The Experts below are selected from a list of 735 Experts worldwide ranked by ideXlab platform
Jiao Sun - One of the best experts on this subject based on the ideXlab platform.
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sio2 nanoparticle induced impairment of mitochondrial energy metabolism in hepatocytes directly and through a kupffer cell mediated pathway in vitro
International Journal of Nanomedicine, 2014Co-Authors: Yang Xue, Qingqing Chen, Tingting Ding, Jiao SunAbstract:The liver has been shown to be a primary target organ for SiO2 nanoparticles in vivo, and may be highly susceptible to damage by these nanoparticles. However, until now, research focusing on the potential toxic effects of SiO2 nanoparticles on mitochondria-associated energy metabolism in hepatocytes has been lacking. In this work, SiO2 nanoparticles 20 nm in diameter were evaluated for their ability to induce dysfunction of mitochondrial energy metabolism. First, a Buffalo Rat liver (BRL) cell line was directly exposed to SiO2 nanoparticles, which induced cytotoxicity and mitochondrial damage accompanied by decreases in mitochondrial dehydrogenase activity, mitochondrial membrane potential, enzymatic expression in the Krebs cycle, and activity of the mitochondrial respiRatory chain complexes I, III and IV. Second, the role of Rat-derived Kupffer cells was evaluated. The supernatants from Kupffer cells treated with SiO2 nanoparticles were transferred to stimulate BRL cells. We observed that SiO2 nanoparticles had the ability to activate Kupffer cells, leading to release of tumor necrosis factor-α, nitric oxide, and reactive oxygen species from these cells and subsequently to inhibition of mitochondrial respiRatory chain complex I activity in BRL cells.
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kupffer cell mediated hepatic injury induced by silica nanoparticles in vitro and in vivo
International Journal of Nanomedicine, 2013Co-Authors: Qingqing Chen, Yang Xue, Jiao SunAbstract:Silica nanoparticles (SiO2 NPs) have been shown to exert cytotoxic effects in hepato-cytes and to cause liver injury. In the liver, Kupffer cells (KCs), as the resident macrophages, play an important role in the normal physiology and homeostasis of the liver. Nevertheless, few studies have attempted to clarify the role of KCs in hepatic injury induced by SiO2 NPs. In this study, we treated Buffalo Rat liver (BRL) cells with the supernatants of SiO2 NP-stimulated KCs to determine KC-mediated hepatotoxicity and its underlying preliminary mechanism. We also examined the response of KCs and liver injury in vivo after the administRation of SiO2 NPs. The results showed that KCs stimulated by SiO2 NPs release large amounts of reactive oxygen species, tumor necrosis factor-α and nitric oxide. After BRL cells were cultured with the supernatants of SiO2 NP-stimulated KCs, the viability of BRL cells was reduced, and increases in aspartate aminotransferase and lactate dehydrogenase leakage were observed. Exposure to SiO2 NPs in vivo caused KC hyperplasia, hepatic inflammation, and oxidative stress, which led to changes in the biochemical composition of the liver. These data suggest that SiO2 NPs activate KCs to mediate hepatic injury and that the preliminary mechanism involves the release of bioactive substances from KCs.
Feng Zhang - One of the best experts on this subject based on the ideXlab platform.
