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Objectives: Female obesity may be improved by the consumption of a high-polyphenolic-rich diet. Lycium ruthenicum Murray is a renowned edible plant, the fruit of which is abundant in anthocyanins and exhibits many biological activities. This study aimed to investigate the potential impact of anthocyanins derived from Lycium ruthenicum Murray (ACN) intervention on improving obesity by regulating the gut microbiota and bile acids (BAs) metabolism in high-fat diet (HFD)-induced female mice. Methods: A total of 32 C57BL/6J female mice were divided into four distinct groups: the Ctrl group (fed a normal diet), Ctrl + ACN group (fed a normal diet plus 8 mg/mL extract of ACN), HFD group (fed a high-fat diet), and HFD + ACN group (fed a HFD plus 8 mg/mL extract of ACN). Results: The findings showed that ACN significantly reduced the body weight, periovarian adipose mass, and adipocyte diameter, ameliorated lipid accumulation in the liver, and lowered the serum total cholesterol and low-density lipoprotein (LDL-C) levels in HFD-induced female mice. In addition, ACN exhibited a reversal of gut microbial dysbiosis in HFD-fed female mice, such as by enhancing the quantity of Lactobacillus and Allobaculum and reducing the abundance of Blautia and Faecalibaculum. Moreover, the results of fecal BAs showed that ACN led to a decrease in the ratio of primary to secondary BAs, mainly attributed to decreased levels of primary BAs, including CA, CDCA, αMCA, and HCA in HFD-induced female mice. Further analysis revealed that ACN may exert its anti-obesity effect by increasing the relative abundance of Lactobacillus_ jonsonii and Lactobacillus_reuteri within the gut and subsequently affecting the metabolism of fecal HDCA and GUDCA. Conclusion: These results indicated that ACN effectively inhibits HFD-induced obesity in female mice by regulating gut microbiota-related BA metabolism. [ABSTRACT FROM AUTHOR]

The high heterogeneity of receptor expression and varied chemotherapeutic sensitivity seriously compromise the therapeutic outcome of triple‐negative breast cancer (TNBC)‐targeting nanodrugs. In this work, a TNBC‐targeting nanodrug (designated as CPU) equipped with self‐promoted targeting property through chemotherapeutic upregulation of CD47 is constructed, enabling synergistic chemo/photodynamic therapy. Specifically, the hydrophobic docetaxel (DOC), which can upregulate the expression of CD47 in TNBC cells, is loaded in the nanomicelles (designated as P‐Pep) assembled from a protoporphyrin IX (PPIX)‐labeled amphiphilic chimeric peptide of Fmoc‐K(PPIX)‐AWSATWSNYWRH, obtaining the ca. 196 nm CPU. Aided by the enhanced permeability and retention effect and guidance of CD47‐binding peptide sequence, CPU is verified to prefer to accumulate in CD47 overexpressed TNBC cells, which can recruit more CPU by upregulating CD47 expression post‐treatment of DOC. Both in vitro and in vivo results demonstrate the superior tumor targeting ability, which can extensively amplify chemotherapeutic and photodynamic therapeutic effects while evading obvious adverse effects. The self‐promoted targeting strategy will inspire the design of nanodrugs for the personalized therapy of tumors with high heterogeneity and resistance. [ABSTRACT FROM AUTHOR]