KJCKorea
Journal Central

Modified SOUL-tang (MST) has been known to improve recovery of energy, regulation of body heat, and improvement of qi circulation, but the scientific evidence of MST has not been established. Here, we aimed to determine the energy-regulating effect of MST on performance in the forced swimming test (FST) and on RAW264.7 macrophage activity. MST was administered orally once a day for 28 days. On the 28 days, the immobility time in the FST was significantly decreased in the MST-fed group in comparison with the control group. MST induced a significant increase in serum interferon-γ, interlukin-2, and tumor necrosis factor (TNF)-α levels compared with the control group. In vitro experiments demonstrated that MST significantly increased the expression of TNF-α, nitric oxide (NO), and inducible NO synthase in RAW264.7 macrophages. Furthermore, MST stimulation induced the phosphorylation of IκBα, subsequently promoting the nuclear translocation of nuclear factor-κB. These results indicate that MST enhances energy by boosting immune function, suggesting its potential as an energizer for individuals with energy deficiency.

Objective: Bromodomain-containing protein 4 (BRD4) is a critical transcriptional regulator of cell growth and differentiation. BRD4 inhibitors have the potential to curb cancer cell proliferation by downregulating the expression of associated genes. This study investigated the anticancer effects of a novel BRD4 inhibitor, OPT-0010, on human hepatic carcinoma cell lines. Materials and Methods: Two hepatic carcinoma cell lines, SK-Hep1 and Huh-7, were subjected to 48-h OPT-0010 treatment. Cell viability and proliferation were evaluated using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and adenosine triphosphate assays, respectively. Flow cytometry was used to detect cell cycle arrest. Apoptotic cell death was evaluated using Annexin V and caspase 3 assays. BRD4 and apoptosis-related genes (e.g., BCL2 and BAX) and proteins (e.g., cleaved caspase-3, cleaved PARP, and BCL2) were evaluated using real-time polymerase chain reaction and western blotting, respectively. Additionally, a mouse xenograft model was used to analyze tumor growth, weight, and messenger RNA (mRNA) levels. Results: OPT-0010 significantly decreased cell viability and proliferation, inducing cell cycle arrest and apoptotic cell death in both SK-Hep1 and Huh-7 cell lines. OPT-0010 showed substantial anti-tumor efficacy in a mouse xenograft model, affecting tumor growth and the expression of BRD4 and apoptosis-related proteins. Furthermore, in synergy with sorafenib, OPT-0010 exhibited an enhanced effect, increasing apoptotic cell death, and effectively suppressing tumor growth in vitro and in vivo. Conclusion: This study provided comprehensive insights into the mechanisms and therapeutic effects of OPT-0010 on human hepatic carcinoma cell lines and in vivo mouse xenograft models. These results suggest that OPT-0010 is a promising therapeutic agent for treating human hepatocellular carcinoma.

Objective: Obesity is a complex chronic disease linked to over 200 chronic diseases and has increased in prevalence worldwide to date. This absolutely requires drastic lifestyle changes including practice of exercise and intake of low-calorie diet. However, many pharmacotherapies, approved by FDA, have recently been developed to improve obesity. Especially glucagon-like peptide 1 (GLP-1), a gut hormone that reduces appetite and promotes insulin secretion, has recently attracted much attention as a promising anti-obesity target. We developed ‘NEXITOP’ consisting of several natural substances that have previously been proven to help with obesity and aimed to evaluate the anti-obesity effects via GLP-1 modulation in high-fat diet (HFD)-induced obese mice. Method: After early feeding HFD for 2 weeks, forty of C57BL/6J mice were divided into five groups: normal diet, HFD control, metformin (200 mg/kg), and NEXITOP (1300 or 2600 mg/kg). And then, NEXTOP and metformin were administered for 8 weeks. Results: Feeding of HFD for 10 weeks dramatically increased both caloric intake and body weight (1.4 and 1.6-fold, respectively). While the administration of NEXITOP significantly improved both elevated caloric intake (19%) and body weight (12%). The administration of NEXITOP also showed reducible effects of abdominal fats (visceral; 2.1-fold, epididymal; 4.8-fold, retroperitoneal; 1.5-fold) in HFD-fed mice. Also, the administration of NEXITOP greatly elevated serum GLP-1 levels at 2, 4 and 6 weeks as well as its effects were superior to metformin at 2 and 4 weeks. Conclusion: Our findings suggest that NEXITOP exerted an anti-obesity effect, and its underlying mechanism may involve regulation of the serum GLP-1 level.