Ginseng berry prevents alcohol-induced liver damage.

PMID: 

Int J Mol Sci. 2019 Jul 18 ;20(14). Epub 2019 Jul 18. PMID: 31323789

Abstract Title: 

Ginseng Berry Prevents Alcohol-Induced Liver Damage by Improving the Anti-Inflammatory System Damage in Mice and Quality Control of Active Compounds.

Abstract: 

The ginseng berry contains a variety of biologically active compounds and has a higher ginsenoside content than its roots. This study focused on the hepatoprotective activity of ginseng berry extract prepared by enzyme treatment (EGB) compared to the non-enzyme-treated ginseng berry extract (GB) and quality control of EGB. The feeding effect of EGB on alcohol-induced liver damage (AILD) was investigated by measuring the serum levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) compared with those of EtOH-fed mice. Furthermore, cytokine levels in the culture supernatants of EGB- or GB-treated RAW 264.7 cells were determined by enzyme-linked immunosorbent assay. The developed method was applied to the simultaneous quantification of four major ginsenosides in EGB using UPLC-QTOF/MS. Treatment with EGB at a dose of 0.5 or 1 mg/mouse significantly suppressed the AST and ALT levels in mice with AILD. Enzyme-treated ginseng berry was also found to suppress the production of inflammatory mediators like nitric oxide (NO), tumor-necrosis factor-α (TNF-α), interleukin-6 (IL-6), and prostaglandin E2 (PGE2) in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages, showing higher activity than that of GB. The amount of ginsenoside Re, F5, F3, and Rd in the EGB obtained using UPLC-QTOF/MS was 45.9, 3.3, 4.0, and 6.2 mg/g, respectively. These results suggest that EGB has a potential effect on AILD, and its hepatoprotective effect provides beneficial insights into developing new candidates for the prevention and cure of AILD. Also, this study demonstrated the utility of UPLC-QTOF/MS-based major compounds for quality control (QC) of EGB.

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Total ginsenosides extract induce autophagic cell death in NSCLC cells through activation of endoplasmic reticulum stress.

PMID: 

J Ethnopharmacol. 2019 Jul 17 ;243:112093. Epub 2019 Jul 17. PMID: 31325602

Abstract Title: 

Total ginsenosides extract induce autophagic cell death in NSCLC cells through activation of endoplasmic reticulum stress.

Abstract: 

ETHNOPHARMACOLOGICAL RELEVANCE: Ginseng (Panax ginseng C. A. Mey) has been widely used in Asian countries for thousands of years. It has auxiliary anticancer efficacy and its derived preparations (e.g. Shenmai injection) are prescribed for cancer patients as Traditional Chinese Medicines clinically in China.AIM OF THE STUDY: The involved adjuvant anticancer mechanisms of ginseng are still unknown. The present study evaluated the anti-cancer effect of total ginsenosides extract (TGS) and determined the anticancer mechanisms of TGS-induced cell death in human non-small cell lung cancer (NSCLC) cells.MATERIALS AND METHODS: The anti-cancer effect of TGS was evaluated in NSCLC by cell proliferation assay. The autophagy flux induction of TGS were tested and validated by Western blot, immunofluorescence and transmission electron microscope. The mechanisms of TGS in inducing autophagic cell death were validated by Western blot, gene knockdown and quantitative real time PCR assay.RESULTS: We found TGS could induce cell death in concentration and time dependent manners, and the cell morphology of NSCLC changed from cobblestone shape to elongated spindle shape after treated with TGS. In the study of cell autophagy, we confirm that TGS could upregulate autophagy flux and induce autophagic cell death through activation endoplasmic reticulum stress. Further investigations demonstrated this process was mediated by the ATF4-CHOP-AKT1-mTOR axis in NSCLC cells.CONCLUSION: Our findings suggested that TGS could induce autophagic cell death in NSCLC cells through activation of endoplasmic reticulum stress, disclosing another characteristic of TGS-induced cell death and a novel mechanism of TGS and its derived preparations in clinical treatment of cancer patients.

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Anti-inflammatory effect of artemisinin on uric acid-induced NLRP3 inflammasome activation.

PMID: 

Biochem Biophys Res Commun. 2019 Jul 26. Epub 2019 Jul 26. PMID: 31358323

Abstract Title: 

Anti-inflammatory effect of artemisinin on uric acid-induced NLRP3 inflammasome activation through blocking interaction between NLRP3 and NEK7.

