Kushenol C from Sophora flavescens protects against UVB-induced skin damage in mice through suppression of inflammation and oxidative stress.

Sophora flavescens has been used in traditional medicine for the treatment of various diseases such as viral hepatitis, fever, cancer, and pain. It is known to contain many bioactive compounds including prenylated flavonoids such as kurarinone, sophoraflavanone G, kuraridine and isoxanthohumol. These flavonoids have been confirmed to have anti-inflammatory, α-glucosidase inhibitory and antioxidant performances. However, the protective activities against UV-induced skin damage of kushenol C from S. flavescens have not yet been elucidated. In this study, we explored the protective effect of kushenol C against the skin damage induced by UVB in mice. Our results showed that kushenol C treatment significantly recovered UVB-induced skin damage, the degradation of collagen, mast cell infiltration, together with epidermal hyperplasia in mice. Furthermore, the treatment of kushenol C remarkably suppressed the generation of pro-inflammatory mediators in the mice irradiated by UVB. More so, treatment with kushenol C suppressed the oxidative stress in mice irradiated by UVB. In conclusion, these results showed that kushenol C from S. flavescens has potentialities to treat skin injury via suppressing skin damage induced by UVB and oxidative stress.

Anti-inflammatory of disenecionyl cis-khellactone in LPS-stimulated RAW264.7 cells and the its inhibitory activity on soluble epoxide hydrolase.

The objective of the present study was to investigate anti-inflammatory effects of disenecionyl cis-khellactone (DK) isolated from Peucedanum japonicum Thunberg, a traditional edible plant, in RAW264.7 cells stimulated with lipopolysaccharide (LPS). Anti-inflammatory effects of DK were analyzed using various techniques, including NO assay, Western blot analysis, enzyme-linked immunosorbent assay (ELISA), real-time PCR, and immunofluorescence staining. It was revealed that DK reduced the production of pro-inflammatory cytokines including Monocyte chemoattractant protein-1 (MCP-1), Tumor necrosis factor-α (TNF-α), Interleukin 1ß (IL-1ß), and Interleukin 6 (IL-6) in RAW264.7 cells stimulated with LPS. It was revealed that DK effectively downregulated expression levels of iNOS and COX-2 due to inhibition of NF-κB activation and suppressing the phosphorylation of p38 and jun N-terminal kinase (JNK) mitogen-activated protein kinase (MAPK) phosphorylation. Also, soluble epoxide hydrolase activity and expression were decreased by the proinflammatory inhibitor, DK. Finally, findings of this study suggest that DK isolated from P. japonicum might have potential as a therapeutic candidate for inflammatory diseases.

Diospyros lotus leaf extract and its main component myricitrin regulate pruritus through the inhibition of astrocyte activation.

Diospyros lotus is a deciduous plant native to Asian countries, including Korea, Japan and China, and southeast Europe. In traditional medicine, Diospyros lotus is used as an anticancer, antidiabetic and antipyretic agent. The present study aimed to evaluate the effect of Diospyros lotus leaf extract (DLE) in ameliorating histamine-independent pruritus. Activation of signal transducer and activator of transcription 3 (STAT3) in astrocytes contributes to pruritus. In this study, the effects of DLE and its main component, myricetin (MC), on the activation of STAT3, expression of glial fibrillary acidic protein (GFAP), and production of lipocalin-2 (LCN2) in IL-6-treated astrocytes and chloroquine-injected mice were investigated through western blot, reverse transcription-quantitative PCR, and immunofluorescence staining. DLE and MC inhibited STAT3 activation, GFAP expression and LCN2 release via inositol 1,4,5-trisphosphate receptor type 1 blockade in astrocytes. DLE and MC ameliorated scratching behavior, expression of GFAP, mast cell infiltration and serum IL-6 levels in chloroquine-injected mice. These results suggested that DLE and MC can be used as oral therapeutic agents for the treatment and management of pruritus.

Anti-inflammatory effect of red ginseng marc, Artemisia scoparia, Paeonia japonica and Angelica gigas extract mixture in LPS-stimulated RAW 264.7 cells.

