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Author

June Zhang

Bio: June Zhang is an academic researcher from Jiangxi Normal University. The author has contributed to research in topics: Zebrafish & Apoptosis. The author has an hindex of 3, co-authored 6 publications receiving 31 citations.

Papers
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Journal ArticleDOI
TL;DR: Investigation of the toxic effects and molecular mechanisms of GO exposure in larval and adult zebrafish embryos and pharmacological activation of PPAR-α expression demonstrated that GO induced hepatic dysfunction mainly through the ROS and PPar-α mediated innate immune signaling in zebra fish.
Abstract: Graphene oxide (GO) is an increasingly important nanomaterial that exhibits great promise in the area of bionanotechnology and nanobiomedicine. However, the toxic effects of GO on the vertebrate developmental system are still poorly understood. Here, we aimed to investigate the toxic effects and molecular mechanisms of GO exposure in larval and adult zebrafish. The results showed that the major hepatotoxic phenotype induced by GO in zebrafish embryos was a significant decrease in liver area and a dose-dependent decrease in the hepatocytes. Moreover, the number of macrophages and neutrophils in zebrafish embryos were reduced but the expressions of pro-inflammatory cytokines were increased after GO treatment. High through-put RNA-Seq identified 314 differentially expressed genes (DEGs) in GO-induced zebrafish embryos including 192 up-regulated and 122 down-regulated. KEGG and GO functional analysis revealed that steroid hormone biosynthesis, lipoprotein metabolic process, and PPAR signaling pathway were significantly enriched. Most of the lipid metabolism genes were down-regulated while majority of the immune genes were up-regulated after GO treatment. Moreover, GO induced NF-κB p65 into the nucleus and increased the protein levels of NF-κB p65, JAK2, STAT3, and Bcl2 in adult zebrafish liver. In addition, pharmacological experiments showed that inhibition of ROS and blocking the MAPK signaling could rescue the hepatotoxic phenotypes induced by GO exposure. On the contrary, pharmacological activation of PPAR-α expression have increased the hepatotoxic effects in GO-induced larval and adult zebrafish. Taken together, these informations demonstrated that GO induced hepatic dysfunction mainly through the ROS and PPAR-α mediated innate immune signaling in zebrafish.

23 citations

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TL;DR: It is suggested that SPEE had an important role in the antioxidant and anti-inflammatory effects in zebrafish and some of the components identified may be served as potential sources of new hepatoprotective compounds for the treatment of inflammatory diseases.

21 citations

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TL;DR: In this article, the effects of baicalein on liver development and its anti-inflammatory effects in zebrafish larvae were investigated and the results showed that baicalin has significant anti-embryonic developmental toxicity and significant antioxidant and antiinflammatory capabilities.

20 citations

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TL;DR: In this paper, the authors evaluated whether quercetin can prevent TAA-induced inflammation and liver damage in zebrafish larvae and investigated the molecular mechanisms involved, finding that quercETin has anti-inflammatory, antioxidant, and liver-protective effects.
Abstract: Quercetin is a flavonoid compound with a variety of biological properties that is widely distributed throughout the plant kingdom. Studies have found that quercetin has anti-inflammatory, antioxidant, and liver-protective effects, while thioacetamide (TAA) can cause inflammation and liver damage in zebrafish larvae. The purpose of this study was to evaluate whether quercetin can prevent TAA-induced inflammation and liver damage in zebrafish larvae and to investigate the molecular mechanisms involved. Zebrafish Tg transgenic lines were used as the experimental animals. Behavioral, oxidative stress level, proliferative antigen chromogenic antibody, and western blot analyses were carried out on zebrafish larvae in the control group and groups treated with TAA and 12 μM quercetin. The results indicated that quercetin promoted the development of zebrafish larvae damaged by TAA, exhibited antioxidant and anti-inflammatory properties, and promoted cell proliferation. Quercetin reduced the expression of p53 protein in zebrafish larvae injured by TAA, resulting in decreased levels of Bax and increased levels of Bcl-2. The findings suggested quercetin has antiapoptotic action. Quercetin reduced the expression of DKK1 and DKK2 genes related to the Wnt signaling pathway in zebrafish larvae damaged by TAA and increased the expression of Lef1 and wnt2bb. Quercetin may regulate the development of zebrafish larvae damaged by TAA through the Wnt signaling pathway. This study provides the scientific basis for the development and utilization of quercetin and the development of new related drugs.

10 citations

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TL;DR: Zhang et al. as discussed by the authors investigated the function of chlorogenic acid in the hepatic development in thioacetamide (TAA)-induced zebrafish embryos, and found that CGA exerted certain beneficial effects on zebra fish larvae from TAA-exposed ZEB embryos, such as increasing liver size, body length, heart rate, acetylcholinesterase activity, and motor ability.

4 citations


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Journal ArticleDOI
TL;DR: This review paper has primarily focused on the toxic effects of graphene and GO caused on aquatic invertebrates and fish (cell line and organisms) and aims to point out the current understanding and knowledge gaps of grapheneand GO toxicity.
Abstract: Graphene and its oxide are nanomaterials considered currently to be very promising because of their great potential applications in various industries. The exceptional physiochemical properties of graphene, particularly thermal conductivity, electron mobility, high surface area, and mechanical strength, promise development of novel or enhanced technologies in industries. The diverse applications of graphene and graphene oxide (GO) include energy storage, sensors, generators, light processing, electronics, and targeted drug delivery. However, the extensive use and exposure to graphene and GO might pose a great threat to living organisms and ultimately to human health. The toxicity data of graphene and GO is still insufficient to point out its side effects to different living organisms. Their accumulation in the aquatic environment might create complex problems in aquatic food chains and aquatic habitats leading to debilitating health effects in humans. The potential toxic effects of graphene and GO are not fully understood. However, they have been reported to cause agglomeration, long-term persistence, and toxic effects penetrating cell membrane and interacting with cellular components. In this review paper, we have primarily focused on the toxic effects of graphene and GO caused on aquatic invertebrates and fish (cell line and organisms). Here, we aim to point out the current understanding and knowledge gaps of graphene and GO toxicity.

