Evaluation of the value of combined detection of tumor markers CA724, carcinoembryonic antigen, CA242, and CA19-9 in gastric cancer.

BACKGROUND: Gastric cancer is a global health concern that poses a significant threat to human well-being. AIM: To detecting serum changes in carcinoembryonic antigen (CEA), carbohydrate antigens (CA) 724, CA242, and CA19-9 expression among patients with gastric cancer. METHODS: Eighty patients diagnosed with gastric cancer between January 2020 and January 2023 were included in the observation group, while 80 patients with benign gastric diseases were included in the control group. Both groups were tested for tumor markers (CA724, CEA, CA242, and CA19-9]. Tumor marker indicators (CA724, CEA, CA242, and CA19-9) were compared between the two groups, assessing positive rates of tumor markers across various stages in the observation group. Additionally, single and combined detection of various tumor markers were examined. RESULTS: The sensitivity, specificity, accuracy, positive predictive value, and negative predictive value observed for the combined detection of CA724, CEA, CA242, and CA19-9 were higher than those of CA724, CEA, CA242, and CA19-9 individually. Therefore, the combined detection of CA724, CEA, CA242, and CA19-9 has a high diagnostic accuracy and could reduce the occurrence of missed or misdiagnosed cases, facilitating the early diagnosis and treatment of patients. CONCLUSION: CA724, CEA, CA242, and CA19-9 serum levels in gastric cancer patients significantly surpassed those in non-gastric cancer patients (P < 0.05). Their combined detection can improve the diagnostic accuracy for gastric cancer, warranting clinical promotion.

Purification and Structural Characterization of Dendrobium officinale Polysaccharides and Its Activities.

In this study, Dendrobium officinale polysaccharide (named DOPS-1) was isolated from the stems of Dendrobium officinale by hot-water extraction and purified by using Sephadex G-150 column chromatography. The structural characterization, antioxidant and cytotoxic activity were carried out. Based on the results of HPLC, GC, Congo red experiment, together with periodate oxidation, Smith degradation, SEM, FT-IR, and NMR spectral analysis, it expressed that DOPS-1 was largely composed of mannose, glucose and galacturonic acid in a molar ratio of 3.2 : 1.3 : 1. The molecular weight of DOPS-1 was 1530 kDa and the main chain was composed of (1→4)-ß-D-Glcp, (1→4)-ß-D-Manp and 2-O-acetyl-(1→4)-ß-D-Manp. The measurement results of antioxidant activity showed that DOPS-1 had the strong scavenging activities on hydroxyl radicals, DPPH radicals and superoxide radicals and the high reducing ability in vitro. Moreover, DOPS-1 was cytotoxic to all three human cancer cells of MDA-MB-231, A549 and HepG2.

Effects of volatile oil from ginger on the murine B16 melanoma cells and its mechanism.

In this study, the inhibitory effects of volatile oil from ginger on melanogenesis and its antioxidant characteristics were investigated. The effects of volatile oil from ginger on cell proliferation, melanin content and tyrosinase activity were determined using a microplate reader. In addition, the expression of melanogenesis-related protein was determined by western blotting. The results indicate that the tested concentrates of volatile oil from ginger showed inhibitory effects on cell proliferation and melanogenesis. This revealed that volatile oil from ginger exhibited apparent capacities for scavenging ROS and lipid peroxidation. Furthermore, volatile oil from ginger improved the activities of GSH, SOD and CAT in B16 melanoma cells. These results demonstrated that volatile oil from ginger suppressed melanin synthesis through its antioxidant properties and the inhibitory effects on tyrosinase activity and melanogensis-related proteins. Hence, volatile oil from ginger could be used as an effective skin-whitening agent applied in food industry.

Astaxanthin attenuated pressure overload-induced cardiac dysfunction and myocardial fibrosis: Partially by activating SIRT1.

BACKGROUND: Myocardial fibrosis contributes to cardiac dysfunction. Astaxanthin (AST), a member of the carotenoid family, is a well-known antioxidant, but its effect on and underlying mechanisms in myocardial fibrosis are poorly understood. METHODS: In vivo, myocardial fibrosis and cardiac dysfunction were induced using transverse aortic constriction (TAC). AST was administered to mice for 12weeks post-surgery. In vitro, transforming growth factor ß1 (TGF-ß1) was used to stimulate human cardiac fibroblasts (HCFs). EX-527 (6-chloro-2, 3, 4, 9-tetrahydro-1H-carbazole-1-carboxamide) and SIRT1 siRNA were used to inhibit SIRT1 in vivo and in vitro, respectively. The effects of AST on cardiac function and fibrosis were determined. SIRT1 expression and activity were measured to explore the mechanisms underlying its effects. RESULTS: AST improved cardiac function and attenuated fibrosis. Receptor activated-SMADs (R-SMADs), including SMAD2 and SMAD3, played important roles in these processes. The TAC surgery-induced increases in the expression of phosphorylated and acetylated R-SMADs were attenuated by treatment with AST, the translocation and transcriptional activity of R-SMADs were also restrained. These effects were accompanied by an increase in the expression and activity of SIRT1. Inhibiting SIRT1 attenuated the acetylation and transcriptional activity of R-SMADs, but not their phosphorylation and translocation. CONCLUSIONS: Our data demonstrate that AST improves cardiac function and attenuates fibrosis by decreasing phosphorylation and deacetylation of R-SMADs. SIRT1 contributes to AST's protective function by reducing acetylation of R-SMADs. GENERAL SIGNIFICANCE: These data suggest that AST may be useful as a preventive/therapeutic agent for cardiac dysfunction and myocardial fibrosis.