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galangin alleviates liver ischemia reperfusion injury in a Rat model by mediating the pi3k akt pathway
Cellular Physiology and Biochemistry, 2018Co-Authors: Yang Li, Liquan Tong, Jingyan Zhang, Yafeng Zhang, Feng ZhangAbstract:Background/Aims: Liver ischemia-reperfusion (I/R) injury is a pathological process that often occurs during liver and trauma surgery. There are numerous causes of liver I/R injury, but the mechanism is unknown. Galangin (GA) is a flavonoid, a polyphenolic compound widely distributed in medicinal herbs that has anti-inflammatory, antioxidant, and antitumor activity. This study evaluated the protective effect of GA on hepatic I/R injury. Methods: An I/R model was created in male Wistar Rats by clamping the hepatoportal vein, hepatic artery and hepatic duct for 30 min followed by reperfusion for 2 h. A hypoxia/restoRation (H/R) model was established in Buffalo Rat liver (BRL) cells by hypoxia for 4 h followed by normoxic conditions for 10 h. The extent of liver injury was assayed by serum ALT/AST, hepatic histology, and MPO activity. Oxidative stress was assayed by serum superoxide dismutase (SOD), catalase (CAT), glutathione (GSH) and malondialdehyde (MDA). Expression of apoptosis-related proteins in BRL cells was assayed in western blots. Expression of AKT and p-AKT proteins in vivo and vitro were assayed in western blots. Results: GA significantly decreased ALT/AST expression, reversed changes in oxidative stress markers induced by I/R, and mediated caspase-3 activity expression of apoptosis-related proteins in vivo and in vitro. Methylthiazol tetrazolium (MTT) assay, flow cytometry, and Hoechst 33258 staining confirmed that GA inhibited apoptosis of BRL cells. GA also increased the expression of phosphorylated AKT after H/R. Conclusion: GA reduced liver I/R injury both in vivo and vitro and inhibited BRL cell apoptosis. PI3K/AKT signaling have been involved. GA may protect against liver I/R and be a potential therapeutic candidate.
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Carvacrol Alleviates Ischemia Reperfusion Injury by Regulating the PI3K-Akt Pathway in Rats
2016Co-Authors: Lida Suo, Kai Kang, Xun Wang, Yonggang Cao, Haifeng Zhao, Xueying Sun, Liquan Tong, Feng ZhangAbstract:Background: Liver ischemia reperfusion (I/R) injury is a common pathophysiological process in many clinical settings. Carvacrol, a food additive commonly used in essential oils, has displayed antimicrobials, antitumor and antidepressant-like activities. In the present study, we investigated the protective effects of carvacrol on I/R injury in the Wistar Rat livers and an in vitro hypoxia/restoRation (H/R) model. Methods: The hepatoportal vein, hepatic arterial and hepatic duct of Wistar Rats were isolated and clamped for 30 min, followed by a 2 h reperfusion. Buffalo Rat liver (BRL) cells were incubated under hypoxia for 4 h, followed normoxic conditions for 10 h to establish the H/R model in vitro. Liver injury was evaluated by measuring serum levels of alanine aminotransferase (ALT) and aspatate aminotransferase (AST), and hepatic levels of superoxide dismutase (SOD), catalase (CAT), glutathione (GSH) and malondiadehyde (MDA), and hepatic histology and TUNEL staining. MTT assay, flow cytometric analysis and Hoechst 33258 staining were used to evaluate the prolifeRation and apoptosis of BRL cells in vitro. Protein expression was examined by Western Blot analysis. Results: Carvacrol protected against I/R-induced liver damage, evidenced by significantly reducing the serum levels of ALT and AST, histological alteRations and apoptosis of liver cells in I/R Rats. Carvacrol exhibited anti-oxidative activity in the I/R Rats, reflected by significantly reducing the activity of SOD and the content of MDA, and restoring the activity of CAT and th
Qingqing Chen - One of the best experts on this subject based on the ideXlab platform.
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sio2 nanoparticle induced impairment of mitochondrial energy metabolism in hepatocytes directly and through a kupffer cell mediated pathway in vitro
International Journal of Nanomedicine, 2014Co-Authors: Yang Xue, Qingqing Chen, Tingting Ding, Jiao SunAbstract:The liver has been shown to be a primary target organ for SiO2 nanoparticles in vivo, and may be highly susceptible to damage by these nanoparticles. However, until now, research focusing on the potential toxic effects of SiO2 nanoparticles on mitochondria-associated energy metabolism in hepatocytes has been lacking. In this work, SiO2 nanoparticles 20 nm in diameter were evaluated for their ability to induce dysfunction of mitochondrial energy metabolism. First, a Buffalo Rat liver (BRL) cell line was directly exposed to SiO2 nanoparticles, which induced cytotoxicity and mitochondrial damage accompanied by decreases in mitochondrial dehydrogenase activity, mitochondrial membrane potential, enzymatic expression in the Krebs cycle, and activity of the mitochondrial respiRatory chain complexes I, III and IV. Second, the role of Rat-derived Kupffer cells was evaluated. The supernatants from Kupffer cells treated with SiO2 nanoparticles were transferred to stimulate BRL cells. We observed that SiO2 nanoparticles had the ability to activate Kupffer cells, leading to release of tumor necrosis factor-α, nitric oxide, and reactive oxygen species from these cells and subsequently to inhibition of mitochondrial respiRatory chain complex I activity in BRL cells.
