in Zucker diabetic fatty rats by preventing oxidative stress, apoptosis and inactivation of autophagy.

Abstract: 

Redox balance, autophagy and apoptosis are main processes involved in the development of diabetic nephropathy. Epidemiological and animal studies suggest that cocoa might reduce the risk of diabetic complications. However, the molecular mechanisms responsible for these potential preventive activities and whether cocoa exerts beneficial effects on dysregulated signalling pathways involved in cellular antioxidant defence, autophagy and apoptosis in the diabetic kidney remain largely unknown. Therefore, this work investigated the effect of a cocoa-rich diet on the mentioned processes in the renal cortex of Zucker Diabetic Fatty (ZDF) rats. Male ZDF rats were fed either a control or cocoa-rich diet (10%), and Zucker lean animals received the control diet (10-20 weeks-of-life). ZDF rats fed with cocoa decreased body weight and glucose and insulin levels, and improved renal function. Cocoa intake further prevented the enhanced renal cortical oxidative stress in diabetic rats by regulating the antioxidant defence system and close-related proteins to cytoprotection and cell response; thus, cocoa diminished oxidative markers (reactive oxygen species and carbonyl groups) and NADPH-oxidase-4 levels, and restored key enzymatic antioxidant activities (superoxide dismutase and catalase), nuclear-erythroid-2-related factor-2, and ERK-MAPK levels, as well as sirtuin-1/5'-AMP-activated-protein kinase signalling. Moreover, in ZDF rats cocoa-rich diet contributed to alleviation of the renal cortical injury through autophagy activation (p62 upregulation, and downregulation of beclin-1 and LC3), and inhibition of apoptosis (Bcl-xL stimulation and suppression of Bax and caspases-9 and -3). These findings provide the first in vivo evidence on the molecular mechanisms of cocoa to circumvent renal cortical damage that involve improvement of antioxidant competences, stimulation of autophagy and suppression of apoptosis in ZDF rats.

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PMID: 

Biol Trace Elem Res. 2019 Aug 5. Epub 2019 Aug 5. PMID: 31385202

Abstract Title: 

Effects of Choline and Magnesium Concurrent Supplementation on Coagulation and Lipid Profile in Patients with Type 2 Diabetes Mellitus: a Pilot Clinical Trial.

Abstract: 

Metabolic failure is associated with dyslipidemia and coagulation which can result in a higher risk of cardiovascular disease (CVD) in type 2 diabetes mellitus (T2DM). The aim of this study was to assess the effects of choline and magnesium co-supplementation on lipid profile and coagulation parameters in patients with T2DM. In a randomized, double-blind, placebo-controlled trial, supplements of choline bitartrate (1000 mg), magnesium oxide (500 mg), choline plus magnesium, or placebo were administered for 2 months to 96 diabetic participants of both sexes aged 30-60 years. Anthropometric characteristics, dietary intake, physical activity, serum lipids, and coagulation markers were measured in all subjects. Significant differences were observed in plasminogen activator inhibitor-1 (PAI-1) levels in the magnesium and choline-magnesium groups (p 

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