Appearance of proteomics technology can fleetly filt and reveal specificity biomarkers of disease, this will help to reveal the pathogenesis of femur head necrosis and help early diagnosis, find more effective methods and therapeutic targets. At present, they are hot spots that find out the occurred mechanism,related proteins of early diagnosis and early treatment and its functional identification; set up the early related database; optimize the protein extraction methods for research of femur head necrosis. This article reviews the application of study technology of related proteins of femur head necrosis on bone tissue, serum,related animal model,and in order to provide further research ideas.
Early Diagnosis ; Femur Head Necrosis ; diagnosis ; metabolism ; Humans ; Proteomics ; methods

Thirty-six cases of necrotizing lymphadenitis--including 33 cases of unknown etiology, 1 typhoid lymphadenopathy, and 2 cases of suspicious lupus lymphadenopathy--were clinico-pathologically reviewed and analyzed with immunostaining for s-100 and lysozyme. All cases histologically showed architectural effacement by paracortical lesions composed of nuclear karyorrhexis and mononuclear cell proliferation. Immunohistochemical study revealed proliferation of lysozyme-positive macrophages in the necrotizing areas and an increase in the number of s-100-positive cells in the uninvolved paracortical areas. This observation suggests that necrotizing lymphadenitis may be a common morphologic expression of a T cell-mediated hyperimmune condition induced by diverse etiologies.
Adolescent ; Adult ; Female ; Humans ; Immunohistochemistry ; Lymphadenitis/etiology/metabolism/*pathology ; Male ; Muramidase/metabolism ; Necrosis ; S100 Proteins/metabolism

Cell Line ; Glucose ; metabolism ; pharmacology ; Humans ; Mesangial Cells ; drug effects ; metabolism ; Tumor Necrosis Factor-alpha ; metabolism

Inflammation underlies a wide variety of physiological and pathological processes, and plays a pivotal role in controlling pathogen infection. C1q/tumor necrosis factor (TNF) related proteins (CTRPs), a newly discovered adipokine family with conservative structure and wide distribution, has attracted increasing attention. The CTRP family consists of more than 15 members which fall into the characteristic C1q domain. Increasing studies have demonstrated that CTRPs are involved in the onset and development of inflammation and metabolism as well as related diseases, including myocardial infarction, sepsis and tumors. Here, we first clarified the characteristic domains of CTRPs, and then elucidated their roles in inflammatory-related diseases. Taken together, the information presented here provides new perspectives for therapeutic strategies to improve inflammatory and metabolic abnormalities.
Humans ; Complement C1q/metabolism* ; Tumor Necrosis Factor-alpha/metabolism* ; Inflammation/metabolism* ; Myocardial Infarction

This study aimed to explore the potentiating effect and mechanism of the extract of Jingfang Granules(JFG) on the activation of macrophages. The RAW264.7 cells were treated with JFG extract and then stimulated by multiple agents. Subsequently, mRNA was extracted, and reverse transcription-polymerase chain reaction(RT-PCR) was used to measure the mRNA transcription of multiple cytokines in RAW264.7 cells. The levels of cytokines in the cell supernatant were detected by enzyme-linked immunosorbent assay(ELISA). In addition, the intracellular proteins were extracted and the activation of signaling pathways was determined by Western blot. The results showed that JFG extract alone could not promote or slightly promote the mRNA transcription of TNF-α, IL-6, IL-1β, MIP-1α, MCP-1, CCL5, IP-10, and IFN-β, and significantly enhance the mRNA transcription of these cytokines in RAW264.7 cells induced by R848 and CpG in a dose-dependent manner. Furthermore, JFG extract also potentiated the secretion of TNF-α, IL-6, MCP-1, and IFN-β by RAW264.7 cells stimulated with R848 and CpG. As revealed by mechanism analysis, JFG extract enhanced the phosphorylation of p38, ERK1/2, IRF3, STAT1, and STAT3 in RAW264.7 cells induced by CpG. The findings of this study indicate that JFG extract can selectively potentiate the activation of macrophages induced by R848 and CpG, which may be attributed to the promotion of the activation of MAPKs, IRF3, and STAT1/3 signaling pathways.
Tumor Necrosis Factor-alpha/metabolism* ; Interleukin-6/metabolism* ; Plant Extracts/metabolism* ; Lipopolysaccharides/pharmacology* ; Macrophages ; Cytokines/metabolism* ; RNA, Messenger/metabolism*

OBJECTIVETo investigate the effects of TNF-alpha, TNF-beta and the acceptor expression about mechanical renal trauma with extraneous ADM.

METHODSThere were 104 healthy adult plain grade Wistar rat, randomly divided into four groups:8 in the group of control, 32 in the group of trauma, 32 in the group injected ADM before trauma, 32 in the group injected ADM post trauma. The experimental model of rat kidney with mechanical trauma was prepared by striking the area of rat skin reflecting by kidney with free dropping ferrous hammer in the last three groups. ADM (0.1 nmol/kg) administrated by intraperitoneal injection at 10 minutes before trauma or post trauma respectively in injected groups. All rats were executed by drawing-out all the blood in their hearts. Renal tissue was investigated to study positive expression of TNF-alpha, TNF-beta, TNFR after SABC stained.