A normal inflammatory response is essential in protecting the body from foreign substances. However, excessive inflammation contributes to diseases such as oxidative stress, heart disease, and cancer. In this study, we evaluated the anti-inflammatory effects of RAPA (red ginseng marc, Artemisia scoparia Waldst.et Kit, Paeonia japonica Miyabe & Takeda, and Angelica gigas Nakai extract mixture) in LPS-stimulated RAW 264.7 cells (macrophages). RAPA suppressed the expression of inflammatory factors such as iNOS and COX-2 and decreased the production of nitric oxide. In addition, RAPA decreased the expression of the inflammatory cytokines TNF-α and IL-6. Furthermore, RAPA inhibited the phosphorylation of MAPKs such as JNK and ERK as well as IκB and NF-κB. In conclusion, RAPA inhibited production of inflammatory mediators via downregulation of the MAPK and NF-κB signaling pathways in LPS-stimulated RAW 264.7 cells. The results of this study demonstrated that RAPA regulates excessive inflammatory responses at the cellular level. Therefore, it is necessary to investigate whether the same effect is observed in vivo through further research.

Ameliorative effects of Cirsium japonicum extract and main component cirsimaritin in mice model of high-fat diet-induced metabolic dysfunction-associated fatty liver disease.

The objective of this study was to determine biological effects of Cirsium japonicum extract and its main component cirsimaritin on high-fat diet (HFD)-induced metabolic dysfunction-associated fatty liver disease (MAFLD) in a mouse model. Mice were fed with a HFD to induce MAFLD and simultaneously administered with C. japonicum extract (CJE) or cirsimaritin. Various MAFLD biomarkers were evaluated using biological methods. Results demonstrated that triglyceride, aspartate aminotransferase, alanine aminotransferase, and malondialdehyde levels in the liver of mice were significantly reduced upon administration of CJE or cirsimaritin. Treatment with CJE or cirsimaritin also reduced the severity of liver injury in the experimental mouse model of MAFLD by inhibiting hepatic steatosis, oxidative stress, inflammation, and liver fibrosis. These results demonstrate that CJE and cirsimaritin as its main compound have a preventive action against the progression of hepatic steatosis to fibrosis and cirrhosis. Our study suggests that CJE and cirsimaritin might be promising agents for preventing and/or treating MAFLD.

Citric acid and enzyme-assisted modification of flavonoids from celery (Apium graveolens) extract and their anti-inflammatory activity in HMC-1.2 cells.

Apium graveolens (celery) of the family Apiaceae contains bioactive compounds including luteolin and apigenin. The purpose of this study was to increase the extraction yield of apigenin and luteolin in celery extract using green technology and to evaluate their biological activities. The results showed that CA and ß-glucosidase-assisted celery extraction transformed apiin in the celery to apigenin with an increase in luteolin concentration. The CA and ß-glucosidase-treated celery extract (CAGE) improved the anti-inflammatory properties of celery extract by inhibiting the expression and production of inflammatory cytokines (IL-6, IL-8, IL-31, and TNF-α) in IL-33-stimulated mast cells (HMC-1.2 cells). Their mechanism of action was tied to the inhibition of ERK, JNK, IKKα, IκBα, and NF-κB activation by CAGE in the stimulated cells. In conclusion, CA and enzyme treatment can be considered as a useful biotechnology tool for the improvement of bioactive compounds in celery and hence improve on their bioactivity. PRACTICAL APPLICATIONS: Apium graveolens commonly called celery is an edible agricultural product cultivated throughout the world and known as a "superfood." Celery contains bioactive compounds including apigenin and luteolin that contribute to their described biological activities. However, extracting celery using normal extraction procedures such as hot water and ethanol methods yields only a small amount of apigenin and luteolin. In the present study, we introduced an eco-friendly method using citric and ß-glucosidase to obtain apigenin and luteolin-rich celery extract with improved anti-inflammatory activities. The present work will spark studies on the conversion of less biologically active compounds in functional food materials to more active compounds using CA and ß-glucosidase, and the development of functional food with specifically enriched bioactive substances at the industrial levels.

