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Weifang, China

Weifang Medical University is a university based in Weifang city, Shandong province, China which offers courses in Medicine. Wikipedia.

Niu N.,Weifang Medical University
Investigative ophthalmology & visual science | Year: 2013

RPE is a key component of the blood-ocular barrier (BOB) and is equipped with immunological molecules such as toll-like receptors (TLRs) and complement receptors, which together orchestrate the innate and adaptive immunity of the eye. Immunoglobulin G (IgG) in the aqueous humor and vitreous body has traditionally been thought to be derived from serum via transcytosis across the BOB. Our previous work validated production of endogenous IgG by RPE cells locally. However, the function and role of this IgG in the intraocular immunity is poorly understood. After confirming IgG production in a human RPE cell line (ARPE-19) with immunofluorescence, in situ hybridization, and RT-PCR, we further investigated the function of endogenous IgG in RPE biology with MTS, flow cytometry, and cell invasion analysis after downregulation of IgG by siRNA. Involvement of the TLR4 pathway was also studied using Western blot, ELISA and confocal microscopy. Endogenous IgG is crucial for support of proliferation, mitosis, migration, and inhibition of apoptosis of RPE. Moreover, production of endogenous IgG by RPE is regulated by the TLR4 pathway in a concentration- and duration-dependent manner, and IgG affects the activation of the TLR4 pathway in a synergistic manner. Activation of the FcγR I pathway and production of IL-10 could be induced by IgG derived from RPE. These data suggest that endogenous IgG may be a molecule that is essential for the physiological function of RPE, and suggest IgG is important for regulating intraocular immune responses under physiologic and pathologic conditions.

Xu W.,Weifang Medical University
African journal of traditional, complementary, and alternative medicines : AJTCAM / African Networks on Ethnomedicines | Year: 2013

The objective of the paper was to study the anti-tumor effect of total glycosides from Radix paeoniae rubra in S180 tumor-bearing mice, and to preliminarily explore its mechanism of action. Mice were made into S180 solid tumor model, grouped and administered with the extracts; tumor inhibition rate was measured by harvesting the tumors, and serum IL-2 and IL-4 levels were measured by taking blood samples. Total glycosides of Radix paeoniae rubra significantly inhibited the growth of tumor cells in tumor-bearing organisms, enhanced the cytotoxic activity of NK cells, and increased the serum IL-2 and IL-4 levels. Total glycosides of Radix paeoniae rubra have some anti-tumor effect in vivo, which might have been accomplished through the regulation of the immune system.

Lin W.,Weifang Medical University | Tongyi S.,Weifang Medical University
Tumor Biology | Year: 2014

Green tea polyphenol (GTP) is one of the most promising chemopreventive agent for cancer; it can inhibit cancer cell proliferation and induce apoptosis through p53-dependent cell signaling pathways. Unfortunately, many tumor cells lack the functional p53, and little is known about the effect of GTP on the p53-deficient/mutant cancer cells. To understand the p53-independent mechanisms in GTP-treated p53-dificient/mutant cancer cells, we have now examined GTP-induced cytotoxicity in human hepatoma Hep3B cells (p53-deficient). The results showed that GTP could induce Bax and Bak activation, cytochrome c release, caspase activation, and necroptosis of Hep3B cells. Bax and Bak, two key molecules of mitochondrial permeability transition pore (MPTP), were interdependently activated by GTP, with translocation and homo-oligomerization on the mitochondria. Bax and Bak induce cytochrome c release. Importantly, cytochrome c release and necroptosis were diminished in Hep3B cells (Bax−/−) and Hep3B cells (Bak−/−). Furthermore, overexpression of Bcl-2 could ameliorate GTP-induced cytochrome c release and necroptosis. Together, the findings suggested that GTP-induced necroptosis was modulated by the p53-independent pathway, which was related to the translocation of Bax and Bak to mitochondria, release of cytochrome c, and activation of caspases. © 2014, International Society of Oncology and BioMarkers (ISOBM).

Zeng H.,Capital Medical University | Ding M.,Weifang Medical University | Chen X.-X.,Weifang Medical University | Lu Q.,Capital Medical University
Neuroscience | Year: 2014

Accumulating evidence supports that nicotinamide adenine dinucleotide phosphate (NADPH) oxidase contributes to microglia-mediated neurotoxicity in the CNS neurodegenerative diseases. Several studies, including ours, suggest that microglial activation is involved in the retinal degeneration in the animal models of retinitis pigmentosa (RP). In the present study, we investigated the activation of NADPH oxidase in the rod degeneration in rd mice and further explored its role in the microglia-mediated photoreceptor apoptosis. Expression of gp91phox protein, a major subunit of NAPDH oxidase in the whole retina of rd mice at postnatal days (P) 8, 10, 12, 14, 16 and 18 was assessed by western blot analysis. Location of gp91phox in the rd retina at each age group and its cellular source were studied by immunohistochemical analysis and double labeling respectively. The generation of superoxide radicals in the rd retinas was demonstrated by intraperitoneal injection of hydroethidine. Apocynin was applied intraperitoneally in the rd mice from P8 to P14 to inhibit the activity of NAPDH oxidase and the outer nuclear layer (ONL) thickness was measured before and after apocynin treatment. Our results demonstrated that during the rod degenerative process, the expression of gp91phox started to increase in the outer part of rd retina at P10 and reached a peak at P14. Double labeling of gp91phox with CD11b showed co-localization of gp91phox in the retinal microglial cells. Increasing generation of superoxide radicals visualized by hydroethidine was noted at P8 and reached a peak at P14. Apocynin markedly reduced the production of superoxide radicals and preserved the rod cells. The results suggested that NADPH oxidase might play an important role in the rod degeneration in the rd mice. Inhibition of NAPDH oxidase could be a possible approach to treat RP in the early degenerative stage. © 2014 IBRO.

Sheng J.,Weifang Medical University | Sun Y.,Weifang Medical University
Carbohydrate Polymers | Year: 2014

Different molecular weight polysaccharides were prepared by degradation of polysaccharides extracted from Athyrium multidentatum (Doll.) Ching rhizome (CPA) with hydrogen peroxide and ascorbic acid. Four low molecular polysaccharides derivatives (CPA-1, CPA-2, CPA-3 and CPA-4) were successfully obtained and had their antioxidant activities investigated employing various established in vitro systems. All CPA derivatives showed pronounced antioxidant activity, and had stronger antioxidant ability than CPA in certain tests. CPA-1 exhibited the strongest scavenging ability on 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical among all samples, and the IC50 value was 25 μg/mL. CPA-2 possessed the highest scavenging ability against superoxide radical at 200 μg/mL. The scavenging activity of CPA-4 on hydroxyl radical was higher than CPA from 120 to 200 μg/mL. The mechanism on influence the antioxidant activity of CPA and its degraded derivatives was indicated. © 2014 Elsevier Ltd.

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