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Agent for RNA extraction and QuantiTect SYBR Green PCR Mix were obtained from Qiagen, Inc (Valencia, CA). The AMV 1st Strand cDNAPostnatal day 3 (P3) Long Evans rat pups (mean body weight 10 g) were given 3 alternate day intra-peritoneal (i.p.) injections of 20 g NDEA or vehicle. Upon weaning, male rats (N = 8-10 per group) were pair-fed for 8 weeks with high fat (HFD) or low fat (LFD) chow diets.
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Xidative stress and neurodegeneration. Cerebellar protein homogenates were used to measure (A) GSK-3b; (B) phospho (p)-GSK-3b; (C) GFAP; (D) GAPDH; (E) HNE; (F) malondialdehyde, MDA; (G) Nitrotyrosine, N-TYR; or (H) b-Actin; by direct binding ELISA. Immunoreactivity was detected with HRP-conjugated secondary antibody and Amplex Red soluble fluorophor. Fluorescence light units (FLU) were measured (
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Ative stress with lipid peroxidation, as occur in AD. The finding that chronic HFD feeding did not significantly alter tau or AbPP expression also supports our previous conclusion that HFD feeding contributes to, but is not sufficient to cause AD-type neurodegeneration [45,46]. The combined effect of early, limited NDEA exposure plus chronic HFD feeding significantly reduced insulin and ChAT mRNA
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Ysiol Cell Physiol. 2012;302(2):C383?91. 68. Sachdev U, Cui X, Hong G, Namkoong S, Karlsson JM, Baty CJ, et al. High mobility group box 1 promotes endothelial cell angiogenic behavior in vitro and improves muscle perfusion in vivo in response to ischemic injury. J Vasc Surg. 2012;55(1):180?1.Yang et al. Cell Bioscience (2015) 5:Page 10 of69. Kang R, Livesey KM, Zeh HJ, Loze MT, Tang D. HMGB1: a
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D (Ex 579 nm/Em 595 nm) in a Spectromax M5, and results were normalized to sample protein content in the wells. Box plots depict mean, range ?S.D. of results (N = 8-10/group). Inter-group comparisons were made using ANOVA with the post-hoc Bonferroni multiple comparisons test of significance. Significant P-values are indicated within the panels.Tong et al. BMC Endocrine Disorders 2010, 10:4 http:/
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Xidative stress and neurodegeneration. Cerebellar protein homogenates were used to measure (A) GSK-3b; (B) phospho (p)-GSK-3b; (C) GFAP; (D) GAPDH; (E) HNE; (F) malondialdehyde, MDA; (G) Nitrotyrosine, N-TYR; or (H) b-Actin; by direct binding ELISA. Immunoreactivity was detected with HRP-conjugated secondary antibody and Amplex Red soluble fluorophor. Fluorescence light units (FLU) were measured (
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E formation of DNA and protein adducts [105-107] that can serve as persistent sources of oxidative stress, and cause further DNA damage and protein dysfunction. Recently, we demonstrated a role for ceramidemediated neurodegeneration in a model of diet-induced obesity with T2DM [45], and showed that in vitro ceramide exposure causes neurodegeneration with impairments in neuronal viability, energy m
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Ration have soared over the past several decades, suggesting that exposures rather than genetics dictate their etiologies. Our over-arching hypothesis is that shifts in lifestyles and economics have led us to chronically consume excess fat, and get exposed to agents that cause insulin resistance. Consideration given to potential pathogenic agents was focused by the experimental evidence showing th