Fig. 3: Hepatocyte-specific TMEM16A deficiency ameliorates inflammation during hepatic I/R injury.

A Representative immunofluorescence staining and quantification of infiltrating CD3⁺, LY6G⁺, or CD68⁺ cells (red) in the livers of TM^LKO or AAV-TM mice and their counterpart control mice subjected to 90 min of hepatic ischemia followed by 24 h of reperfusion (n = 6). ^#P < 0.05 versus TM^Flox or AAV-Con. B Flow cytometry histogram showing neutrophils and macrophages in liver samples from indicated mice subjected to 90 min of ischemia and 24 h of reperfusion (n = 6). ^#P < 0.05, ##P < 0.01 versus TM^Flox I/R or AAV-Con I/R. Levels of C serum and D hepatic mRNA levels of pro-inflammatory factors (TNF-α, IL-1β, Il-6, MCP-1, and CXCL-1) in TM^LKO or AAV-TM-treated mice and their counterparts subjected to 90 min of hepatic ischemia followed by 24 h of reperfusion (n = 6). **P < 0.01 versus TM^Flox sham or AAV-Con sham; ^#P < 0.05, ^##P < 0.01 versus TM^Flox I/R or AAV-Con I/R. E TNF-α, MCP-1, and CXCL-1 levels in hepatocytes isolated from TM^LKO or AAV-TM-treated mice and their counterpart control mice after H/R challenge (4 h of hypoxia and 12 h of reoxygenation) (n = 6). **P < 0.01 versus TM^Flo or AAV-Con; ^#P < 0.05, ^##P < 0.01 versus TM^Flox H/R or AAV-Con H/R. F Total and phosphorylated IKKβ, IκBα, and p65 levels in livers of TM^LKO or AAV-TM-treated mice after sham operation or hepatic I/R treatment (90 min of ischemia and 24 h of reperfusion) (n = 6). G Relative levels of the aforementioned proteins. *P < 0.05, **P < 0.01 versus TM^Flox sham or AAV-Con sham; #P < 0.05 versus TM^Flox I/R or AAV-Con I/R. Data were presented as the mean ± SD.