We have previously demonstrated the anticancer effect of anthocyanins. In this study, we explored the biological activities of delphinidin, the most common of the anthocyanidin monomers, that were related to autophagy in HER-2 positive breast cancer MDA-MB-453 and BT474 cells. The effects of various doses of delphinidin on the proliferation and apoptosis of MDA-MB-453 and BT474 cells were analysed. Autophagy was identified as a critical factor that influenced chemotherapy, and the autophagic mechanism in delphinidin-treated cells was investigated. The autophagy inhibitors, 3-MA and BA1, were used to analyse the effects of autophagy inhibition. Delphinidin inhibited proliferation, promoted apoptosis, and induced autophagy in MDA-MB-453 and BT474 cells in a dose-dependent manner. The inhibition of autophagy enhanced the delphinidin-induced apoptosis and antiproliferative effect in both HER-2 positive breast cancer cells. In addition, delphinidin induced autophagy via suppression of the mTOR signalling pathway and activation of the AMPK signalling pathway in HER-2 positive breast cancer cells. Collectively, the results showed that delphinidin induced apoptosis and autophagy in HER-2 positive breast cancer cells and that autophagy was induced via the mTOR and AMPK signalling pathways. The suppression of autophagy promoted the anticancer effects of delphinidin.

Background: Prostate cancer is the second leading cause of cancer-related death among males in America. The patients’ survival time is significantly reduced after prostate cancer develops into castration-resistant prostate cancer (CRPC). It has been reported that AKR1C3 is involved in this progression, and that its abnormal expression is directly correlated with the degree of CRPC malignancy. Genistein is one of the active components of soy isoflavones, and many studies have suggested that it has a better inhibitory effect on CRPC. Objective: This study aimed to investigate the antitumor effect of genistein on CRPC and the potential mechanism of action. Design: A xenograft tumor mouse model established with 22RV1 cells was divided into the experimental group and the control group, and the former was given 100 mg/kg.bw/day of genistein, with 22RV1, VCaP, and RWPE-1 cells cultured in a hormone-free serum environment and treated with different concentrations of genistein (0, 12.5, 25, 50, and 100 μmol/L) for 48 h. Molecular docking was used to elucidate the molecular interactions between genistein and AKR1C3. Results: Genistein inhibits CRPC cell proliferation and in vivo tumorigenesis. The western blot analysis confirmed that the genistein significantly inhibited prostate-specific antigen production in a dose-dependent manner. In further results, AKR1C3 expression was decreased in both the xenograft tumor tissues and the CRPC cell lines following genistein gavage feeding compared to the control group, with the reduction becoming more obvious as the concentration of genistein was increased. When the genistein was combined with AKR1C3 small interfering ribonucleic acid and an AKR1C3 inhibitor (ASP-9521), the inhibitory effect on the AKR1C3 was more pronounced. In addition, the molecular docking results suggested that the genistein had a strong affinity with the AKR1C3, and that it could be a promising AKR1C3 inhibitor. Conclusion: Genistein inhibits the progression of CRPC via the suppression of AKR1C3.

