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1.
Yao Xue Xue Bao ; (12): 2388-2398, 2022.
Article in Chinese | WPRIM | ID: wpr-937056

ABSTRACT

In this study, dexamethasone (DXMS) and captopril (CAP) were co-loaded into poly(lactic-co-glycolic acid) (PLGA) nanoparticles with a surface coating of a phospholipid bilayer, and then the core-shell nanoparticles were modified with polyethylene glycol and integrin α8 antibody to obtain immunoliposome-nanoparticle hybrids (DXMS/CAP@PLGA-ILs). The role of nanoparticles on the renal targeting, anti-inflammatory effects, and macrophage differentiation were investigated. The results showed that the particle size of the nanoparticles was 115.9 ± 2.89 nm, and the core-shell structure could be observed under an electron microscope. The drug loading capacity of DXMS and CAP was 5.72% ± 0.37% and 7.51% ± 0.07%, respectively. The results of in vitro experiments showed that DXMS/CAP@PLGA-ILs could reduce the secretion of specific cytokines and the mRNA expression of markers in M2-type macrophages, thus promoting the differentiation of M2-type macrophages in the direction of unpolarized macrophages. In vivo experiments in mice showed that DXMS/CAP@PLGA-ILs had a significant renal targeting effect, which could restore the renal index, serum creatinine, and urea nitrogen levels of mesangial proliferative glomerulonephritis in mice. Moreover, DXMS/CAP@PLGA-ILs could reduce both the secretion of inflammatory cytokines and the mRNA expression levels of M1 and M2 macrophage markers in the kidney. All the animal experiments were in accordance with the regulations of Animal Ethics Committee of Sichuan Agricultural University. In conclusion, renal-targeting DXMS/CAP@PLGA-ILs could effectively regulate the polarization of macrophages and had an "anti-inflammatory/anti-fibrosis" therapeutic effect, providing a new strategy and basis for the targeted therapy of glomerulonephritis.

2.
Yao Xue Xue Bao ; (12): 2636-2641, 2020.
Article in Chinese | WPRIM | ID: wpr-837505

ABSTRACT

The aim of this study was to evaluate the effects and mechanisms of berberine (BBR) against dexamethasone (Dex)-induced metabolic disorders. 3T3-L1 cells were differentiated by Dex treatment and then treated with BBR (2.5, 5, 10 μmol·L-1). Lipid accumulation was detected using oil-red O staining. After review and approval of the ethics committee of the Institute of Materia Medica, Peking Union Medical College, Chinese Academy of Medical Sciences, C57BL/6N mice were randomly divided into three groups. In the BBR treatment group, mice were subcutaneously implanted with an osmotic pump containing Dex and gavaged with BBR (100 mg·kg-1·day-1) for 4 weeks. The model control group was implanted with a Dex osmotic pump with no other treatment. Mice given a saline-filled osmotic pump were used as a negative control. During the study, food intake and body weight were measured weekly. Subcutaneous fat and visceral fat was detected by MRI. At the end of the experiment the plasma levels of total cholesterol (CHO), triglyceride (TG), low-density lipoprotein cholesterol (LDL-c), high-density lipoprotein cholesterol (HDL-c), glucose (Glu), and muscle mass were measured. The expression of peroxisome proliferator-activated receptor γ (PPARγ) and AMP-activated protein kinase α (AMPKα) in 3T3-L1 cells and epididymal fat of C57BL/6N mice was evaluated through RT-PCR and Western blot analysis. The results showed that BBR inhibited Dex-induced adipocyte differentiation in 3T3-L1 preadipocytes by up to 23% in a dose-dependent manner. In C57BL/6N mice, berberine alleviated hyperlipidemia and hyperglycemia and reduced visceral fat accumulation induced by Dex. The results from RT-PCR and Western blot analysis showed that BBR reduced PPARγ expression and increased the phosphorylation of AMPKα in 3T3-L1 cells as well as in adipose tissue. Berberine might alleviate Dex-induced metabolic disorder and visceral fat accumulation by modulating PPARγ and AMPK expression.

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