Anti­inflammatory effect of Chrysanthemum zawadskii, peppermint, Glycyrrhiza glabra herbal mixture in lipopolysaccharide­stimulated RAW264.7 macrophages.

The normal inflammatory reaction protects the body from harmful external factors, whereas abnormal chronic inflammation can cause various diseases, including cancer. The purpose of the present study was to investigate the anti­inflammatory activity of a mixture of Chrysanthemum zawadskii, peppermint and Glycyrrhiza glabra (CPG) by analyzing the expression levels of inflammatory mediators, cytokines and transcription factors in lipopolysaccharide (LPS)­stimulated Raw264.7 cells. A nitric oxide assay, ELISA, western blotting and immunofluorescence staining were performed to investigate the anti­inflammatory activity of the CPG mixture. Pretreatment of Raw264.7 cells with CPG inhibited the increase of inflammatory mediators (inducible nitric oxide synthase, cyclooxygenase­2 and IFN­ß) induced by LPS. Additionally, it inhibited the production of pro­inflammatory cytokines (TNF­α, IL­6 and IL­1ß). CPG suppressed LPS­induced phosphorylation of STAT1, AKT, Iκb and NF­κB. Furthermore, CPG inhibited the translocation of NF­κB into the nucleus. In summary, CPG could inhibit LPS­induced inflammation, which occurs primarily through the AKT/Iκb/NF­κB signaling pathway in RAW264.7 cells.

Protective effects of halophyte complex extract against UVB-induced damage in human keratinocytes and the skin of hairless mice.

Limonium tetragonum, Triglochin maritimum, Artemisia scoparia and red ginseng have been used as folk remedies for treating a variety of diseases. In the current study, the protective effects of halophyte and red ginseng against ultraviolet (UV)-induced skin damage were investigated. Halophyte red ginseng complex extract (HRCE) was prepared and its effects on UV-B irradiated human keratinocytes and mouse skin were studied through ELISA, Western blotting immunofluorescence and histological staining. HRCE inhibited peroxide-induced damage in human keratinocytes. HRCE also inhibited UVB-induced collagen and elastin degradation in human keratinocytes and mouse skin. In addition, HRCE inhibited mast cell infiltration in the skin of mice irradiated with UVB light. This effect was likely due to HRCE inhibiting the activation of MAPK and NF-κB. By protecting the skin from UVB-induced skin damage, HRCE has the potential to be used in the treatment and prevention of UV-induced skin damage and photoaging.

Kushenol C Prevents Tert-Butyl Hydroperoxide and Acetaminophen-Induced Liver Injury.

Sophora flavescens, also known as Kushen, has traditionally been used as a herbal medicine. In the present study we evaluated the ameliorative effects of kushenol C (KC) from S. flavescens against tBHP (tert-Butyl hydroperoxide)-induced oxidative stress in hepatocellular carcinoma (HEPG2) cells and acetaminophen (APAP)-induced hepatotoxicity in mice. KC pretreatment protected the HEPG2 cells against oxidative stress by reducing cell death, apoptosis and reactive oxygen species (ROS) generation. KC pretreatment also upregulated pro-caspase 3 and GSH (glutathione) as well as expression of 8-Oxoguanine DNA Glycosylase (OGG1) in the HEPG2 cells. The mechanism of action was partly related by KC's activation of Akt (Protein kinase B (PKB)) and Nrf2 (Nuclear factor (erythroid-derived 2)-like 2) in the HepG2 cells. In in vivo investigations, coadministration of mice with KC and APAP significantly attenuated APAP-induced hepatotoxicity and liver damage, as the serum enzymatic activity of aspartate aminotransferase and alanine aminotransferase, as well as liver lipid peroxidation and cleaved caspase 3 expression, were reduced in APAP-treated mice. Coadministration with KC also up-regulated antioxidant enzyme expression and prevented the production of proinflammatory mediators in APAP-treated mice. Taken together, these results showed that KC treatment has potential as a therapeutic agent against liver injury through the suppression of oxidative stress.

