Fig. 2: SAA effectively reduced viral loads in LCMV-challenged BALB/c mice through intravenous administration.
a Schematic diagram for in vivo efficacy evaluation with BALB/c mouse model. Mice of 6–8 weeks (n = 5) were randomly divided into vehicle, positive drug control, and experimental groups. In detail, the mice either daily received 20 mg/kg SAA, chebulinic acid, tannic acid, and punicalagin via intragavage (i.g.), or daily received 20 or 40 mg/kg SAA via i.g., intraperitoneal injection (i.p.) or tail vein injection (i.v.) upon challenge of 1 × 105 plaque-forming units of LCMV via i.p. Mice received 300 mg/kg Favipiravir (T-705, a nucleic acid analog drug with broad-spectrum antiviral activity to target viral RNA-dependent RNA polymerase) or 30 mg/kg of Ribavirin (RBV) daily via i.g., as controls. Viral copies in spleens or livers were taken for analysis at 3 days post-infection (dpi). b Body weight changes in mice after treatment with 20 mg/kg of SAA, chebulinic acid, tannic acid, or punicalagin via i.g. upon challenge. 300 mg/kg T-705 administered via i.g. was used as a positive control. c, d Viral copies in livers and spleens were determined at 3 dpi using RT-qPCR through the standard curve method, after the treatments of 20 or 40 mg/kg SAA via i.g., i.p., or i.v., or the treatment of 300 mg/kg T-705 or 30 mg/kg RBV via i.g. Data were represented as mean ± standard deviation from five animals. e Metabolic kinetic data of SAA in rats (n = 3) were determined through both i.g. and i.v. administration routes. The table presents the half-life (t1/2), maximum concentration time (Tmax), maximum blood concentration (Cmax), area under curve (AUC), and bioavailability (F) of SAA across various administration methods. Data were represented as mean ± standard deviation from three animals.
