Figure 3.

ICAC reduced the mortality of the EV71-infected mice by regulating the viral load and cytokine secretion. Two-day-old mice were utilized as the animal model. (A) The acute toxicity of ICAC (12.5–200 mg/kg) on mice was evaluated. In the antiviral study, the mice were challenged intraperitoneally with saline (control) or 1×10⁷ TCID₅₀ of EV71. Then, the infected mice were treated with various doses (1.6–6.4 mg/kg) of ICAC or 10 mg/kg of ribavirin for 14 days. The mice in the model group were injected with saline. The survival rates (B) and body weight ratios (C) were recorded continuously until 14 dpi. The body weight ratio was presented relative to the corresponding treatments on the first day (n = 10). (D) Representative photos of limb paralysis caused by EV71 infection (left) and healthy phenotypes of mice treated with 6.4 mg/kg of ICAC (right) at 6 dpi. The brain tissues were sampled at 3, 6, and 9 dpi. (E) The viral loads in the brains were determined by real-time PCR (n = 6). The IL-6 (F), MCP-1 (G), and TNF-α (H) levels in the brains were determined by ELISA (n = 6). All results were expressed as the means ± SEs. Asterisks indicate that the data significantly differ from the EV71 group at the P < 0.05 level according to one-way analysis of variance.