Luteolin and Apigenin Attenuate LPS-Induced Astrocyte Activation and Cytokine Production by Targeting MAPK, STAT3, and NF-κB Signaling Pathways.

Astrocytes release biologically active substances that cause inflammation in neurodegenerative diseases. The present study investigated the effects of two flavonoids (apigenin and luteolin) on the production of IL-31 and IL-33 in lipopolysaccharide (LPS)-activated astrocytes. Cell viability was investigated using EZ-Cytox assay, mRNA expressions of IL-31 and IL-33 were analyzed by RT-PCR, protein expressions were analyzed by western blot, and cytokine secretion was analyzed by ELISA. Apigenin and luteolin prevented astrocyte activation and inhibited mRNA and protein expression and secretion of IL-31 and IL-33 in the LPS-treated astrocytes. Apigenin's suppression of ERK, NF-κB, and STAT3 activations was responsible for the inhibition of IL-31 and IL-33, while luteolin's suppression of JNK, p38, ERK, NF-κB, and STAT3 activations was responsible for the inhibition of IL-31 in the astrocytes. Also, luteolin's suppression of ERK, NF-κB, and STAT3 activations inhibited IL-33 production in the activated astrocytes. In addition, apigenin and luteolin also prevented the translocation of activated STAT3 and NF-κB to the nucleus of the activated astrocytes and subsequently affected their DNA binding activities. The results suggest that apigenin and luteolin may have potentials as neuroprotective agents for the treatment of diseases involving astrocyte activation and detrimental production of IL-31 and IL-33.

In vitro Anti-Inflammatory and Anti-Oxidative Stress Activities of Kushenol C Isolated from the Roots of Sophora flavescens.

Kushenol C (KC) is a prenylated flavonoid isolated from the roots of Sophora flavescens aiton. Little is known about its anti-inflammatory and anti-oxidative stress activities. Here, we investigated the anti-inflammatory and anti-oxidative stress effects of KC in lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages, and tert-butyl hydroperoxide (tBHP)-induced oxidative stress in HaCaT cells. The results demonstrated that KC dose-dependently suppressed the production of inflammatory mediators, including NO, PGE2, IL-6, IL1ß, MCP-1, and IFN-ß in LPS-stimulated RAW264.7 macrophages. The study demonstrated that the inhibition of STAT1, STAT6, and NF-κB activations by KC might have been responsible for the inhibition of NO, PGE2, IL-6, IL1ß, MCP-1, and IFN-ß in the LPS-stimulated RAW264.7 macrophages. KC also upregulated the expression of HO-1 and its activities in the LPS-stimulated RAW264.7 macrophages. The upregulation of Nrf2 transcription activities by KC in the LPS-stimulated RAW264.7 macrophages was demonstrated to be responsible for the upregulation of HO-1 expression and its activity in LPS-stimulated RAW264.7 macrophages. In HaCaT cells, KC prevented DNA damage and cell death by upregulating the endogenous antioxidant defense system involving glutathione, superoxide dismutase, and catalase, which prevented reactive oxygen species production from tert-butyl hydroperoxide (tBHP)-induced oxidative stress in HaCaT cells. The upregulated activation of Nrf2 and Akt in the PI3K-Akt signaling pathway by KC was demonstrated to be responsible for the anti-oxidative stress activity of KC in HaCaT cells. Collectively, the study suggests that KC can be further investigated as a potential anti-inflammatory candidate for the treatment of inflammatory diseases.

Anti-obesity effects of a mixed extract containing Platycodon grandiflorum, Apium graveolens and green tea in high-fat-diet-induced obese mice.

