The liver injury following ischemia and reperfusion is worse in experimental knockout heterozygote mouse model for expression of connexin 43()

PURPOSE: To evaluate that Connexin (Cx43) plays a role in lesions after hepatic ischemia/reperfusion (IR) injury. METHODS: We use Cx43 deficient model (heterozygotes mice) and compared to a wild group. The groups underwent 1 hour ischemia and 24 hours reperfusion. The heterozygote genotype was confi...

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Detalles Bibliográficos
Autores principales: Trevisan, Alexandre Maximiliano, Cogliati, Bruno, Homem, Adriana Ribeiro, Aloiav, Thiago Pinheiro Arrais, de Aquino, Nelson, Moreira, Jairo Marques, Reno, Leonardo da Cruz, Naumann, Alexandre Moulin, Galvão, Flavio Henrique Ferreira, Andraus, Wellington, D'Albuquerque, Luiz Augusto Carneiro
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Sociedade Brasileira para o Desenvolvimento da Pesquisa em Cirurgia 2019
Materias:
Original Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6912844/
https://www.ncbi.nlm.nih.gov/pubmed/31851211
http://dx.doi.org/10.1590/s0102-865020190100000003
Descripción
Sumario:PURPOSE: To evaluate that Connexin (Cx43) plays a role in lesions after hepatic ischemia/reperfusion (IR) injury. METHODS: We use Cx43 deficient model (heterozygotes mice) and compared to a wild group. The groups underwent 1 hour ischemia and 24 hours reperfusion. The heterozygote genotype was confirmed by PCR. We analyzed the hepatic enzymes (AST, ALT, GGT) and histology. RESULTS: The mice with Cx43 deficiency showed an ALT mean value of 4166 vs. 307 in the control group (p<0.001); AST mean value of 7231 vs. 471 in the control group (p<0.001); GGT mean value of 9.4 vs. 1.7 in the control group (p=0.001); histology showed necrosis and inflammation in the knockout group. CONCLUSIONS: This research demonstrated that the deficiency of Cx43 worses the prognosis for liver injury. The topic is a promising target for therapeutics advancements in liver diseases and procedures.

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