Introduction: Glioblastoma multiforme (GBM) is an aggressive case of primary brain cancer which remains among the most fatal tumors worldwide. Although, some in vitro and in vivo models have been developed for a better understanding of GBM behavior; a natural model of GBM would improve the efficiency of experimental models to human GBM tumors. We aimed at the present study to examine the survival and durability of U87 cells in the brain of wild-type rats. Methods: U87 cells were intracranially implanted in twenty-one wild-type rats. Tumor size and morphology as well as infiltration of immune cells were investigated at three-time points by H&E and immunohistochemistry (IHC). Results: The results demonstrated that the inoculation of GBM cells led to the infiltration of host defense system cells which caused to immunological regression of the tumor mass after six weeks. While the tumors successfully developed without any sign of host defense invasion in the second week of GBM inoculation. Also, the decrease of tumor size and infiltration of immune system cells were observed at the fourth week. Conclusion: These data remarkably suggest that time plays a crucial role in activating the immune system against human GBM tumors in rats; and it shows that the regression of tumor mass depends on a time slope.

Background: Teucrium polium (TP) is a medicinal plant with a long history of consumption as a folk remedy for curing many diseases, including diabetes, common cold, obesity, anxiety, etc. Objectives: The present study aimed at investigating the effects of TP crude extracts (TPCE), as well as its diethyl ether (DE) and petroleum ether (PE) fractions, on the brain, kidney, and liver tissue of male rats in the subchronic phase. Methods: In the study, 45 adult male Wistar rats were randomly assigned to five groups as the PBS (receiving phosphate buffer saline), vehicle (receiving dimethyl sulfoxide), as well as CE, PE, and DE receiving 3 mg/kg (100 µL) TPCE, PE, and DE, respectively, for six weeks. Histopathological examinations by hematoxylin and eosin staining investigated morphological changes in all specimens. Also, the brain samples were stained by the immunohistochemistry (IHC) technique with Ki-67, CD31, p53, Nestin, and GFAP markers. Results: The findings showed that the prolonged consumption of TP caused the formation of histological lesions as apoptosis, degeneration, cytoplasmic vacuolization of neurons, and foamy cells in the brain. The liver, displayed cytoplasmic vacuolization, apoptosis, degeneration, and dilated sinusoids. Moreover, TP led to atrophy, vacuolization, and necrosis in renal cells. IHC studies evidenced an increase in the expression of P53, whereas the expression of Ki67 and CD31 decreased. It should be noted that TP crude extract and fractions were toxic; however, the PE fraction was more cytotoxic than others. Conclusions: The study findings indicated that long-term administration of a sublethal dose of TP impairs cellular integrity in vital orangs, including the liver, brain, and kidney, through triggering the cell death mechanisms.

IntroductionIn the current study, we investigate whether oral administration of agmatine (AGM) could effectively reduce motor and cognitive deficits induced by bile duct ligation (BDL) in an animal model of hepatic encephalopathy (HE) through neuroprotective mechanisms.MethodsThe Wistar rats were divided into four groups: sham, BDL, BDL+ 40 mg/kg AGM, and BDL+ 80 mg/kg AGM. The BDL rats were treated with AGM from 2 weeks after the surgery for 4 consecutive weeks. The open field, rotarod, and wire grip tests were used to assess motor function and muscle strength. The novel object recognition test (NOR) was performed to evaluate learning and memory. Finally, blood samples were collected for the analysis of the liver markers, the animals were sacrificed, and brain tissues were removed; the CA1 regions of the hippocampus and cerebellum were processed to identify apoptosis and neuronal damage rate using caspase‐3 immunocytochemistry and Nissl staining.ResultsThe serological assay results showed that BDL severely impaired the function of the liver. Based on histochemical findings, BDL increased the neuronal damage in CA1 and Purkinje cells, whereas apoptosis was significantly observed only in the cerebellum. AGM treatment prevented the increase of serum liver enzymes, balance deficits, and neuronal damage in the brain areas. Apoptosis partially decreased by AGM, and there were no differences in the performance of animals in different groups in the NOR.ConclusionsThe study suggests AGM as a potential treatment candidate for HE because of its neuroprotective properties and/or its direct effects on liver function.