PMID: 

J Biochem Mol Toxicol. 2019 Nov 12:e22412. Epub 2019 Nov 12. PMID: 31714645

Abstract Title: 

Bisphenol A triggers the malignancy of acute myeloid leukemia cells via regulation of IL-4 and IL-6.

Abstract: 

Acute myeloid leukemia (AML) is a cancer of hematopoietic stem cells with a rapid progression. The progression of AML can be regulated by estrogenic signals. Our present data showed that an industrial endocrine-disrupting chemical, bisphenol A (BPA), can promote the proliferation of AML cells and decrease their sensitivity to daunorubicin and cytarabine treatment. Among the tested cytokines, BPA treatment can decrease the expression of interleukin-4 (IL-4) while increasing the expression of IL-6. Overexpression of IL-4 or neutralization antibody of IL-6 (anti-IL-6) can attenuate BPA-induced proliferation of AML cells and reverse BPA-suppressed chemosensitivity. Furthermore, activation of nuclear factor kappa B is essential for BPA-induced upregulation of IL-6 in AML cells. As to IL-4, BPA can increase the expression of NFAT1 to inhibit its transcription. Collectively, our data showed that BPA can trigger the malignancy of AML cells via regulation of IL-4 and IL-6.

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PMID: 

Chemosphere. 2019 Nov 6 ;243:125301. Epub 2019 Nov 6. PMID: 31726260

Abstract Title: 

Developmental programming: Prenatal bisphenol A treatment disrupts mediators of placental function in sheep.

Abstract: 

Gestational Bisphenol A (BPA) exposure is associated with low birth weight. We hypothesized that the low birth weight is the consequence of reduced placental efficiency and a function of BPA-induced inflammatory, oxidative, lipotoxic, angiogenic, steroidal and fibrotic changes involving epigenetic alterations. Placentomes were collected during early (day 65) and mid (day 90) gestation (term∼147 days) from control and BPA (gestational day 30-90)-treated pregnant sheep. BPA treatment: reduced placental efficiency and fetal weight; increased interleukin 8, lipid peroxidation marker, antioxidants, aromatase, 17 alpha-hydroxylase, estrogen receptor 2, insulin like growth factor (IGF) 2 receptor and IGF binding proteins (IGFBP), and histone deacetylase 1 and 2; reduced tumor necrosis factor alpha and IGF1 receptor at early gestation (Day 65). Gestational BPA-induced mid-gestational changes include: reduced angiogenic factor hypoxia inducible factor 1 alpha; increased IL1beta, oxidative stress markers, triglyceride, 17alpha hydroxylase, IGFBP 1, DNA methyltransferase 3 A and histone deacetylase 1. These findings indicate that gestational BPA, either acting directly or by altering steroidal input, produces early/mid-gestational-specific epigenetic changes culminating in placental disruptions at several levels, in keeping with time-specific/time-lagged pregnancy-associated changes in placental efficiency and fetal weight. The reduced early-gestational placental efficiency may be a function of increased inflammation/oxidative stress and reduced IGF bioavailability with themid-gestational restoration of placental efficiency likely driven by improved IGF bioavailability and the time-lagged response to antioxidant increase. This compensation, the result of time-lagged response to increases in negative mediators of placental function must have failed with pregnancy advancement to explain the low birthweight outcome.

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PMID: 

Afr J Tradit Complement Altern Med. 2017 ;14(3):142-146. Epub 2017 Mar 1. PMID: 28480425

Abstract Title: 

BEHAVIORAL EVIDENCE OF ANTIDEPRESSANT-LIKE ACTIVITY OFL. VAR.IN MICE.

