Gamma-enolase predicts lung damage in severe acute pancreatitis-induced acute lung injury.

Severe acute pancreatitis (SAP) associated acute lung injury (ALI) accounts for about 70% mortality of SAP patients. However, there are no precise biomarkers for the disease currently. Herein, we evaluated the potential of gamma-enolase (ENO2), against its universal isoform alpha-enolase (ENO1), as a marker of SAP-ALI in a rat model. Firstly, 16 male Sprague-Dawley rats were randomly divided into two groups, Sham (n = 8) and SAP-ALI (n = 8), for pancreatitis induction. Ultra-structure examination by electron microscopy and HE staining were used for lung injury assessment. Lung tissue expressions of alpha-enolase and gamma-enolase were evaluated by qRT-PCR and immunohistochemistry. In a prospective validation experiment, 28 rats were used: sham (n = 8), SAP-ALI at 3 h (3 h, n = 10), and SAP-ALI at 24 h (24 h, n = 10). Lung tissue damage, tissue expression and circulating alpha-enolase and gamma-enolase levels were evaluated. Elevated serum levels of α-amylase and TNF-α were observed in SAP rats but not in sham-operated rats. Histological examination of pancreatic and lung tissues indicated marked damage in SAP rats. While alpha-enolase was universally expressed, gamma-enolase was expressed only in damaged lung tissues. Gamma-enolase was detected in lung tissues, BALF, and serum as early as 3 h post-surgery when physical pathological damage was not apparent. Unlike alpha-enolase, secreted and/or circulating gamma-enolase level progressively increased, especially in serum, as lung damage progressed. Thus, gamma-enolase may signal and correlate lung tissue damage well before obvious physical pathological tissue damage and might be a candidate diagnostic and/or prognostic marker.

[Protect role of Netrin-1 in inflammatory response].

OBJECTIVE: Neuronal guidance factor Netrin-1 has been known to be involved in nervous system development by controlling neuronal migration through both chemoattractive and chemo-repulsive signaling by binding different receptors. Netrin-1 has been shown to play a positively regulatory role during inflammatory process recently. Since the chemorepulsive receptors were found in leukocytes, it is suggest that Netrin-1 played a protective role in tissue through inhibiting leukocyte trafficking and accumulating during inflammatory process in researches. It is demonstrated that Netrin-1 can limit inflammatory response through the involvement of inflammatory cascades, attenuate hypoxia-inducible tissue injury and suppress apoptosis concurrently. It is indicated that Netrin-1 can be a novel target in future through preventing and inhibiting inflammatory diseases in these researches. This review will focus on recent relevant advances and in-depth study to elucidate its mechanism of anti-inflammation.