RESULTSTNF-alpha expression:the TNF-alpha expression of trauma group was more positive than it of control group in the wound early time. The expression of group injected post trauma was less than it of trauma group at 1 h (P < 0.01). The expression of group injected before trauma was less than it of trauma group at 6 h (P < 0.05) TNF-beta expression: the TNF-beta expression of trauma group was less than it of control group at 1 h and 6 h (P < 0.05). The TNF-beta expression of group injected post trauma was more positive than it of trauma group at the same time of 1 h and 6 h (P < 0.01). TNFR expression: the TNFR expression of trauma group was less than it of control group at 6 h (P < 0.01). The TNFR expression of group injected before trauma was more positive than it of trauma group in the at the same time of 1 h and 6 h (P < 0.01).

CONCLUSIONSThe TNFR can regulate the TNF-alpha and the TNF-beta in dynamic balancing. The regulation of TNFR is main to TNF-alpha. What the TNF-beta participated in renal trauma mainly is the anti-damage process. ADM can reduce the expression of TNF-alpha. ADM increases the expression of TNF-beta and TNFR.

Adrenomedullin ; pharmacology ; Animals ; Disease Models, Animal ; Female ; Kidney ; injuries ; metabolism ; Lymphotoxin-alpha ; metabolism ; Male ; Rats ; Rats, Wistar ; Receptors, Tumor Necrosis Factor ; metabolism ; Tumor Necrosis Factor-alpha ; metabolism

Programmed necrosis, also known as necroptosis, has recently drawn great attention. As an important cellular regulation mechanism, knowledge of its signaling components is expanding. Necroptosisis demonstrated to be regulated by the RIP1 and RIP3 kinases, and its pathophysiological importance has been confirmed in a number of disease models. Here we review the new members of this necroptosis pathway, MLKL, PGAM5, Drp1 and DAI, and discuss some of their possible applications according to recent findings.
Animals ; Carrier Proteins ; metabolism ; DNA-Binding Proteins ; metabolism ; GTP Phosphohydrolases ; metabolism ; Humans ; Microtubule-Associated Proteins ; metabolism ; Mitochondrial Proteins ; metabolism ; Necrosis ; Phosphoprotein Phosphatases ; Protein Kinases ; chemistry ; metabolism ; Receptor-Interacting Protein Serine-Threonine Kinases ; metabolism ; Signal Transduction ; Tumor Necrosis Factors ; metabolism

Infection of hepatitis B virus (HBV) is a main cause of liver diseases including hepatitis, cirrhosis and hepatocellular carcinoma (HCC). Among the HBV-encoded proteins, the HBV X protein (HBx) has been suspected to be strongly involved in HBV-associated liver pathogenesis. HBx, a virally encoded multifunctional regulator, has been shown to induce apoptosis, anti-apoptosis, proliferation, and transformation of cells depending on the cell lines, model systems used, assay protocols, and research groups. Among the several activities of HBx, the pro-apoptotic function of HBx will be discussed in this review. Given that the disruption of apoptosis pathway by HBx contributes to the liver pathogenesis, a better understanding of the molecular interference in the cellular pro-apoptotic networks by HBx will provide useful clues for the intervention in HBV-mediated liver diseases.
*Apoptosis ; Hepatitis B/etiology ; Liver Diseases/metabolism/virology ; Trans-Activators/*metabolism ; Tumor Necrosis Factors/metabolism ; Tumor Suppressor Protein p53/metabolism

Endothelial dysfunction is implicated in a variety of cardiovascular diseases although the detailed mechanisms are not yet completely understood. A relationship has been suggested to exist between inflammation and endothelial dysfunction. TNF-α serves as one of the most important pro-inflammatory cytokines. The main objectives of the present study were to explore the effect of PKC-ζ on TNF-α-impaired endothelial function as well as the underlying mechanisms. Acetylcholine-induced endothelium-dependent vasodilation of mouse thoracic aorta stimulated by TNF-α was initially determined. PKC-ζ deficient mice and the specific inhibitor of NADPH oxidase were respectively applied to elucidate their roles in TNF-α-induced endothelial dysfunction. In vitro superoxide generation in HAECs was detected by DHE staining after administration of TNF-α. Meanwhile, the regulatory p47(phox) subunit of NADPH oxidase was evaluated by Western blotting and RT-PCR. The results showed that TNF-α conspicuously impaired endothelium-dependent vasodilation and the impairment was attenuated by either depleting PKC-ζ or inhibiting NADPH oxidase. In vitro TNF-α increased superoxide production and p47(phox) expression in HAECs, and such increases could be ameliorated by the specific PKC-ζ inhibitor. Our findings suggest that superoxide over-production triggered by PKC-ζ-dependent NADPH oxidase activation contributes to TNF-α-induced endothelial dysfunction.
Animals ; Endothelium, Vascular ; metabolism ; Male ; Mice ; NADPH Oxidases ; metabolism ; Protein Kinase C ; metabolism ; Tumor Necrosis Factor-alpha ; metabolism

Animals ; Coxsackievirus Infections ; metabolism ; Enterovirus B, Human ; Female ; Male ; Mice ; Myocarditis ; metabolism ; Myocardium ; metabolism ; Tumor Necrosis Factor-alpha ; metabolism