Capsicum annuum L. var. “Chile de árbol” combined with poly(lactic-co-glycolic acid) (PLGA) and TiO₂-ZnO oxides synthesized at different molar ratios and pH (Ti-Zn A and B 3:1, 1:1, and 1:3) via the sol-gel method was characterized by the Brunauer–Emmett–Teller (BET) method, a UV-Vis spectrophotometer (UV-Vis), Fourier transform infrared spectroscopy (FT-IR), High-Performance Liquid Chromatography (HPLC-DAD), and a release profile through mathematical models to explain its behavior. Furthermore, FTIR revealed the presence of PLGA, TiO₂, and ZnO as well as amino group characteristics from oleoresin components, principally alkaloid groups (capsaicin and dihydrocapsaicin), as evidenced by HPLC, to identify the presence of capsaicin and dihydrocapsaicin. The UV-Vis spectra showed a slight hypsochromic shift in the PLGA treatments. The release profile demonstrated a higher controllable release in the PLGA treatments than in the double nanoemulsions. Moreover, it is important to note that the effect of NPs influenced the release profile itself, increasing the release when NPs were synthesized at an acidic pH. Therefore, the TiZnOl/PLGA A characteristics suggest that these results have potential for pharmaceutical (as drug carriers) and medical applications.

Salmonella spp. is one of the most common food poisoning pathogens and the main cause of diarrheal diseases in humans in developing countries. The increased Salmonella resistance to antimicrobials has led to the search for new alternatives, including natural compounds such as curcumin, which has already demonstrated a bactericidal effect; however, in Gram-negatives, there is much controversy about this effect, as it is highly variable. In this study, we aimed to verify the antibacterial activity of curcumin against the Salmonella enterica serovar Typhimurium growth rate, virulence, and pathogenicity. The strain was exposed to 110, 220 or 330 µg/mL curcumin, and by complementary methods (spectrophotometric, pour plate and MTT assays), we determined its antibacterial activity. To elucidate whether curcumin regulates the expression of virulence genes, Salmonella invA, fliC and siiE genes were investigated by quantitative real-time reverse transcription (qRT-PCR). Furthermore, to explore the effect of curcumin on the pathogenesis process in vivo, a Caenorhabditis elegans infection model was employed. No antibacterial activity was observed, even at higher concentrations of curcumin. All concentrations of curcumin caused overgrowth (35–69%) and increased the pathogenicity of the bacterial strain through the overexpression of virulence factors. The latter coincided with a significant reduction in both the lifespan and survival time of C. elegans when fed with curcumin-treated bacteria. Our data provide relevant information that may support the selective antibacterial effects of curcumin to reconsider the indiscriminate use of this phytochemical, especially in outbreaks of pathogenic Gram-negative bacteria.

The mechanisms underlying oxidative stress (OS) resistance are not completely clear. Caenorhabditis elegans (C. elegans) is a good organism model to study OS because it displays stress responses similar to those in mammals. Among these mechanisms, the insulin/IGF-1 signaling (IIS) pathway is thought to affect GABAergic neurotransmission. The aim of this study was to determine the influence of heat shock stress (HS) on GABAergic activity in C. elegans. For this purpose, we tested the effect of exposure to picrotoxin (PTX), gamma-aminobutyric acid (GABA), hydrogen peroxide, and HS on the occurrence of a shrinking response (SR) after nose touch stimulus in N2 (WT) worms. Moreover, the effect of HS on the expression of UNC-49 (GABA_A receptor ortholog) in the EG1653 strain and the effect of GABA and PTX exposure on HSP-16.2 expression in the TJ375 strain were analyzed. PTX 1 mM- or H₂O₂ 0.7 mM-exposed worms displayed a SR in about 80 % of trials. GABA exposure did not cause a SR. HS prompted the occurrence of a SR as did PTX 1 mM or H₂O₂ 0.7 mM exposure. In addition, HS increased UNC-49 expression, and PTX augmented HSP-16.2 expression. Thus, the results of the present study suggest that oxidative stress, through either H₂O₂ exposure or application of heat shock, inactivates the GABAergic system, which subsequently would affect the oxidative stress response, perhaps by enhancing the activity of transcription factors DAF-16 and HSF-1, both regulated by the IIS pathway and related to hsp-16.2 expression.