Abstract: 

OBJECTIVE: Artemisinin is a potent anti-malarial agent that plays a potent role in regulating inflammatory disorders. NEK7 is a major interacting partner with NLRP3 in NLRP3 inflammasome. The aim of this study was to clarify the anti-inflammatory effect of artemisinin on activation of uric acid-induced NLRP3 inflammasome through regulation of NEK7.METHODS: Human macrophage U937 cells treated with lipopolysaccharide (LPS), monosodium urate (MSU) crystals, or artemisinin were used in in vitro study. Intracellular potassium (K) level was measured in U937 cells treated with and without artemisinin. Expression of target genes or proteins NEK7, NLRP3, ASC, caspase-1, interleukin-1β (IL-1β), and NF-κB signaling molecules was measured. MSU crystal-induced arthritis model was used for in vivo study.RESULTS: Gout patients showed higher NLRP3 and NEK7 mRNA expression, compared to controls. Enhanced expression of NLRP3, caspase-1, and IL-1β was noted in macrophages treated with LPS (10 ng/ml) and MSU crystals (0.1 mg/ml), which was markedly suppressed by treatment with artemisinin (1, 10, and 100 μM). Artemisinin significantly inhibited interaction between NLRP3 and NEK7 in NLRP3 inflammasome activation. Artemisinin (10 and 100 μM) attenuated intracellular Kefflux in macrophages stimulated with LPS and MSU crystals. Artemisinin suppressed foot and ankle swelling in MSU crystal-induced arthritis mice.CONCLUSION: This study revealed that artemisinin inhibited activation of NLRP3 inflammasome by suppressing interaction between NEK7 and NLRP3 in uric acid-induced inflammation.

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Electromagnetic fields have a greater influence on women with a predisposition to allergic responses who are exposed to toxic traffic emissions than women without predispostions to allergic responses.

PMID: 

Ind Health. 2000 Jul ;38(3):294-300. PMID: 10943077

Abstract Title: 

Combined effects of traffic and electromagnetic fields on the immune system of fertile atopic women.

Abstract: 

Object of this preliminary study was the immune response to high or low frequency electromagnetic fields (ELMF) of non-atopic and atopic fertile women with uniform exposure to toxic compounds produced by traffic. Women were divided in group A (non-atopic, non-exposed to ELMF); B (atopic, non-exposed to ELMF); C (non-atopic, exposed to ELMF); D (atopic, exposed to ELMF)."In vitro"cell proliferation of peripheral blood mononuclear cells (PBMC) of atopic women (groups B and D) stimulated by phytohaemoglutinin (PHA) was reduced. The ELMF exposed women (groups C and D) showed lower levels of blood NK CD16(+)-CD56+ lymphocyte subpopulations and of"in vitro"production of interferon-gamma (both spontaneously and in presence of PHA) by PBMC, suggesting that ELMF reduces blood cytotoxic activity. Serum IgE of the atopic women exposed to ELMF (group D) was higher than that of the other groups. Linear discriminant analysis including serum zinc and copper (essential enzymes for immune functions), blood lead and urinary transtrans muconic acid, a metabolite of benzene (markers of exposure to traffic) and key parameters of immune functions (CD16(+)-CD56+ lymphocyte subset, serum IgE, interferon-gamma produced by PBMC in presence of PHA, stimulation index of blastogenesis) showed absence of significant difference between groups A and C and a marked separation of groups B and D. This datum suggests that ELMF have a greater influence on atopic women exposed to traffic than on non-atopic ones.

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This study concludes that exposure of professional military personnel to anti-aircraft radars that existed in Western Europe from the 1960s until the 1990s may have resulted in an increase in the incidence of hemolymphatic cancers.

PMID: 

Int J Cancer. 2009 Feb 15 ;124(4):945-51. PMID: 19035449

Abstract Title: 

Causes of death among Belgian professional military radar operators: a 37-year retrospective cohort study.

Abstract: 

Concerns have been raised about the safety of the electromagnetic (microwave) emissions of radars, as well as about the ionizing radiation that is emitted on short distances (

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Paternal average extremely low frequency magnetic field exposure was weakly associated with neuroblastoma in offspring whereas maternal exposure was not.

PMID: 

Epidemiology. 2001 Sep ;12(5):508-17. PMID: 11505168

Abstract Title: 

Parental occupational exposures to electromagnetic fields and radiation and the incidence of neuroblastoma in offspring.

