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Aim: The present study is aimed to examine olvanil's effect in preadipocyte cell culture and on a murine model of diet-induced obesity. We hypothesized that olvanil by being a capsaicinoid will reduce the differentiation to mature adipocytes and reduce the weight of fat tissue in the studied mice. Methods: To determine the effect of olvanil on adipogenesis, 3T3-L1 cells were cultured. Oil red staining was performed to determine lipid accumulation, whereas triglycerides were measured by biochemical determination. Expression of PPAR-γ and PREF-1 were measured by RT-PCR. Therefore, male C57BL/6J mice (CICUAL:2018-020B) were fed with a high-fat diet for 12 weeks to develop a murine model of diet-induced obesity (DIO). Animals were separated into 6 experimental groups: control (standard diet), DIO (high-fat diet), DIO + orlistat (10 mg/kg), DIO + olvanil (10 mg/kg), DIO + olvanil (25 mg/kg) and DIO + olvanil (50 mg/kg), olvanil was administered for 4 weeks. Results: Olvanil inhibits adipogenesis, reduces lipid accumulation and triglycerides in 3T3-L1 adipocytes. PPAR-ɣ gene expression was suppressed while PREF-1 was increased in adipocytes treated with olvanil. Whereas protein expression of FABP4 and PPAR-ɣ decreases significantly with olvanil. The results suggest that olvanil can inhibit the differentiation of preadipocytes to adipocytes through the overexpression or maintenance of PREF-1 levels and the suppression of PPAR-ɣ, and FABP4. Therefore, in diet-induced obesity in mice, olvanil decreases fat accumulation in the body and improve lipid profile by decreasing LDL, VLDL and triglycerides in serum. Conclusion: Olvanil inhibits adipocyte differentiation in 3T3-L1 cells and reduces fat accumulation and ameliorate lipid profile in diet-induced obese mice.

Current efforts to find novel treatments that counteract multiple sclerosis (MS) have pointed toward immunomodulation and remyelination. Currently, cell therapy has shown promising potential to achieve this purpose. However, disadvantages such as poor survival, differentiation, and integration into the target tissue have limited its application. A series of recent studies have focused on the cell secretome, showing it to provide the most benefits of cell therapy. Exosomes are a key component of the cell secretome, participating in the transfer of bioactive molecules. These nano-sized vesicles offer many therapeutical advantages, such as the capacity to cross the blood-brain barrier, an enrichable cargo, and a customizable membrane. Moreover, integrating of biomaterials into exosome therapy could lead to new tissue-specific therapeutic strategies. In this work, the use of exosomes and their integration with biomaterials is presented as a novel strategy in the treatment of MS.

IntroductionThe response to the SARS-CoV-2 coronavirus epidemic requires increased research efforts to expand our knowledge of the disease. Questions related to infection rates and mechanisms, the possibility of reinfection, and potential therapeutic approaches require us not only to use the experimental models previously employed for the SARS-CoV and MERS-CoV coronaviruses but also to generate new models to respond to urgent questions.DevelopmentWe reviewed the different experimental models used in the study of central nervous system (CNS) involvement in COVID-19 both in different cell lines that have enabled identification of the virus’ action mechanisms and in animal models (mice, rats, hamsters, ferrets, and primates) inoculated with the virus. Specifically, we reviewed models used to assess the presence and effects of SARS-CoV-2 on the CNS, including neural cell lines, animal models such as mouse hepatitis virus CoV (especially the 59 strain), and the use of brain organoids.ConclusionGiven the clear need to increase our understanding of SARS-CoV-2, as well as its potential effects on the CNS, we must endeavor to obtain new information with cellular or animal models, with an appropriate resemblance between models and human patients.

There is considerable controversy with regard to the genotoxicity of glyphosate, with some reports stating that this compound is non-toxic for fish, birds and mammals. In this work, we used the comet assay to examine the genotoxicity of glyphosate isopropylamine (0.7, 7, 70 and 700 µM) in human lymphocytes, erythrocytes of Oreochromis niloticus and staminal nuclei of Tradescantia (4430) in vitro and in vivo. Cells, nuclei and fish that had and had not been exposed to 5 mM N-nitrosodiethylamine (NDEA) were used as positive and negative controls, respectively. Significant (p < 0.01) genetic damage was observed in vivo and in vitro in all cell types and organisms tested. Human lymphocytes and Tradescantia hairs showed lower genetic damage in vivo compared to in vitro, possibly because of efficient metabolization of the herbicide. In O. niloticus erythrocytes, significant (p < 0.001) genotoxicity was observed at > 7 µM, whereas in vitro, glyphosphate was genotoxic in human lymphocytes and Tradescantia hairs at > 0.7 µM. These results indicate that glyphosate is genotoxic in the cells and organisms studied at concentrations of 0.7-7 µM.