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. Author manuscript; available in PMC: 2020 Sep 25.
Published in final edited form as: Alcohol Clin Exp Res. 2020 Apr 8;44(5):1046–1060. doi: 10.1111/acer.14326

Fig 4.

Fig 4.

Fig 4.

DHM significantly reduces hepatic enzyme release, exhibits dose-dependent anti-inflammatory actions, and maintains serum BDNF levels. A) DHM administration at both 5 and 10 mg/kg significantly inhibited the activities of serum ALT and AST comparable to control values (n=6/group). B) DHM dose-dependently decreased serum cytokine markers compared to untreated ethanol-fed mice serum (n=4/group). C) DHM administration, at both 5 and 10 mg/kg, significantly reduced ethanol-mediated hepatic TNF-α expression relative to ethanol only controls (n=3/group; See Data S4A for Image J quantification of triplicates). D) Hepatic cytokine analysis of mice chronically-fed EtOH and either treated with DHM (5 or 10 mg/kg) or untreated (n=4/group). E) DHM administration at both 5 and 10 mg/kg significantly reversed ethanol-mediated reductions in serum BDNF concentrations (n=6/group). Color key and histogram illustrate the intensity of red being associated with larger fold increases in expression relative to normalized control values (white), and intense greens are associated with fold-decreases (0.5-fold the lowest) relative to normalized control values. Blue solid lines indicate average fold values relative to control (dotted blue line). Data represented as mean ± SEM. *p<0.05 compared with corresponding ethanol controls. *p<0.05 and **p < 0.01 compared with corresponding ethanol controls. E = ethanol; D5 = 5 mg/kg DHM; D10 = 10 mg/kg DHM.