45 citations

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TL;DR: Diverse interactions of NMs with the liver are reviewed, specifically on major liver cell types including Kupffer cells (KCs), liver sinusoidal endothelial cells (LSECs), hepatic stellate cells (HSCs), and hepatocytes as well as the detailed molecular mechanisms involved.
Abstract: Nanomaterials (NMs) are widely used in commercial and medical products, such as cosmetics, vaccines, and drug carriers. Exposure to NMs via various routes such as dermal, inhalation, and ingestion has been shown to gain access to the systemic circulation, resulting in the accumulation of NMs in the liver. The unique organ structures and blood flow features facilitate the liver sequestration of NMs, which may cause adverse effects in the liver. Currently, most in vivo studies are focused on NMs accumulation at the organ level and evaluation of the gross changes in liver structure and functions, however, cell‐type‐specific uptake and responses, as well as the molecular mechanisms at cellular levels leading to effects at organ levels are lagging. Herein, the authors systematically review diverse interactions of NMs with the liver, specifically on major liver cell types including Kupffer cells (KCs), liver sinusoidal endothelial cells (LSECs), hepatic stellate cells (HSCs), and hepatocytes as well as the detailed molecular mechanisms involved. In addition, the knowledge gained on nano‐liver interactions that can facilitate the development of safer nanoproducts and nanomedicine is also reviewed.

35 citations

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TL;DR: In this article, the authors focus on graphene-based nanomaterials as, in addition to modulating nanotopography, elastic modulus and viscoelastic features of the scaffold, they can also regulate its conductivity.
Abstract: Leading-edge regenerative medicine can take advantage of improved knowledge of key roles played, both in stem cell fate determination and in cell growth/differentiation, by mechano-transduction and other physicochemical stimuli from the tissue environment This prompted advanced nanomaterials research to provide tissue engineers with next-generation scaffolds consisting of smart nanocomposites and/or hydrogels with nanofillers, where balanced combinations of specific matrices and nanomaterials can mediate and finely tune such stimuli and cues In this review, we focus on graphene-based nanomaterials as, in addition to modulating nanotopography, elastic modulus and viscoelastic features of the scaffold, they can also regulate its conductivity This feature is crucial to the determination and differentiation of some cell lineages and is of special interest to neural regenerative medicine Hereafter we depict relevant properties of such nanofillers, illustrate how problems related to their eventual cytotoxicity are solved via enhanced synthesis, purification and derivatization protocols, and finally provide examples of successful applications in regenerative medicine on a number of tissues

33 citations

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TL;DR: Exposure of zebrafish embryos to GO-COOH specifically induced neurodevelopmental abnormalities and altered tendency of locomotor in larval fish and it was found that Parkinson's disease-related genes' expression were disordered after GO- COOH treatment.

31 citations

Journal Article
TL;DR: The effects of baicalin, baicalein, and LR-JB3 on attenuating the virulence of H. pylori infections are revealed.
Abstract: Helicobacter pylori infection is associated with chronic gastritis, peptic ulcers, and gastric cancer. The flavonoid compounds baicalin and baicalein found in many medicinal plants exhibit an anti-inflammatory effect. The administration of Lactobacillus strains reducing the risk of H. pylori infection is well accepted. In this study, the therapeutic effects against H. pylori infection of baicalin, baicalein, and L. rhamnosus JB3 (LR-JB3), isolated from a dairy product, were investigated. Compared to baicalin, baicalein exhibited stronger anti-H. pylori activity and cytotoxicity on human gastric cancer epithelial AGS cells. Baicalin and baicalein both suppressed the vacA gene expression of H. pylori and interfered with the adhesion and invasion ability of H. pylori to AGS cells, as well as decreased H. pylori-induced interleukin (IL)-8 expression. In the mice infection model, high dosages of baicalin and baicalein inhibited H. pylori growth in the mice stomachs. Serum IL-1β levels and H. pylori-specific serum IgM and IgA levels in mice treated with baicalin and baicalein were decreased. Moreover, a synergistic therapeutic effect of baicalein and LR-JB3 on eradicating H. pylori infections was observed. Thus, administrating baicalin, baicalein, or LR-JB3 for an H. pylori infection could offer similar therapeutic effects to administering antibiotics while not disturbing the balance of gut microbiota. This study revealed the effects of baicalin, baicalein, and LR-JB3 on attenuating the virulence of H. pylori. The synergistic effect with baicalein and LR-JB3 provides the experimental rationale for testing the reliability, safety, and efficacy of this approach in higher animals and perhaps ultimately in humans to eradicate H. pylori infections. PRACTICAL APPLICATION: Baicalin and baicalein exert health promotion and avoidance of H. pylori infections by interfering with H. pylori growth and virulence. Lactobacillus rhamnosus JB3 was used to reduce the gastric inflammation caused by H. pylori infection.

25 citations