Furthermore, in vivo study showed that subcutaneously administration of 5 mg/kg RTD-1 could improve the survival rate and suppress the levels of a number of inflammatory cytokines and chemokines in two sepsis mouse models (received either intraperitoneal injection of E. coli or CLP).
The BxPC-3 pancreatic cancer xenogeneic mice model received treatment with physiological saline, inhibition of SIRT1, gemcitabine, and combination therapy with inhibition of SIRT1 and gemcitabine in vivo and the results showed that the tumor volumes decreased and the survival rate within 45 days increased according to the order of the given drugs and the difference was significant (P < 0.05).
For the experiments in the AAV-FlexOFF-α-synuclein mouse model, animals received i.p injections of CsA (20 mg/kg, Sigma-Aldrich) every other day from the day following the last injection of tamoxifen and until the time of sacrifice.
Mouse models have various advantages.
In line with this idea, recent studies showed that GBE induced hippocampal neurogenesis, a very energy demanding process, in young and old transgenic AD mouse model (TgAPP/PS1) after receiving a diet supplemented with GBE for 1 month [43].
Delay of melanoma tumors implantation was also observed after 21 days of chronic treatment with crotamine (1 μg per animal, per day), in a mice model that received B16-F10 cells (10 cells) by subcutaneous injection.
In a mouse model in which mice received passive transfer of anti-MV antibodies, Grote et al. found that intratumoral MV-Edm therapy of human lymphoma xenografts resulted in effective tumor regression without compromise through the presence of anti-MV antibodies [ 52].
Although in patients treated by TCR gene therapy such toxicity was not reported so far, lethal autoimmune pathology due to mispaired TCR dimers was seen in a mouse model in which animals received TCR-Tg T cells using a protocol mimicking clinical application 5.
In an orthotopic ovarian cancer xenograft model, mice receiving the nanoparticles with both paclitaxel and 90Y at a dose of 500 µg nanoparticles/mouse (20 µg paclitaxel and 1.85 MBq 90Y per mouse) showed significant survival advantage over those receiving monotherapies.
Similar to the AOM/DSS model, mice receiving the colon carcinogens (PhIP and DMH) followed by DSS treatment have a higher incidence of tumors [124], [127].