Abstract: 

BACKGROUND: Currently-available antidepressant agents produce various adverse effects, and are expensive. At present, various plants are being evaluated for their possible role against numerous diseases, and no doubt, the role of traditional and complementary medicines in the development of effective therapy is incredible. The present study was designed to evaluate antidepressant-like activity ofL. Var.at different doses in mice.MATERIALS AND METHODS: Antidepressant potential of ethanolic extract ofL. was evaluated at three different doses 250 mg/kg, 500 mg/kg and 1000 mg/kg by using forced swim test and tail suspension test on albino male mice. The results were compared with control and standard mice groups administered with normal saline and Fluoxetine respectively. In both parameters immobility period was recorded two times during 60 days dosing.RESULTS: The ethanol extract at all three tested doses (250 mg/kg, 500 mg/kg and 1000 mg/kg) and standard fluoxetine demonstrated notable antidepressant-like activity (p

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PMID: 

Food Sci Nutr. 2019 Oct ;7(10):3327-3337. Epub 2019 Sep 9. PMID: 31660146

Abstract Title: 

Fermented black radish (L. var.) attenuates methionine and choline deficient diet-induced nonalcoholic fatty liver disease in mice.

Abstract: 

As one of the wide-ranging form of chronic liver disease, there are only limited therapeutic options for nonalcoholic fatty liver disease (NAFLD). We evaluated whether fermented black radish (L. var.; FBR) ameliorates lipid accumulation, inflammation, and hepatic fibrosis, which are characteristics of the pathogenesis of NAFLD. Fermented black radish treatment reduced lipid accumulation in 3T3-L1 adipocytes, which appeared to be associated with the downregulation of adipogenic transcription factors, including sterol regulatory element-binding protein 1c, CCAAT/enhancer-binding proteinα, peroxisome proliferator-activated receptor γ, and lipid accumulation-related genes including adipocyte protein-2 and fatty acid synthase. Administration of FBR to C57BL/6J mice challenged with methionine and choline deficient (MCD) diet significantly attenuated the increased serum levels of alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, and triglyceride. In addition, treatment with FBR interestingly repressed the hepatic inflammation induced with MCD diet, by lowering the expression of inducible nitric oxide synthase and suppressing the inactivation of macrophages and Kupffer cells in the liver. Fermented black radish was also shown to mitigate liver fibrosis through the inhibition of alpha-smooth muscle actin, transforming growth factor beta-1, and collagen type I alpha 1 chain. Our results indicate that FBR ameliorates NAFLD and its related metabolic disease by regulating multiple pathways, suggesting that FBR may be an effective dietary supplement for ameliorating NAFLD.

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PMID: 

Eur J Pharmacol. 2019 Sep 5 ;858:172483. Epub 2019 Jun 21. PMID: 31233753

Abstract Title: 

Anti-colorectal cancer biotargets and biological mechanisms of puerarin: Study of molecular networks.

Abstract: 

Based on network pharmacology analysis, this study was to uncover the anti-colorectal cancer (CRC) targets and molecular mechanisms exerted by puerarin. Pathological genes of CRC and therapeutic genes of puerarin were collected through well-established databases. The crucial targets of puerarin against CRC were further used for function and pathway enrichment assays to elucidate the biological processes and signaling pathways, followed by experiment-based verification. In network data, the most significant targets of tyrosyl-DNA phosphodiesterase-1 (TDP1), aldehyde dehydrogenase 1 family member A-1 (ALDH1A1), muscleblind like splicing regulator 1 (MBNL1), aldehyde dehydrogenase-2 (ALDH2), and nicotinamide adenine dinucleotide (HPGD) were screened and defined in anti-CRC effects exerted by puerarin. In further enrichment assays, the functional processes of puerarin against CRC were associated with energy pathways, metabolism, cell communication, signal transduction, aldehyde metabolism, DNA repair. Meanwhile, key ten signaling pathways from bioinformatic findings were ascertained respectively. As revealed in human data, CRC patients showed up-regulated expressions of endogenous TDP1, ALDH1A1, accompanied with visible hematoxylin-eosin (HE) and Ki-67 stains and elevated blood tumor marker expressions. In further study in vitro, puerarin-treated human CRC cells resulted in inhibited cell growth, increased cell apoptosis in a dose-dependent way. Further, down-regulated expressions of TDP1, ALDH1A1 and proliferating cell nuclear antigen (PCNA) were detected in puerarin-treated CRC cells. In conclusion, the molecular network data manifest the biotargets and signaling pathways of puerarin against CRC, followed by verification of both human and cell line studies. Furthermore, the pharmacological molecules of TDP1, ALDH1A1 seem to be the possible targets for managing CRC.