The anti-obesity effect of a combination of extracts made of Platycodon grandiflorum (PGE), Apium graveolens (AGE) and green tea (GTE) extracts was investigated in a high-fat diet-induced obese C57BL/6N mouse model. Body weight, epididymal adipose tissue weight, liver weight, adipocytes size and serum lipid profile, insulin, leptin and glucose levels were investigated. Additionally, hepatic steatosis, injury and oxidative burden were evaluated in the present study. The current study demonstrated that the PGE, AGE, and GTE (PAG) mixture were most effective in preventing obesity and its associated complications compared with the single extracts used alone. This was evidenced by the PAG's prevention of weight gain, reduction of adipocyte size, beneficial effects in serum lipid profile, levels of insulin, leptin and glucose, and the prevention of liver injury by reducing fat accumulation in the liver, decreased GOT and GPT enzymes and the upregulation of liver antioxidant enzymes. These results suggested that PAG may provide insights into functional food ingredients for use in the prevention of obesity.

Effect of Luteolin and Apigenin on the Production of Il-31 and Il-33 in Lipopolysaccharides-Activated Microglia Cells and Their Mechanism of Action.

Microglia cells are resident cells of the central nervous system (CNS) charged with modulating inflammation in the CNS. Overstimulation of microglia cells continuously releases inflammatory mediators that contribute to neurodegenerative diseases. Apigenin and Luteolin are flavonoids with reported anti-inflammatory activities. However, their effects on IL-31 and IL-33 production in microglial cells are unknown. Here, we investigated the effects of apigenin and luteolin on the production of IL-31 and IL-33 by microglia cells. SIM-A9 microglial cells were pre-treated with apigenin or luteolin and stimulated with lipopolysaccharides to evaluate the production of IL-31 and IL-33. The study revealed that apigenin and luteolin inhibited the production of IL-31 and IL-33 at the gene and protein expressions and the secretion levels. Using potent inhibitors of MAPK, NF-κB, and STAT3 signaling pathways, we demonstrated that apigenin and luteolin's suppression of ERK and JNK contributed to the inhibition of IL-31 and IL-33 in the MAPK pathway. Luteolin's suppression of NF-κB and STAT3 also contributed to the inhibition of IL-31 and IL-33. Further analysis revealed that both compounds prevented nuclear translocation of activated NF-κB and STAT3, an act that subsequently prevented their DNA binding activities. Collectively, the study suggested that apigenin and luteolin's regulation of signaling pathways contributed to the inhibition of IL-31 and IL-33, thus suggesting its importance for the improvement of neurodegenerative diseases involving these two cytokines.

Luteolin suppresses IL-31 production in IL-33-stimulated mast cells through MAPK and NF-κB signaling pathways.

IL-31 and IL-33 are cytokines, which are expressed in many inflammatory and pathological disorders, thus suggesting an IL-31/IL-33 axis interaction in pathological diseases. Luteolin from natural products is known for its anti-inflammatory activities associated with the regulation of inflammatory signaling pathways. Here, we investigated the effects of luteolin in the regulation of IL-33-stimulated production and secretion of IL-31 in HMC-1.2 mast cells. Human mast cells (HMC-1.2) were treated with luteolin and stimulated with IL-33. Real-time PCR was used to measure IL-31 mRNA expression. Western blot and immunofluorescence assays were used to measure IL-31 expression. ELISA techniques were used to measure IL-31 secretion and NF-κB-DNA-binding activities. The results revealed that luteolin inhibited the expression of IL-31 in IL-33-stimulated HMC-1.2 cells at the mRNA and protein levels. Also, Luteolin inhibited the secretion of IL-31 into the cell culture media of the IL-33-stimulated HMC-1.2 cells. Further findings demonstrated that luteolin inhibited the activation of ERK, JNK, p38, and NF-κB p65 in the IL-33-stimulated HMC-1.2 cells. In addition, luteolin also prevented the nuclear translocation and binding of p65 to its DNA-binding site. Based on the results, luteolin may be considered as a potential therapeutic or functional food agent for the prevention and/or treatment of IL-31 and IL-33-related diseases.

Anti-atopic dermatitis effects of hydrolyzed celery extract in mice.

