A win-win scenario for antibacterial activity and skin mildness of cationic surfactants based on the modulation of host-guest supramolecular conformation.

The commercial cationic surfactants (CSAa) with quaternary ammonium (QA) groups have proved to be broad-spectrum bactericide against bacteria, fungi, and viruses. Nevertheless, they inevitably exhibit potent irritation on the skin. In this work, we systematically investigated the regulatory mechanism of the host-guest supramolecular conformation with ß-cyclodextrin (ß-CD) on the bactericidal performance and skin irritation of CSAa with different head groups and chain lengths. When the ratio of incorporated ß-CD is not greater than 1:1, the bactericidal efficiency of CSAa@ß-CD (n > 12) remained above 90 % due to the free QA groups and hydrophobic fraction that can act on negatively charged bacterial membranes. And once the ratio of ß-CD exceeded 1:1, the ß-CD attracted to the bacterial surface by hydrogen bonding might prevent CSAa@ß-CD from acting on bacteria, resulting in a decrement in antibacterial performance. Even so, the antibacterial activity of CSAa with long alkyl chains (n = 16, 18) was independent from the complexation of ß-CD. Accordingly, both the zein solubilization assay and the neutrophil migration assay on zebrafish skin evidenced that ß-CD attenuated the interaction of surfactant with skin model proteins and the inflammatory effect on zebrafish, thereby enhancing skin mildness. In this way, we hope to create a simple but effective brainpower using the host-guest approach to guarantee both bactericidal efficiency and skin mildness without modifying the chemical structure of these commercial biocides.

Nesfatin-1 alleviates high glucose/high lipid-induced injury of trophoblast cells during gestational diabetes mellitus.

Gestational diabetes mellitus (GDM) is a common disease in pregnant women, imposing risks on both mother and fetus. Dysregulated nesfatin-1 has been observed in women with GDM, but the specific role of nesfatin-1 underlying the pathological process of GDM is unclear. The main objective of this study is to investigate the role and the molecular mechanism of nesfatin-1 in GDM. HTR-8/SVneo cells were treated with high glucose (HG)/high lipid (HL) to mimic the injured trophoblast of GDM in vitro. Cell viability, cytotoxicity and apoptosis were measured using CCK-8, LDH and TUNEL assays, respectively. The levels of inflammatory cytokines and antioxidant factors were detected using their commercial kits. ATP level and cytochrome c were determined with corresponding detecting kits. Quantitative real-time PCR and Western blot were performed to detect the expression of corresponding genes. The results showed that nesfatin-1 was downregulated upon HG/HL stimulation. Nesfatin-1 treatment greatly alleviated HG/HL-induced cell viability loss, cytotoxicity, inflammatory response, oxidative stress, and apoptosis in HTR-8/SVneo cells. In addition, nesfatin-1 promoted ATP generation, reduced the leakage of cytochrome c from mitochondria to cytoplasm, and upregulated mitochondrial transcription factor A (TFAM) and nuclear respiratory factor 1 (NRF1), alleviating mitochondrial dysfunction. Furthermore, nesfatin-1 inhibited p38 MAPK signaling. p79350, an agonist of p38 MAPK signaling, remarkably hindered the protective role of nesfatin-1 in HG/HL-induced HTR-8/SVneo cells. In conclusion, nesfatin-1 exerted a protective effect on GDM model in vitro, by regulating p38 MAPK signaling pathway, providing novel insights of treating GDM.

[Effect of human bone morphogenetic protein 2, 3, 6, and 12 on osteosarcoma cell line UMR106].

OBJECTIVE: To investigate the effect of human bone morphogenetic protein (hBMPs) 2/3/6 and 12 on osteosarcoma cell UMR106. METHODS: Adenovirus-BMP2/3/6 and 12 (AdBMP2/3/6 and12) were used to treat the cell line. Their proliferation, apoptosis, and transmigration were detected by Trypan blue exclusion test, TdT-mediated biotinylated-dUTP nick end labeling (TUNEL), acridine orange-ethidium bromide (AO/EB) double fluorescent dye staining, and transwell-room test, respectively. The alkaline phosphatase (ALP) activity was detected to reflect the differentiation of tumors. RESULTS: Compared with the control groups, the cell survival rate of the experimental groups treated with AdBMP2/3/6 and 12 showed a significant time-dependent decrease (P<0.01). The apoptosis indexes were increased significantly (P<0.01) and the results from TUNEL and AO/EB method were consistent. The cell numbers of transmembrane significantly decreased at 24,48, and 72 h (P<0.01). AdBMP2/3/6 and 12 treatment enhanced the activity of ALP activity from day 3 and this effect might still be observed up to day 9 of the treatment (P<0.01). CONCLUSION: hBMPs2/3/6 and 12 can inhibit the proliferation and transmigration, and induce their apoptosis and differentiation in osteosarcoma cell line UMR106.