Abstract: 

We examined parental occupational exposures to electromagnetic fields and radiation and the incidence of neuroblastoma in offspring. Cases were 538 children diagnosed with neuroblastoma between 1992 and 1994 in the United States or Canada. Age-matched controls were selected by random-digit dialing. Occupational exposures to electrical equipment and radiation sources were classified by an industrial hygienist, and average exposures to extremely low frequency magnetic fields were estimated using a job exposure matrix. Maternal exposure to a broad grouping of sources that produce radiofrequency radiation was associated with an increased incidence of neuroblastoma (odds ratio = 2.8; 95% confidence interval = 0.9-8.7). Paternal exposure to battery-powered forklifts was positively associated with neuroblastoma (odds ratio = 1.6; 95% confidence interval = 0.8-3.2), as were some types of equipment that emit radiofrequency radiation (odds ratios congruent with 2.0); however, the broad groupings of sources that produce ELF fields, radiofrequency radiation, or ionizing radiation were not associated with neuroblastoma. Paternal average extremely low frequency magnetic field exposure>0.4 microTesla was weakly associated with neuroblastoma (odds ratio = 1.6; 95% confidence interval = 0.9-2.8), whereas maternal exposure was not. Overall, there was scant supportive evidence of strong associations between parental exposures in electromagnetic spectrum and neuroblastoma in offspring.

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Wogonin alleviates hyperglycemia through increased glucose entry into cells via AKT/GLUT4 pathway.

PMID: 

Curr Pharm Des. 2019 Jul 22. Epub 2019 Jul 22. PMID: 31333118

Abstract Title: 

Wogonin alleviates hyperglycemia through increased glucose entry into cells via AKT/GLUT4 pathway.

Abstract: 

Insulin resistance and type 2 Diabetes mellitus resulting in chronic hyperglycemia is a major health problem in the today modern world. Many drugs have been tested to control hyperglycemia which is believed to be main factor behind many of the diabetes related late term complications. Wogonin is a famous herbal medicine which has been shown to be effective in controlling diabetes and its complications. In our previous work we have shown that wogonin is beneficial in many ways in controlling diabetic cardiomyopathy. In this review, we have mainly explained wogonin anti-hyperglycemic property through AKT/GLUT4 pathway. Here we briefly discussed that wogonin increases Glut4 trafficking to plasma membrane which allow increased entry of glucose and thus alleviate hyperglycemia. Conclusion: Wogonin can be used as anti-diabetic and anti-hyperglycemic drug and works via AKT/GLUT4 pathway.

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This study suggests that there are no adverse auditory effects from mobile phone use, however the findings were limited by the self-reporting method used.

PMID: 

Int J Audiol. 2007 Mar ;46(3):113-8. PMID: 17365064

Abstract Title: 

Survey of mobile phone use and their chronic effects on the hearing of a student population.

Abstract: 

Mobile phone ownership and usage is now widespread and public concern has developed over possible harmful physiological effects of their use. This study aimed to investigate the prevalence of student mobile phone ownership and any possible chronic effects of usage on hearing, tinnitus and balance. Questionnaires for electronic self-completion were distributed to University of Southampton postgraduates, and 117 out of 160 returned met the criteria for analysis. A total of 94% were current mobile phone users, and only 2% had never used a mobile phone. Duration of ownership and daily usage ranged from 0-7 years and 0-45 minutes respectively. Text-messaging was more popular than talking. High or long-term users reported no worse hearing, tinnitus, or balance than low or short-term users. The results of this study confirm that the prevalence of mobile phone ownership amongst students is extremely high. However there appear to be no harmful effects of mobile phone usage on their audiovestibular systems within the range of exposure of the study, insofar as can be detected by the self-report method employed.

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Wogonin can attenuate liver fibrosis via regulating the activation and apoptosis of hepatic stellate cells.

PMID: 

Int Immunopharmacol. 2019 Aug 1 ;75:105671. Epub 2019 Aug 1. PMID: 31377590

Abstract Title: 

Wogonin attenuates liver fibrosis via regulating hepatic stellate cell activation and apoptosis.

Abstract: 

Liver fibrosis is the representative features of liver chronic inflammation and the characteristic of early cirrhosis. To date, effective therapy for liver fibrosis is lacking. Recently, Traditional Chinese Medicine (TCM) has attracted increasing attention due to its wide pharmacological effects and more uses in clinical. Wogonin, as one major active constituent of Scutellaria radix, has been reported it plays an important role in anti-inflammatory, anti-cancer, anti-viral, anti-angiogenesis, anti-oxidant and neuro-protective effects. However, the anti-fibrotic effect of wogonin is never covered in liver. In this study, we evaluated the protect effect of wogonin in liver fibrosis. Wogonin significantly attenuated liver fibrosis both in CCl-induced mice and TGF-βactivated HSCs. Meanwhile, wogonin can enhances apoptosis of TGF-βactivated HSC-T6 cell from rat and LX-2 cell from human detected by flow cytometry. Additionally, wogonin can largely enhances cle-caspase3, cle-caspase9 expression and the ratio of Bax/Bcl-2 in T6 cells. Pro-apoptosis effect of wogonin in vivo was further verified in situ. In conclusion, wogonin can attenuate liver fibrosis via regulating the activation and apoptosis of hepatic stellate cells, and may be an effective drug to treat and prevent liver fibrosis.

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