This study investigated the ameliorative effects of acid hydrolyzed celery extract (HCE) and celery extract (CE) in an atopic dermatitis (AD) mice model. The results of the study showed that HCE, more than CE improved AD-like skin lesions caused by fluoro-2,4-dinitrobenzene and house dust mite antigen administration. Further analysis also showed the dominance of HCE than CE in preventing mast cell infiltration in the dermis; inhibiting the IL-31 expression in mice skin and reducing the immunoglobulin-E, IL-4, IL-5, TNF-α, IFN-γ, IL-31, and TSLP in serum of mice. Using in vitro studies in a murine macrophage cell line, we showed that apigetrin, luteolin, and apigenin present in both extracts could be accountable for the observed effects as these three compounds and not apiin prevented the nitric oxide production in the murine macrophage. Based on this study, we suggest that hydrolyzing celery extracts can improve the therapeutic efficacy of celery extracts for management of AD. PRACTICAL APPLICATIONS: Apigenin, apigetrin, and luteolin are known biologically active compounds present in celery. Acid hydrolysis could increase the biologically active compounds in natural products. The research investigated the effects of acid HCE in a mice model of atopic dermatitis. The data obtained from this study sheds light on the use of hydrolysis methods to improve the biological activities of plant extracts used in nutraceutical industries.

Anti-obesity effects of enzyme-treated celery extract in mice fed with high-fat diet.

The present study demonstrated the anti-obesity effects of enzyme-treated celery extract (ECE) in mice on high-fat diet (HFD). In vitro studies showed that ECE has anti-adipogenic properties by inhibiting lipid accumulations in adipose cells. In vivo studies indicated that the administration of ECE markedly prevented HFD-induced body weight gain, food efficiency ratio, and epididymal fat and liver weights. ECE reduced lipid parameters, cardiac risk factor, and atherogenic index in obese mice. ECE prevented a diabetes state by improving adipokines levels, reducing glucose levels, and preventing insulin resistance. Moreover, ECE prevented HFD-induced liver damage by preventing hepatic steatosis and upregulation of liver antioxidant enzymes. The mechanism of ECE was partially investigated to involve the activation of 5' adenosine monophosphate-activated protein kinase and hence the downregulation of CCAAT/enhancer binding protein α and peroxisome proliferator-activated receptor γ by ECE. Our results suggest that ECE could be used as functional food materials for the prevention of obesity. PRACTICAL APPLICATIONS: Apium graveolens is a popular plant with nutritive and medicinal benefits. It contains bioactive compounds such as apiin, apigenin, and luteolin. However, these compounds are rendered insoluble due to their interaction with polysaccharides in the cell wall thus making them less bioavailable. Hydrolyzing them could increase the yield of bioactive compounds in celery. This pilot study demonstrates that pectinase-treated celery extract has anti-obesity effects. The results of this research demonstrate the use of enzymes in improving the biological activities of plant extracts and suggest the use of enzyme-assisted extraction techniques in the industrial production of health functional food from celery.

Anti-inflammatory effect of hydrolyzed celery leaves extract in murine primary splenocyte.

Apium graveolens (celery) has been used in traditional medicine for the treatment of various ailments. However, its molecular mechanism of action in inflammatory response is unclear. In this study, we sought to investigate the anti-inflammatory properties of celery leaves. We prepared an acid-hydrolyzed extract of celery leaves (HCE) and studied its effects on concanavalin A (ConA)-stimulated primary splenocytes. HCE at noncytotoxic concentrations, inhibited ConA-induced proliferation of splenocytes. HCE treatment reduced CD4+ T cell population and decreased expressions and production of cytokines in stimulated splenocytes. In addition, HCE significantly inhibited NO production and reduced the expression of COX-2 mRNA in the stimulated splenocytes. The effects seen were probably due to HCE's downregulation of NF-κB/p65 activation in splenocytes. By providing the anti-inflammatory mechanism of action of HCE, these findings are potentially important for future studies that may, ultimately result in the potential use of celery for the treatment/prevention of inflammatory diseases. PRACTICAL APPLICATIONS: Apium graveolens is a well-known edible plant with high concentrations of bioactive compounds such as apigenin, luteolin, and kaempferol. The research investigated the effects of A. graveolens leaves in splenocyte proliferation, and production of inflammatory mediators and cytokines. The data obtained from this study shed light on the use of plant extracts and plant-based bioactives in nutraceutical industries as potential functional food materials for preventing inflammatory diseases.