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PMID: 

Med Sci Monit. 2019 Aug 31 ;25:6523-6531. Epub 2019 Aug 31. PMID: 31471534

Abstract Title: 

Alleviation of Inflammatory Response of Pulmonary Fibrosis in Acute Respiratory Distress Syndrome by Puerarin via Transforming Growth Factor (TGF-β1).

Abstract: 

BACKGROUND Acute respiratory distress syndrome (ARDS) in infants is acute and progressive hypoxic respiratory failure caused by various extrapulmonary pathogenic factors besides cardiogenic factors. Diffuse alveolar injury and progression to pulmonary fibrosis are pathological features of ARDS. The present study sought to determine how puerarin influences the inflammatory response caused by pulmonary fibrosis in ARDS in infants. MATERIAL AND METHODS The human lung fibroblasts cell line HLF1 was treated with different concentrations of puerarin in different groups for various times. TGF-ß1 was overexpressed by TGF-ß1 (2 ng/mL) in routine experiments, and the treated cells and culture supernatant were collected for analysis in each step. Cell apoptosis was measured by flow cytometry, TUNEL assay, and detection of caspase 3 and Bcl-2. Cell proliferation was assessed by CCK-8 assay.Real-time PCR and Western blot assay were used to assess mRNA and protein levels of TGF-ß1 and Smad3, respectively. The related cytokines were assessed by ELISA. RESULTS Results showed that puerarin promoted the apoptosis and inhibited the proliferation of HLF1 cells. Caspase 3 was upregulated, whereas Bcl-2, TGF-ß1, and Smad3 were downregulated by puerarin. IL-1, IL-2, and IL-4, secreted by HLF1 cells, were reduced, but IL-10 showed the opposite trend. When TGF-ß1 was overexpressed, Smad3 was promoted, and IL-1, IL-2, and IL-4 was increased in HLF1 cells. Finally, overexpression of TGF-ß1 reversed the effect of puerarin in HLF1 cells. CONCLUSIONS Puerarin regulated the proliferation and apoptosis of pulmonary fibrosis cells, and affected the secretion of inflammatory cytokines. Thus, puerarin alleviated the inflammatory response resulting from pulmonary fibrosis by regulating the TGF-ß1/Smad3 pathway in infants with ARDS.

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PMID: 

BMC Complement Altern Med. 2019 Oct 15 ;19(1):269. Epub 2019 Oct 15. PMID: 31615565

Abstract Title: 

Puerarin inhibits the osteoclastogenesis by inhibiting RANKL-dependent and -independent autophagic responses.

Abstract: 

BACKGROUND: Puerarin exerts therapeutic effect on osteoporosis due to its inhibitory effect on the formation of osteoclasts. Puerarin is also widely established as an autophagy inhibitor. The study aimed to investigate the significance of autophagy in Puerarin-treated osteoclast formation.METHODS: Osteoclast precursors (OCPs) derived from bone marrow-derived macrophages (BMMs) were treated with Puerarin along with RANKL or without RANKL, and then the autophagic parameters of OCPs (including autophagic proteins, LC3 transformation, autophagosome or LC3-puncta) were observed through Western Blotting, Transmission Electron Microscopy and Immunofluorescence assays. Next, after using overexpression vectors of autophagic genes (Atg7, Atg5 and BECN1) to alter autophagy activity, OCP proliferation was measured by Ethynyl deoxyuridine (EdU) assays and Cell Counting Kit-8 (CCK-8) kit, and osteoclast differentiation was assessed by Tartrate-resistant acid phosphatase (TRAP) staining.RESULTS: The results showed that Puerarin could directly inhibit the autophagy and proliferation of OCPs. Importantly, overexpression of autophagic genes Atg5, Atg7 and BECN1 reversed Puerarin-inhibited OCP autophagy and proliferation. What's more, RANKL could promote the autography of OCPs, which was recovered by Puerarin treatment. Interestingly, different from single-Puerarin treatment, we found that in the presence of RANKL, only BECN1 overexpression significantly reversed Puerarin-inhibited osteoclast differentiation and OCP autophagy.CONCLUSION: In conclusion, Puerarin could inhibit the OCP autophagy in the presence or absence of RANKL, which blocked the OCP proliferation and osteoclast differentiation respectively. Moreover, BECN1 plays an essential role in Puerarin-inhibited osteoclastogenesis. Our study provides potential clue to further complete the intrinsic mechanism of Puerarin in treating osteoporosis.