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kupffer cell mediated hepatic injury induced by silica nanoparticles in vitro and in vivo
International Journal of Nanomedicine, 2013Co-Authors: Qingqing Chen, Yang Xue, Jiao SunAbstract:Silica nanoparticles (SiO2 NPs) have been shown to exert cytotoxic effects in hepato-cytes and to cause liver injury. In the liver, Kupffer cells (KCs), as the resident macrophages, play an important role in the normal physiology and homeostasis of the liver. Nevertheless, few studies have attempted to clarify the role of KCs in hepatic injury induced by SiO2 NPs. In this study, we treated Buffalo Rat liver (BRL) cells with the supernatants of SiO2 NP-stimulated KCs to determine KC-mediated hepatotoxicity and its underlying preliminary mechanism. We also examined the response of KCs and liver injury in vivo after the administRation of SiO2 NPs. The results showed that KCs stimulated by SiO2 NPs release large amounts of reactive oxygen species, tumor necrosis factor-α and nitric oxide. After BRL cells were cultured with the supernatants of SiO2 NP-stimulated KCs, the viability of BRL cells was reduced, and increases in aspartate aminotransferase and lactate dehydrogenase leakage were observed. Exposure to SiO2 NPs in vivo caused KC hyperplasia, hepatic inflammation, and oxidative stress, which led to changes in the biochemical composition of the liver. These data suggest that SiO2 NPs activate KCs to mediate hepatic injury and that the preliminary mechanism involves the release of bioactive substances from KCs.
K C Worrilow - One of the best experts on this subject based on the ideXlab platform.
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co culture with assisted hatching of human embryos using Buffalo Rat liver cells
Human Reproduction, 1998Co-Authors: Wayne S Maxson, David I Hoffman, Julie Dupre, Steve Ory, Sue Eager, K C WorrilowAbstract:Commercially obtained Buffalo Rat liver (BRL) cells were grown in monolayer culture. The effect of BRL cell co-culture with assisted hatching on embryo development, implantation and pregnancy was investigated in a population of 200 'first-time' in-vitro fertilization (IVF) patients, subdivided into three groups according to the methods of fertilization [IVF; intracytoplasmic sperm injection (ICSI); ICSI/IVF]. Assisted hatching was performed on all embryos chosen for transfer. Following co-culture, the overall embryo quality, implantation Rate and pregnancy Rates were not significantly different from the controls. However, when grouped according to fertilization method, co-culture was found to have an impact on pregnancy and implantation Rates in the group undergoing conventional IVF. Using co-culture with assisted hatching, we were able to achieve a 58% (38/65) clinical pregnancy Rate with a 49% (32/65) live birth Rate and a 26% (60/235) implantation Rate. No changes in the pregnancy and implantation Rates were apparent in ICSI or ICSI/IVF subgroups. This is the first prospective, randomly controlled study which reports the use of BRL cell co-culture for human IVF for a large number of patients undergoing IVF for the first time.
