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Diabetes mellitus is a metabolic disorder, with a large prevalence in low- and middle-income countries. Numerous studies highlighted the use of medicinal plants for diabetes in Algeria. This use is influenced by cultural considerations. The industrialization of the country leads to the transformation of the trend of the utilization of plants, and the increase of polymedication. In this context, there is no information about the profile of diabetic patients using plants and the potential of herb-drug interactions.

The objective was to evaluate the use of plants by diabetic patients and to search the drug interactions with the most cited species.

Descriptive and comparative studies were carried out among diabetic patients and traditional healers, in the west of Algeria, to inventory the plants used in diabetes. Bivariate and multivariate analysis by logistic regression were performed to evaluate the associated factors with the use, to determine the profile of users. Bibliometric research in PubMed, Googleion of information sources. Patients under ODA must be educated about the use and the risk of herb-drug interactions.

The root of Achyranthes bidentata Blume, Achyranthis Radix (AR), is used as a traditional medicine ingredient in East Asia. It has anti-inflammatory, anti-oxidative, and anti-diabetic activities.

In the present study, we aimed to evaluate the oral toxicity and genotoxicity of single-dose and 4-week repeated-doses of AR hot water extract (ARE), under the good laboratory practice principles.

For oral toxicity studies, SD rats (n=5 per sex and group) were administered ARE at concentrations of 500, 1000, and 2000mg/kg/day once (single dose) or once per day for 4 weeks (repeated dose). The non-clinical genotoxicity study consisted of bacterial reverse mutation using Escherichia coli (WP2 uvrA) and Salmonella typhimurium (TA98, TA100, TA1535, and TA1537), in vitro chromosomal aberration test with Chinese hamster lung cells (CHL/IU), and in vivo mouse bone marrow micronucleus test using bone marrow cells collected from male ICR mice (n=5) that were orally administered ARE.

In the single-dose oral toxicity study, mortality and treatment-related changes in body weight were not observed throughout the study, and the lethal dose was estimated to be>2000mg/kg in rats. In the 4-week repeated-dose oral toxicity study, ARE did not induce significant changes in body weight, organ weight, food intake, or hematological and serum biochemical parameters in any group. In the bacterial reverse mutation test, ARE did not induce gene mutations in any tested strain. In the chromosomal aberration test, ARE did not cause chromosomal aberrations. The micronucleus test showed no significant increase in the number of micronucleated polychromatic erythrocytes or the mean ratio of polychromatic to total erythrocytes.

These results showed that ARE does not induce oral toxicity and genotoxicity in the in vivo and in vitro test systems.

These results showed that ARE does not induce oral toxicity and genotoxicity in the in vivo and in vitro test systems.Deamidation is a spontaneous modification of peptides and proteins that has potent repercussions on their activity and stability in vivo and in vitro. Being able to implement easy techniques to detect and quantify protein deamidation is a major goal in this field. Here we focus on electrophoretic methods that can be deployed to assess protein deamidation. We provide an update on the use of Taurine/Glycinate as trailing ions to assist the detection of several examples of deamidated proteins, namely the small GTPases RhoA, Rac1 and Cdc42, but also the oncogene Bcl-xL and calcium-binding Calmodulin. We also report on the use of imidazole as a counter ion to improve the focusing of deamidated bands. Finally, we provide examples of how these gels proved useful to compare on full-length proteins the effect of ions and pH on the catalytic rates of spontaneous deamidation. Taken together, the electrophoretic method introduced here proves useful to screen at once the effect of various conditions of pH, ionic strength and buffer ions on protein stability. Direct applications can be foreseen to tailor buffer formulations to control the stability of proteins drug products.In this study, we identified elevated levels of LPS and suppressed neurogenesis in a successfully established mouse model of gut microbiota dysbiosis. We mimicked these phenotypes using mouse and chicken embryos exposed to LPS and found that dramatic variation in gene expression was due to changes in the dorsal-ventral patterning of the neural tube. Cell survival and excess ROS were also involved in this process. Neratinib order Antioxidant administration alleviated LPS-activated NF-κB signaling, while directly blocking NF-κB signaling altered the LPS-induced inhibition of neurogenesis. Furthermore, IL-6 was proven to play a vital role in the expression of crucial neurogenesis-related genes and NF-κB. In summary, we found that the suppression of neurogenesis induced by dysbacteriosis-derived LPS was significantly reversed in mice with fecal microbiota transplantation. This study reveals that gut dysbacteriosis-derived LPS impairs embryonic neurogenesis, and that the NF-κB/IL-6 pathway could be one of the main factors triggering the downstream signaling cascade.Diversiform ways of intercellular communication are vital links in maintaining homeostasis and disseminating physiological states. Among intercellular bridges, tunneling nanotubes (TNTs) discovered in 2004 were recognized as potential pharmacology targets related to the pathogenesis of common or infrequent neurodegenerative disorders. The neurotoxic aggregates in neurodegenerative diseases including scrapie prion protein (PrPSc), mutant tau protein, amyloid-beta (Aβ) protein, alpha-synuclein (α-syn) as well as mutant Huntington (mHTT) protein could promote TNT formation via certain physiological mechanisms, in turn, mediating the intercellular transmission of neurotoxicity. In this review, we described in detail the skeleton, the formation, the physicochemical properties, and the functions of TNTs, while paying particular attention to the key role of TNTs in the transport of pathological proteins during neurodegeneration.