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PMID: 

Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2019 Jul 28 ;35(4):355-358. PMID: 31701722

Abstract Title: 

[Effects of puerarin on rats with type 2 diabetes mellitus].

Abstract: 

OBJECTIVE: To investigate the therapeutic effects of puerarin on rats with type 2 diabetes mellitus (T2DM).METHODS: T2DM models were established by high fat and high glucose feeding combined with a one-time intraperitoneal injection of streptozotocin (STZ, 60 mg/kg). Then the rats were randomly divided into normal group, model group, metformin group (MET, 40 mg/kg), puerarin low-dose group, medium-dose group and high-dose group (40, 80, 160 mg/kg), n=10. After the model was successfully established, rats were treated with corresponding drug intervention by intragastrical administration for 4 weeks. The body weight and fasting blood glucose (FBG) were measured per week, and blood samples were collected 24 h after the last administration, and serum levels of blood glucose, serum triglyceride (TG), total cholesterol (TC), low-density lipoprotein-cholesterol (LDL-C), high-density lipoprotein-cholestrol (HDL-C), serum enzyme activities of aspartate aminotransferase (AST), alanine aminotransferase (ALT), blood urea nitrogen (BUN), serum creatinine (SCr), and blood uric acid (UA) were measured.RESULTS: As compared with normal group, the body weight was decreased after 4 weeks-intervention in the model group, and the levels of FBG, TC, TG, LDL-C, ALT, AST, BUN, SCr and UA were all increased,while HDL-C level was decreased (P＜0.05). As compared with model group,the body weight was increased after 4 weeks-intervention in metformin group and puerarin groups, and the levels of FBG, TC, TG, LDL-C, ALT, AST, BUN, SCr and UA were decreased (P＜0.01); meanwhile, HDL-C level was increased significantly (P＜0.05).CONCLUSION: Puerarin can reduce the weight loss of T2DM rats, decrease the blood lipid and blood glucose levels of T2DM rats, which can be used to control T2DM.

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PMID: 

Mar Pollut Bull. 2019 Nov 9:110712. Epub 2019 Nov 9. PMID: 31718860

Abstract Title: 

Can microplastics pose a threat to ocean carbon sequestration?

Abstract: 

Global climate change has attracted worldwide attention. The ocean is the largest active carbon pool on the planet and plays an important role in global climate change. However, marine plastic pollution is getting increasingly serious due to the large consumption and mismanagement of global plastics. The impact of marine plastics on ecosystem responsible for the gas exchange and circulation of marine COmay cause more greenhouse gas emissions. Consequently, in this paper, threats of marine microplastics to ocean carbon sequestration are discussed. Marine microplastics can 1) affect phytoplankton photosynthesis and growth; 2) have toxic effects on zooplankton and affect their development and reproduction; 3) affect marine biological pump; and 4) affect ocean carbon stock. Phytoplankton and zooplankton are the most important producer and consumer of the ocean. As such, clearly, further research should be needed to explore the potential scale and scope of this impact, and its underlying mechanisms.

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PMID: 

Biomed Res Int. 2019 ;2019:4516730. Epub 2019 Jul 18. PMID: 31396529

Abstract Title: 

Assessment of the Protective Effect ofagainst Aluminum-Induced Liver and Kidney Effects in Albino Rat.

Abstract: 

Background and Objectives: Environmental pollution with the different Aluminum (Al) containing compounds has been increased. Liver and kidney are two vital organs targeted by Al accumulation. The aim of this study was to assess the possible protective and curative effects ofLinn (LS) against Al-induced impairment of liver and kidney in albino rat and to explore the mechanism behind this effect.Materials and Methods: This experimental animal-based study included fifty albino rats divided into five groups, the control, LS-treated (20 mg/kg), AlCl-treated (10 mg/kg), AlClthen LS, and AlClplus LS-treated, simultaneously for 8 weeks. At the end of the experiment, hepatic and renal functions as well as the biomarkers of antioxidants activities were assessed in the serum. Both liver and kidney were dissected out and histopathologically examined.Results: This study showed that administration of AlClcaused a significant (p

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