Background: Laparoscopic resection is increasingly used in colorectal cancer (CRC). It has been suggested to carry short-term benefits in safety, recovery, and preservation on immune function for patients with CRC. However, the impact of laparoscopic resection on natural killer (NK) cells is largely unclear. Methods: A total of 200 patients with CRC across Dukes A/B/C stages were randomly assigned to laparoscopic or open resection. The blood samples were collected before and after the surgery. The total number of NK cells was quantified by flow cytometer. Lytic units 35 toward K562 was used to quantify NK cells activity. The outcomes between the groups across pathological stages were also analyzed. Results: The number and activity of NK cells decreased after the surgery in both groups. The laparoscopic group showed a faster recovery rate of NK cells function than the control group as assessed by cell count and lytic activity. Natural killer cells were impaired in a higher degree in patients at Dukes B/C stages. The recovery of NK cells to baseline level at day 7 postsurgery was observed in the laparoscopic group across all 3 stages. Conclusion: Generally, laparoscopically assisted surgery resulted in a better preservation on NK cells function. A better outcome was observed in patients with CRC at Dukes B/C stages.

Increasing evidence highlights the multiple roles of microRNAs (miRs) in the tumorigenesis of colorectal cancer (CRC); however, the molecular mechanism, particularly the target of miR-146b-5p in CRC has not been fully elucidated. The present study aimed to elucidate the influence of miR-146b-5p via regulating tumor necrosis factor receptor-associated factor 6 (TRAF6) in CRC. The expression levels of miR-146b-5p and TRAF6 in CRC tissue and cells were determined by reverse transcription quantitative PCR and western blotting. Binding between miR-146b-5p and TRAF6 was examined using a dual luciferase reporter gene assay. The impact of miR-146b-5p and TRAF6 on proliferation and migration of CRC cells was determined using Cell Counting Kit-8 and Transwell assays, respectively. An animal model of CRC was established to determine the carcinogenic effect of the miR-146b-5p-TRAF6 axis. The results demonstrated that miR-146b-5p was highly expressed in CRC tissue samples compared with in normal adjacent tissue samples and in CRC cells compared with in the normal NCM460 cell line, whereas TRAF6 was expressed at low levels. Overexpression of miR-146b-5p decreased TRAF6 expression in CRC HT29 and SW620 cells. miR-146b-5p targeted and inhibited TRAF6 expression in CRC cells. Furthermore, transfection with a miR-146b-5p mimic promoted the proliferation, migration and invasion of CRC cells and tumor growth; however, these effects were abolished by TRAF6 overexpression. Transfection with a miR-146b-5p inhibitor suppressed the proliferation of CRC cells. Taken together, the results from the present study demonstrated that miR-146b-5p could enhance the initiation and tumorigenesis of CRC by targeting TRAF6. These results will help elucidate the mechanisms underlying CRC development and will facilitate the development of targeted therapy for CRC.

Post-traumatic stress disorder (PTSD) has become a major disease that threatens human health. Neurotransmitters and the amygdala are found to be critical in the development and maintenance of PTSD. We aim to investigate the role of glycyrrhizin in treating PTSD. Contextual fear extinction and elevated plus maze test were applied to evaluate the anxiety and fear memory. Microdialysis and high-performance liquid chromatography were used to analyze the expression of amygdala neurotransmitters in PTSD animal models and to verify the effects of glycyrrhizin on major neurotransmitters. The protein levels of tryptophan hydroxylase 2 (TPH2) were examined by western bolt. Glycyrrhizin treatment significantly reduced anxiety and fear memory after 1 and 7 days of PTSD modelling. In addition, glycyrrhizin treatment restored the circadian rhythm changes of serotonin and TPH2. The present study found a significant circadian rhythm change of serotonin in the amygdala in PTSD rats. Besides, glycyrrhizin treatment restored the altered serotonin diurnal fluctuations, which raises important implications for PTSD treatment.

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Homoharringtonine (HHT) exhibits an anti-inflammatory activity. The potential protective effects and mechanisms of HHT on dextran sulfate sodium- (DSS-) induced colitis were investigated. DSS-induced colitis mice were intraperitoneally injected with HHT. Body weight, colon length, disease activity index (DAI), and histopathological change were examined. The relative contents of interleukin- (IL-) 1β, tumor necrosis factor- (TNF-) α, IL-6, and the chemokine (C-C motif) ligand 2 (CCL2) in the colon tissues and HHT-treated RAW264.7 cells were detected with the enzyme-linked immunosorbent assay. In the meantime, the levels of p-p65 and p-IκBα were detected by Western blot. The proportion of macrophages (CD11b+F4/80+) in the colon tissues was detected by flow cytometry. HHT alleviated DSS-induced colitis with downregulated TNF-α, IL-1β, IL-6, and CCL2 expression; reduced activation of nuclear factor-kappa B (NF-κB) signaling; and diminished proportion of recruited macrophages in colon tissues. It was further testified that HHT inhibited lipopolysaccharide-induced macrophage activation with reduced activation of NF-κB signaling. In addition, HHT inhibited the M1 polarization of both human and mouse macrophages, while HHT did not affect the differentiation of human CD4 T cells into Th17, Th1, or Treg cells and did not affect the proliferation and migration of human colon epithelial cells. In summary, HHT attenuates DSS-induced colitis by inhibiting macrophage-associated NF-κB activation and M1 polarization, which could be an option for the treatment of ulcerative colitis.