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growth factor expression by human oviduct and Buffalo Rat liver coculture cells
Fertility and Sterility, 1997Co-Authors: Larry I Barmat, K C Worrilow, Barbara V PayntonAbstract:Abstract Objective: To characterize growth factor gene expression by passaged coculture cell lines demonstRated to enhance in vitro pre-embryo growth. Design: Ribonucleic acids isolated from the isthmus, ampullary, and fimbriae portions of the human oviduct, and from Buffalo Rat liver cell monolayers were subjected to Northern analysis using probes for growth factors. Setting: Academic tertiary care hospital. Patient(s): Two reproductive age women undergoing a hysterectomy and bilateral salpingectomy for benign gynecologic conditions consented to experimental use of their oviducts. Intervention(s): Cell cultures were established from fresh human oviduct segments and commercially purchased Buffalo Rat liver cells. After two passages, total RNA was isolated from these confluent monolayers, fractionated on denaturing agarose gels, transferred to nylon membranes, and analyzed by Northern hybridization using complementary DNAs from epidermal growth factor (EGF), stem cell factor, also known as Kit-ligand, colony-stimulating factor-1 (CSF), leukemia inhibitory factor, and interleukin-6 (IL-6). Radioactively labeled probes were prepared by in vitro transcription or by 5' end labeling. After hybridization, blots were washed at increasing strigencies to remove nonspecifically bound radioactivity and subjected to autoradiography. Result(s): Human oviduct coculture cells express EGF (kit-ligand), CSF, leukemia inhibitory factor, and IL-6. Buffalo Rat liver cells contain the messenger RNA transcripts for kit-ligand and CSF. Conclusion(s): Human oviduct and Buffalo Rat liver coculture cells express specific growth factors. These results support the theory that coculture systems may enhance pre-embryo growth via the production of embryotrophic factors. The identification of these ligands may provide the Rationale for selecting specific growth factors for media supplementation as well as contribute to our understanding of the general mechanisms involved in regulating early embryonic growth and development.
Yang Xue - One of the best experts on this subject based on the ideXlab platform.
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sio2 nanoparticle induced impairment of mitochondrial energy metabolism in hepatocytes directly and through a kupffer cell mediated pathway in vitro
International Journal of Nanomedicine, 2014Co-Authors: Yang Xue, Qingqing Chen, Tingting Ding, Jiao SunAbstract:The liver has been shown to be a primary target organ for SiO2 nanoparticles in vivo, and may be highly susceptible to damage by these nanoparticles. However, until now, research focusing on the potential toxic effects of SiO2 nanoparticles on mitochondria-associated energy metabolism in hepatocytes has been lacking. In this work, SiO2 nanoparticles 20 nm in diameter were evaluated for their ability to induce dysfunction of mitochondrial energy metabolism. First, a Buffalo Rat liver (BRL) cell line was directly exposed to SiO2 nanoparticles, which induced cytotoxicity and mitochondrial damage accompanied by decreases in mitochondrial dehydrogenase activity, mitochondrial membrane potential, enzymatic expression in the Krebs cycle, and activity of the mitochondrial respiRatory chain complexes I, III and IV. Second, the role of Rat-derived Kupffer cells was evaluated. The supernatants from Kupffer cells treated with SiO2 nanoparticles were transferred to stimulate BRL cells. We observed that SiO2 nanoparticles had the ability to activate Kupffer cells, leading to release of tumor necrosis factor-α, nitric oxide, and reactive oxygen species from these cells and subsequently to inhibition of mitochondrial respiRatory chain complex I activity in BRL cells.
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kupffer cell mediated hepatic injury induced by silica nanoparticles in vitro and in vivo
International Journal of Nanomedicine, 2013Co-Authors: Qingqing Chen, Yang Xue, Jiao SunAbstract:Silica nanoparticles (SiO2 NPs) have been shown to exert cytotoxic effects in hepato-cytes and to cause liver injury. In the liver, Kupffer cells (KCs), as the resident macrophages, play an important role in the normal physiology and homeostasis of the liver. Nevertheless, few studies have attempted to clarify the role of KCs in hepatic injury induced by SiO2 NPs. In this study, we treated Buffalo Rat liver (BRL) cells with the supernatants of SiO2 NP-stimulated KCs to determine KC-mediated hepatotoxicity and its underlying preliminary mechanism. We also examined the response of KCs and liver injury in vivo after the administRation of SiO2 NPs. The results showed that KCs stimulated by SiO2 NPs release large amounts of reactive oxygen species, tumor necrosis factor-α and nitric oxide. After BRL cells were cultured with the supernatants of SiO2 NP-stimulated KCs, the viability of BRL cells was reduced, and increases in aspartate aminotransferase and lactate dehydrogenase leakage were observed. Exposure to SiO2 NPs in vivo caused KC hyperplasia, hepatic inflammation, and oxidative stress, which led to changes in the biochemical composition of the liver. These data suggest that SiO2 NPs activate KCs to mediate hepatic injury and that the preliminary mechanism involves the release of bioactive substances from KCs.