Background: Organism can lead to excessive nutrient consumption in the infected state and increase nutritional risk, which is detrimental to the control of the infection and can further aggravate the disease.Objectives: To investigate the impact of nutritional risk and the NRS2002 score on disease progression and prognosis in patients with COVID-19.Methods: This was a retrospective cohort study including 1,228 COVID-19 patients, who were divided into a with-nutritional risk group (patients with NRS2002 score ≥ 3) and a without-nutritional risk group (patients with NRS2002 score < 3) according to the NRS2002 score at admission. The differences in clinical and outcome data between the two groups were compared, and the relationship between the NRS2002 score and the disease progression and prognosis of COVID-19 patients was assessed.Results: Of 1,228 COVID-19 patients, including 44 critical illness patients and 1,184 non-critical illness patients, the rate of harboring nutritional risk was 7.90%. Compared with those in the without-nutritional risk group, patients in the with-nutritional risk group had a significantly longer coronavirus negative conversion time, significantly lower serum albumin (ALB), total serum protein (TP) and hemoglobin (HGB) at admission, discharge or 2 weeks, a significantly greater proportion with 3 or more comorbidities, and a significantly higher rate of critical illness and mortality (all p < 0.001). Multiple regression analysis showed that nutritional risk, NRS2002 score and ALB at admission were risk factors for disease severity. In addition, nutritional risk, NRS2002 score and TP at admission were risk factors for prognosis. The NRS2002 score showed the best utility for predicting critical illness and death in COVID-19 patients.Conclusion: Nutritional risk and a high NRS2002 score are closely related to disease progression and poor prognosis in COVID-19 patients. For patients with NRS2002 score > 0.5, early intervention of malnutrition is needed to reduce the occurrence of critical disease. Additionally, for patients with NRS2002 score > 5.5, continuous nutritional support therapy is needs to reduce mortality and improve prognosis.Clinical Trial registration: [https://www.chictr.org.cn/historyversionpub.aspx?regno=ChiCTR2000034563], identifier [Chinese Clinical Trial Register ChiCTR2000034563].

Retinal photochemical damage (RPD) can be the main cause of various ophthalmic diseases, such as age-related macular degeneration (AMD) and retinitis pigmentosa (RP). Patients' vision can be severely impaired in the late stages of these eye diseases. Delphinidin, one of the major functional components of anthocyanins, has shown preventive effects on RPD and ophthalmic diseases induced by RPD, but the underlying mechanisms are complex and unclear. This study investigated the protective effect of delphinidin on photochemically damaged retinal photoreceptors in vivo and in vitro and characterized the underlying mechanisms. In vivo experiments showed that delphinidin downregulated the expression levels of caspase-3, and reduced the apoptosis rate of retinal photoreceptor cells in SD rats, thus protecting the structural integrity of the retina. In vitro experiments showed that delphinidin could maintain the normal ultrastructure of the mitochondrial endoplasmic reticulum membrane, reduce the apoptosis rate caused by light injury and improve the survival rate of light-damaged 661W cells. In addition, we found that delphinidin increased the mRNA and activated protein expression of NF-κB p65, NF-κB p50, and IκBα in photochemically injured 661W cells, and decreased the mRNA and protein expression of AP-1 (c-fos/c-jun) and Caspase-3/-8/-9. Compared with the model group, phospho-NF-κB p65 in delphinidin-treated cells was translocated into the nucleus, and the nuclear phospho-NF-κB p65 expression was increased, while nuclear c-jun expression was decreased. These results suggested that delphinidin resisted RPD-induced apoptosis of retinal photoreceptors by regulating the expression of factors involved in the NF-κB/AP-1/caspase-3 pathway.

Background: Dietary patterns play an important role in obesity and metabolic syndrome, and there are few studies on the relationship between dietary patterns and obesity phenotype. In order to identify the main dietary patterns in Hechuan and clarify how they are associated with obesity phenotypes. Methods: The data were derived from the baseline survey data of Hechuan Cohort, a general population cohort study in Southwest China. A semi-quantitative food frequency questionnaire was used to investigate dietary habits of the subjects in the past year. Principal component analysis was used to identify the main dietary patterns, and multinomial logistic regression analysis was used to describe the correlation between dietary patterns and obesity phenotypes. Results: Three major dietary patterns were identified. The subjects followed the wheaten food dietary pattern had a higher likelihood having MHO (OR 1.05, 95%CI 1.02-1.08), MUNW (OR 1.08, 95%CI 1.00-1.16) and MUO (OR 1.07, 95%CI 1.04-1.11). Specifically, those with the highest wheaten food dietary pattern were 1.60 times more likely to have MHO (OR 1.60, 95%CI 1.25-2.05), 2.62 times more likely to have MUNW (OR 2.62, 95%CI 1.28-5.37) and 2.01 times more likely to have MUO (OR 2.01,95%CI 1.51-2.69) than those with the lowest wheaten food pattern. Conclusions: wheaten food dietary pattern can increase the risk of obesity and metabolic abnormalities, and timely intervention should be carried out for this group of people.