An asymmetrically dimethylarginated nuclear 90 kDa protein (p90aDMA) induced by interleukin (IL)-2, IL-4 or IL-6 in the tumor microenvironment is selectively degraded by autophagy.

Protein arginine methylation is a common posttranslational modification resulting in the generation of asymmetric dimethylarginine (aDMA) and symmetric dimethylarginine (sDMA). Currently, the regulation of aDMA or sDMA by hypoxia, nutrient stavation or cytokines in the tumor microenvironment remains largely unknown. Here we show that p90aDMA, p70aDMA and p90sDMA, endogenous proteins containing aDMA or sDMA with mass 70 or 90 kDa, were widely and dominantly expressed in breast cancer cell lines. Notably, it was p90aDMA rather than p90sDMA that accumulated in the nucleus upon stimulation of cancer cells with interleukin (IL)-2, IL-4, IL-6 but not IL-8. In addition, the p90aDMA accumulation could be inhibited after treatment with a global methyltrasferase inhibitor, adenosine-2',3'-dialdehyde (AdOx). It seemed that some endogenous proteins in cancer cells were asymmetrically arginine-methylated upon exposure to some cytokines.. Furthermore, endogenous proteins of aDMA, such as p90aDMA and p70aDMA, were degraded in response to hypoxia, nutrient starvation and rapamycin treatment in breast and cervical cancer cells. IL-2/4/6 slightly increased basal autophagy but slightly decreased the rapamycin­induced autophagy in cancer cells, suggesting that IL-2/4/6 and autophagy inducers play distinct roles in the regulation of aDMA of proteins. Conversely, rapamycin accumulated p90sDMA in MDA-MB­231 and MCF-7 cells. Taken together, our results add a new dimension to the complexity of arginine methylated regulation in response to various stimuli and provide the first evidence that aDMA serves as one specific degradation signal of selective autophagy.

Profilin-1 promotes the development of hypertension-induced cardiac hypertrophy.

OBJECTIVE: Cardiac hypertrophy is a major cause of heart failure and sudden cardiac death among hypertensive individuals. The present study examined the effects of profilin-1 on hypertension-induced cardiac hypertrophy. METHODS: We used adenovirus injection to knockdown or overexpress profilin-1 in spontaneous hypertensive rats (SHRs). As a control, blank adenovirus was injected into age-matched SHRs and Wistar-Kyoto rats (WKYs). SBP and cardiac mass index were measured. Cardiac tissues were stained with hematoxylin-eosin and sirius red, and cardiac ultrastructure was imaged using transmission electron microscopy. Actin filament was quantified by staining with TRIC-tagged phalloidin. Caveolin-3 abundance and endothelial nitric oxide synthase (eNOS) activity were measured using real-time quantitative PCR, Western blot or immunofluorescence staining. RESULTS: Endogenous profilin-1 was highly expressed in hypertrophic myocardium of SHRs compared with WKYs. Lowering profilin-1 expression in SHRs significantly attenuated hypertension-induced cardiac hypertrophy and fibrosis and displayed a significant preservation of myofibrils, sarcolemmal caveolae, abundance of caveolin-3 protein, activity of eNOS and production of nitric oxide (NO). In contrast, transgenic overexpression of profilin-1 in SHRs induced more serious cardiac hypertrophy and fibrosis with significant reduction of sarcolemmal caveolae, caveolin-3 protein, eNOS activity, and production of NO when compared with SHR controls. CONCLUSION: Profilin-1 promotes cardiac hypertrophy partly through interfering with the formation of sarcolemmal caveolae and attenuating the eNOS/NO pathway. These results demonstrate a crucial role for profilin-1 in hypertensive cardiac hypertrophy.

[Protective effect of Qihuang Mingmu capsule on retina of diabetic mice and its impact on VEGF expression].

OBJECTIVE: To investigate the protective effect of Qihuang Mingmu capsule (QHMM) on retina of diabetic mice and its impact on VEGF expression. METHOD: Forty KK/Upj-Ay mice were randomly divided into the model group and high, middle and low dose QHMM (8.32, 4.16, 2.08 g x kg(-1)) groups. Additional 10 C57BL/6 mice were selected as the control group. Mice were orally administered for three months. Their general appearance, fasting blood-glucose (FBG) and glycosylated hemoglobin (HbA1c) were observed. Pathological changes of retina were observed by light microscope and electron microscope. The expressions of vascular endothelial growth factor (VEGF), growth factor receptors-1 (Flt-1) and growth factor receptors-2 (Flk-1) were examined by Real-time PCR (qPCR) and Western blot. RESULT: QHMM could ameliorate the symptoms of diabetic mice to varying degrees, decrease FBG and HbA1c, alleviate pathological lesions of retina and decrease the expressions of VEGF, Flt-1, Flk-1 mRNA and protein. CONCLUSION: QHMM has the protective effect on diabetic retinopathy of mice by inhibiting the expressions of VEGF, Flt-1 and Flk-1 and intervening VEGF-VEGFR signal transduction pathway.