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Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology 2019-Jan

[Cannabinoid receptor 2 deletion promotes proliferation and activation of hepatic macrophages in mice with acute liver injury induced by concanavalin A].

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Yafeng Wu
Cuizhen Long
Yuanhui Shu
Ping He
Yan Zhou
Junying Gu
Lei Yang
Yuping Wang

Nøgleord

Abstrakt

Objective To investigate the effect of cannabinoid receptor 2 (CB2) gene deletion on liver macrophages in mice with acute liver injury induced by concanavalin A (ConA). Methods The mice with gene deletion were identified by PCR. Twenty 8-week-old wild-type C57BL/6J male mice were randomly divided into control group and model group. Twenty C57BL/6J male mice with the deletion of CB2 were divided into CB2-/- control group and CB2-/- model group. The wild-type and CB2-/- mouse model groups were injected with ConA 20 mg/kg via tail vein to replicate the model of acute liver injury, and the control groups were injected with the same amount of PBS. Nine hours after modeling, the serum was taken for the detection of alanine aminotransferase (ALT); the degree of liver injury in each group was observed by HE staining; the expression levels of CD68 and TNF-alpha proteins related to liver macrophages were detected by Western blotting; and the positive level of F4/80 in the liver tissue was detected by immunohistochemistry. Results Compared with the two control groups, the liver injury degree of mice in the model groups were serious; the serum ALT level significantly increased; the positive expression of F4/80 in the liver tissue; and the expression of CD68 and TNF-alpha proteins were significantly enhanced. Compared with the WT model group, the CB2-/- model group had an increase in the degree and area of liver injury, the serum ALT, the positive expression of F4/80 in the liver tissue, and the expression of CD68 and TNF-alpha proteins. Conclusion The deletion of CB2 gene increases the proliferation and activation of macrophages in the mice with ConA-induced acute liver injury.

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