Background:Serum trace elements and oxidative stress factors are related to diabetic microvascular complications. The study was to investigate the complex relationship between trace elements, oxidative stress factors, and the severity of microvascular complications of diabetes in older adults. Methods:The present study included patients with or without type 2 diabetes, and blood glucose, blood lipids, trace elements (iron, magnesium, zinc), oxidative stress factors (malondialdehyde (MDA), nitric oxide (NO), superoxide dismutase (SOD), and total antioxidant capacity (T-AOC)) were evaluated. Risk factors for the severity of diabetic microvascular complications in older adults with diabetes were also estimated. Results:There were statistically significant differences in fasting blood glucose (FBG), triglycerides (TG), low density lipoprotein (LDL), glycated hemoglobin (HbAlc), MDA, NO, SOD, T-AOC, magnesium, and zinc between the two groups (P<0.05). Iron (rZinc = 0.147, rSOD = 0.180, rT-AOC = 0.193, P < 0.05) was positively correlated with zinc, SOD and T-AOC. Iron was negatively correlated with MDA (rMDA = -0.146, P < 0.05). Magnesium was positively correlated with SOD (rMagnesium = 0.147, P < 0.05). Zinc (rSOD = 0.616, rT-AOC = 0.575, P < 0.01) was positively correlated with SOD and T-AOC. Zinc (rMDA =-0.636, rNO=-0.616, P<0.01) was positively correlated with MDA and negatively correlated with NO. The course of disease (18.653, [5.726; 60.764], P <0.01), FBG (1.265, [1.059; 1.511], P <0.05), HbAlc (1.545, [1.431; 1.680], P <0.01), MDA (2.989, [1.900; 4.702], P <0.01) were risk factor for the severity of diabetic microvascular complications. Zinc (0.680, [0.503; 0.919], P < 0.05) and SOD (0.820, [0.698; 0.964], P < 0.05) were protective factors for the severity of diabetic microvascular complications. Conclusion:Serum trace elements are related to oxidative stress levels in older adults with type 2 diabetes. The more stable trace element in older adults with diabetes, the lower the oxidative stress and the fewer microvascular complications of diabetes.

Dysregulation of reactive oxygen species (ROS) production and ROS-regulated pathways in cancer cells leads to abnormal accumulation of reactive oxygen species, displaying a double-edged role in cancer progression, either supporting transformation/proliferation and stimulating tumorigenesis or inducing cell death. Cancer cells can accommodate reactive oxygen species by regulating them at levels that allow the activation of pro-cancer signaling pathways without inducing cell death via modulation of the antioxidant defense system. Therefore, targeting reactive oxygen species is a promising approach for cancer treatment. Ginsenosides, their derivatives, and related drug carriers are well-positioned to modulate multiple signaling pathways by regulating oxidative stress-mediated cellular and molecular targets to induce apoptosis; regulate cell cycle arrest and autophagy, invasion, and metastasis; and enhance the sensitivity of drug-resistant cells to chemotherapeutic agents of different cancers depending on the type, level, and source of reactive oxygen species, and the type and stage of the cancer. Our review focuses on the pro- and anticancer effects of reactive oxygen species, and summarizes the mechanisms and recent advances in different ginsenosides that bring about anticancer effects by targeting reactive oxygen species, providing new ideas for designing further anticancer studies or conducting more preclinical and clinical studies.

BACKGROUND:Heart failure with preserved ejection fraction (HFpEF) is a multifaceted syndrome with a complex aetiology commonly associated with comorbidities such as diabetes mellitus, obesity, hypertension and renal disease. Various diseases induce systemic, chronic and low-grade inflammation; microvascular dysfunction; metabolic stress; tissue ischemia; and fibrosis, leading to HFpEF. An effective treatment for HFpEF is lacking, largely owing to its pathophysiological heterogeneity. Recent studies have revealed that microRNAs (miRNAs) play crucial roles in regulating the pathogenesis of HFpEF and its comorbidities.METHODS:This narrative review included original articles and reviews published over the past 20 years found through 'PubMed' and 'Web of Science'. The search terms included "HFpEF," "MicroRNAs," "comorbidities," "Microvascular Dysfunction (MVD)," "inflammation," "pathophysiology," "endothelial dysfunction," "energy metabolism abnormalities" "cardiac fibrosis" and "treatment."RESULTS:Inflammation, MVD, abnormal energy metabolism, myocardial hypertrophy and myocardial fibrosis are important pathophysiological mechanisms underlying HFpEF. As gene expression regulators, miRNAs may contribute to the pathophysiology of HFpEF and are expected to serve in the stratification of patients with HFpEF and as prognostic indicators for monitoring treatment responses.CONCLUSIONS:A customized strategy based on miRNAs has emerged as an effective treatment for HFpEF. In this review, we discuss recent research surrounding miRNAs and HFpEF and propose potential miRNA targets for the pathophysiology of HFpEF and its comorbidities. Although current research concerning miRNAs and their therapeutic potential is in its early stages, miRNA-based diagnostics and therapeutics hold great promise in the future.

Objective:To investigate the effects of Zinc sulfate on preventing human umbilical veins endothelial cells ( HUVECs) from oxidative stress. Methods:Hydrogen peroxide was used to stimulate HUVECs to build the oxidative stress model in vitro. HUVECs were divided into normal group, H2 O2 group, Zinc sulfate group and Zinc sulfate treated group. Method of nitrate reductase was used to detect the content of nitric oxide ( NO ) and ELISA was used to detect the content of endothelin ( ET ) in supernatant in different groups. The level of HO-1,SOD and CAT of HUVECs were measured by Western blot. Apoptosis of HUVECs was examined by TUNEL as well. Results: Zinc sulfate could enhance the content of NO and decrease the content of ET in the supernatant,which induced by hydrogen peroxide on HUVECs. Zinc sulfate could also increase the level of HO-1, SOD and CAT obviously and decrease the apoptosis cells significantly induced by H2 O2 . Conclusion: Zinc sulfate play an important role in resisting oxidative stress in HUVECs, and maybe prevent HUVECs from oxidative stress damage. Zinc sulfate is expected to be an effective medicine on improving endothelial cells anti-oxidative ability.