Publications by authors named "Shanzhai Wei"

Autophagy, a cellular degradation process involving the formation and clearance of autophagosomes, is mediated by autophagic proteins, such as microtubule-associated protein 1 light chain 3 (LC3) and sequestosome 1 (p62), and modulated by 3-methyladenine (3-MA) as well as chloroquine (CQ). Senescence, characterised by permanent cell cycle arrest, is marked by proteins such as cyclin-dependent kinase inhibitor 1 (p21) and tumour protein 53 (p53). This study aims to investigate the relationship between cell senescence and renal function in diabetic kidney disease (DKD) and the effect of autophagy on high-glucose-induced cell senescence.

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Objective: To investigate the safety and efficacy of recombinant human erythropoietin (rHuEPO) in combination with different doses of Roxadustat in treating renal anemia in patients on maintenance hemodialysis.

Methods: Eighty patients with renal anemia on maintenance hemodialysis treated in Shuyang Hospital of Traditional Chinese Medicine from January 2020 to December 2021 were selected as study subjects, and they were divided into a study group (n=40, high-dose Roxadustat + rHuEPO therapy) and a control group (Con) (n=40, low-dose Roxadustat + rHuEPO therapy) in accordance with different therapies. The effects of anemia therapy, changes in anemia indicators (hemoglobin (Hb), hematocrit (Hct)), changes in iron metabolism indicators (transferrin saturation (TSAT), serum ferritin (SF)), changes in oxidative stress indicators Malondialdehyde (MDA), Superoxide Dismutase (SOD), and changes in microinflammatory indicators IL6, CRP were compared between the two groups.

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Introduction: Uremia could accelerate atherosclerosis (AS) formation involving Treg/Th17 imbalance. Losartan regulates the imbalance between regulatory T cells (Treg cells) and T helper 17 cells (Th17 cells). However, their interactions in uremia accelerated AS (UAAS) remained poorly understood.

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Objective: To explore the protective roles of Astragalus polysaccharide (APS) on acute renal injury (AKI) induced by sepsis.

Methods: Firstly, an animal model of sepsis-induced AKI was established by injecting lipopolysaccharide (LPS) into mice. The mice were pretreated with an intraperitoneal injection of 1, 3, and 5 mg/(kg·d) APS for 3 consecutive days.

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