Battling Salmonella enteritidis infections: integrating proteomics and in vivo assessment of Galla Chinensis tannic acid.

Salmonella infections pose a significant threat to animal and human health. Phytochemicals present a potential alternative treatment. Galla chinensis tannic acid (GCTA), a hydrolyzable polyphenolic compound, inhibits bacterial growth and demonstrates potential as an alternative or supplement to antibiotics to prevent Salmonella infections. However, little is known about the antimicrobial mechanism of GCTA against Salmonella. Here, we revealed 456 differentially expressed proteins upon GCTA treatment, impacting pathways related to DNA replication, repair, genomic stability, cell wall biogenesis, and lipid metabolism using TMT-labeled proteomic analysis. TEM analysis suggested altered bacterial morphology and structure post-treatment. A Salmonella-infected-mouse model indicated that GCTA administration improved inflammatory markers, alleviated intestinal histopathological alterations, and reduced Salmonella enterica serovar Enteritidis (S. Enteritidis) colonization in the liver and spleen of Salmonella-infected mice. The LD50 of GCTA was 4100 mg/kg with an oral single dose, vastly exceeding the therapeutic dose. Thus, GCTA exhibited antibacterial and anti-infective activity against S. Enteritidis. Our results provided insight into the molecular mechanisms of these antibacterial effects, and highlights the potential of GCTA as an alternative to antibiotics.

miR-186 promotes tumor growth in cutaneous squamous cell carcinoma by inhibiting apoptotic protease activating factor-1.

Cutaneous squamous cell carcinoma (cSCC) accounts for 20% of non-melanoma skin cancer worldwide. MicroRNAs (miRNAs or miRs) are a subtype of non-coding RNA associated with the progression of various types of human cancer. MiR-186 has been demonstrated to act as an oncogene in human tumors. However, the role of miR-186 in cSCC remains unclear. The expression of miR-186 and apoptotic protease activating factor 1 (APAF1) was examined using reverse transcription-quantitative polymerase chain reaction, western blotting and immunofluorescence. The correlation between miR-186 and APAF1 was determined using a dual-luciferase assay. Mimics or inhibitors of miR-186 were transfected into A-431 cells to establish cell lines with overexpressed or knocked-down miR-186, respectively. EdU staining and colony formation assays were performed to detect cell proliferation. Transwell and wound-healing assays were performed to analyze cell invasion and migration, respectively. Hoechst staining and flow cytometry were performed to assess cell apoptosis and cell cycle distribution. MiR-186 expression was significantly increased, while APAF1 expression was significantly decreased in cSCC tissues compared with the controls. An miR-186 binding site was predicted in APAF1 and their expression was negatively correlated in cSCC tissues. Cell proliferation, invasion and migration were significantly enhanced in the miR-186-overexpressed A-431 cells and attenuated in miR-186 knockdown cells compared with the control. APAF1 expression was regulated by miR-186, while APAF1 knockdown significantly promoted cell invasion and inhibited cell apoptosis. In summary, the results of the present study indicate that miR-186 serves as an oncogene in cSCC by inhibiting APAF1.

[Therapeutic effect of Artemisia argyi on oral ulcer in rats].

OBJECTIVE: To determine bacteriostatic abilities of Artemisia argyi extracts, and to explore the effect of Artemisia argyi extracts on oral ulcer in rats.
 Methods: We extracted the mixture of Artemisia argyi volatile oils and water-extraction by leaching method and evaluated the anti-microbial effect of Artemisia argyi extracts on common oral floras in vitro. The rat cheeks were burnt by NaOH to establish the models of oral ulcer. The curative effects of crude drug of Artemisia argyi extracts at 2.0, 1.0, 0.5 g/mL on oral ulcer in rats were evaluated by measuring the oral ulcer healing time. Serum TNF-α level and expression of proliferating cell nuclear antigen (PCNA) were analyzed by ELASA and immunohistochemical staining.
 Results: Artemisia argyi extracts obviously inhibited the Staphylococcus aureus and Streptococcus. NaOH-made oral ulcer in rats were successfully established. The crude drug at 2.0 and 1.0 g/mL obviously reduced healing time, significantly inhibited the release of TNF-α, and improved the PCNA level in the ulcer tissues (All P<0.01). The extracts obviously reduced the local inflammatory reaction and promoted tissue repair of oral ulcer.
 Conclusion: Artemisia argyi extracts promote tissue repair of oral ulcer via inhibiting bacterial growth, reducing the release of TNF-α and improving the PCNA level.