Objective To investigate expression of histone deacetylase 5 (HDAC5) in normal and colorectal cancer (CRC) tissues and its mechanism.Methods Immunohistochemistry was used to detect the expression of HDAC5 in CRC tissues.The relationship between HDAC5 expression content and survival prognosis was analyzed.Proliferation,immigration and apoptosis changes were observed after knockdown of HDAC5.Results Positive expression of HDAC5 in tumor tissue was related with poor prognosis of CRC patients,and HDAC5 could inhibit the LS174T cell proliferation by regulating the SIX1 expression.Conclusion Our results reveal that HDAC5 expression is variant in CRC tissues,and it is correlated with prognosis of colorectal cancer,and can affect cell proliferation by regulating the SIX1 expression.

Objective To investigate expression of histone deacetylase 5 (HDAC5) in normal and colorectal cancer (CRC) tissues and its mechanism.Methods Immunohistochemistry was used to detect the expression of HDAC5 in CRC tissues.The relationship between HDAC5 expression content and survival prognosis was analyzed.Proliferation,immigration and apoptosis changes were observed after knockdown of HDAC5.Results Positive expression of HDAC5 in tumor tissue was related with poor prognosis of CRC patients,and HDAC5 could inhibit the LS174T cell proliferation by regulating the SIX1 expression.Conclusion Our results reveal that HDAC5 expression is variant in CRC tissues,and it is correlated with prognosis of colorectal cancer,and can affect cell proliferation by regulating the SIX1 expression.

ObjectiveTo elucidate the potential mechanisms by which the classic prescription Anmeidan alleviates cognitive impairment in insomnia model rats through metabolic profiling. MethodsA total of 60 SD rats were randomly divided into six groups： blank group， model group， low-， medium-， and high-dose Anmeidan groups， and the Suvorexant group， with 10 rats in each group. Except for the blank group， the insomnia model was established in all other groups via intraperitoneal injection of para-chlorophenylalanine. The Suvorexant group was administered Suvorexant solution （30 mg·kg^-1·d^-1） by gavage， while the low-， medium-， and high-dose Anmeidan groups received Anmeidan decoction （4.55， 9.09， 18.18 g·kg^-1·d^-1） by gavage. The blank group received an equivalent volume of normal saline. The open field test was used to assess spatial exploration and anxiety/depressive-like behaviors in rats. Serum levels of epidermal growth factor （EGF）， brain-derived neurotrophic factor （BDNF）， and vasoactive intestinal peptide （VIP） were measured using enzyme-linked immunosorbent assay （ELISA）. Untargeted metabolomics was employed to identify differential metabolites in rat serum， and systematic biological methods were applied to analyze the potential targets and pathways of Anmeidan. ResultsCompared to the blank group， the model group exhibited significant reductions in total distance traveled， average speed， number of entries into the central area， time spent in the central area， and frequency of upright events （P<0.01）， along with significant decreases in VIP， EGF， and BDNF levels （P<0.05，P<0.01）. A total of 100 differential metabolites were identified between the model and blank groups. Compared to the model group， the low-， medium-， and high-dose Anmeidan groups showed significant increases in total distance traveled， average speed， number of entries into the central area， time spent in the central area， and frequency of upright events （P<0.05，P<0.01）， as well as a significant increase in VIP levels （P<0.05，P<0.01）. Anmeidan significantly reversed abnormal changes in 67 metabolites compared to the model group. A combined analysis identified 134 potential targets of Anmeidan， with network topology analysis suggesting that Caspase-3， B-cell lymphoma 2 （Bcl-2）， nuclear transcription factor-κB （NF-κB）， interleukin-1β （IL-1β）， interleukin-2 （IL-2）， matrix metalloproteinase-9 （MMP-9）， and Toll-like receptor 4 （TLR4）， among others， may serve as key targets of Anmeidan. Kyoto Encyclopedia of Genes and Genomes （KEGG） pathway analysis revealed major enriched pathways， including the cyclic adenosine monophosphate （cAMP） signaling pathway， hypoxia inducible factor-1 （HIF-1） signaling pathway， and IL-17 signaling pathway. ConclusionThis study demonstrates that Anmeidan can recalibrate abnormal metabolic profiles in insomnia model rats to mitigate cognitive impairment， with its mechanisms of action potentially involving the regulation of immune-inflammatory responses， energy metabolism， and apoptosis-related pathways.

Machine Learning ; Image Processing, Computer-Assisted/methods*