Chlorogenic acid-rich Solanum melongena extract has protective potential against rotenone-induced neurotoxicity in PC-12 cells.

Neurodegenerative diseases are major threats to human health. Here, through fluorescence, colorimetric, immunoblotting, spectroscopy, and laser scanning confocal microscopic techniques, we investigated the neuroprotective properties of chlorogenic acid-rich Solanum melongena extracts (SM extract) in rotenone-induced PC-12 cell death. The results showed that rotenone caused apoptosis to PC-12 cells by elevating Bax/Bcl-2 ratio and increasing caspase-3 activity. Rotenone also increased ROS in cells while suppressing SOD and catalase activities. This resulted in the depletion of ATP in cells by blocking mitochondria complex I activity. Pretreatment of the cells with SM extract at concentrations of 100, 250, and 500 µg/ml before incubation for 24 hr with rotenone significantly prevented apoptosis, decreased ROS, and increased ATP production in the cells. SM extract upregulated SOD and catalase activities in the cells. These results unveil evidence that SM extract content neuroprotective properties that can be exploited to prevent and treat neurodegenerative diseases. PRACTICAL APPLICATIONS: Solanum melongena eggplant is a popular ingredient in many traditional recipes and is well known in Asia for its medicinal benefits. Despite numerous scientific reports of the potential health benefits of this plant, reports on its effects in neurodegenerative diseases is still lacking. This pilot study demonstrates that S. melongena eggplant can protect against neurotoxicity in neurodegenerative diseases. The results of this research serves as a base for further research on eggplant that will result in its usage on a larger scale as functional food materials.

Commiphora myrrha inhibits itch-associated histamine and IL-31 production in stimulated mast cells.

Commiphora myrrha (Myrrh) is widely recognized for its anti-inflammatory and antimicrobial properties, which are utilized for the treatment of oral ulcers, gingivitis, sinusitis, glomerulonephritis, brucellosis and a variety of skin disorders. The current study aimed to assess whether myrrh modulates itch-associated interleukin (IL)-31 cytokine production and histamine release in stimulated human mast cells (HMC-1). To realize this, molecular biology techniques including real-time quantitiative PCR, western blotting and ELISA were employed. The results indicated that Myrrh successfully suppressed phorbol myristate acetate and calcium ionophore-stimulated mRNA expression, and reduced the production of IL-31 in HMC-1 cells. In addition, myrrh served as a suppressor of extracellular signal-regulated kinase and NF-κB activation, indicating its mechanism in the prevention of HMC-1 cell IL-31 production. Myrrh also prevented the release of histamine in HMC-1 cells. Whilst the present study awaits in vivo support, the pharmacological actions of myrrh provide new indications as to its potential applicability for itch treatment, which cannot be treated with histamine receptor blockers alone.

Combined effects of Diospyros lotus leaf and grape stalk extract in high-fat-diet-induced obesity in mice.

The aim of this study was to investigate the combined effects of Diospyros lotus leaves extracts (DLE) and Muscat Bailey A grape stalk extracts (MGSE) in obesity induced by high-fat diet (HFD) in mice. The mice were fed with HFD and orally administered daily with DLE, MGSE, a mixture of DLE and MGSE, and Garcinia cambogia extract over a period of 16 weeks. The results revealed that daily administration of DLE and MGSE mixtures markedly prevented HFD-induced weight gain, plasma lipid profile, hepatic steatosis, hepatic fibrosis, diabetic symptoms, and the risk of developing cardiovascular diseases. Also, DLE and MGSE mixtures administration greatly prevented oxidative stress and liver toxicity. The combined effects of DLE and MGSE mixtures were higher than effects of the single extracts and of G. cambogia, a plant known for its anti-obesity effects. In summary, these findings demonstrated that DLE and MGSE mixtures, exhibit anti-obesity activity in HFD-fed mice.