BackgroundA national health literacy scale was developed in China in 2012, though no studies have validated it. In this investigation, we assessed the reliability, construct validity, and measurement invariance of that scale.MethodsA population-based sample of 3731 participants in Hunan Province was used to validate the Chinese Resident Health Literacy Scale based on item response theory and classical test theory (including split-half coefficient, Cronbach’s alpha, and confirmatory factor analysis). Measurement invariance was examined by differential item functioning.ResultsThe overall Cronbach’s alpha of the scale was 0.95 and Spearman-Brown coefficient 0.94. Confirmatory factor analysis showed that the test measured a unidimensional construct with three highly correlated factors. Highest discrimination was found among participants with limited to moderate health literacy. In all, 64 items were selected from the original scale based on factor loading, Pearson’s correlation coefficient, and discrimination and difficulty parameters in item response theory. Measurement invariance was significant but slight. According to the two-level linear model, health literacy was associated with education level, occupation, and income.ConclusionsThe 2012 national health literacy scale was validated, and 64 items were selected based on classical test theory and item response theory. The revised version of the scale has strong psychometric properties with minor measurement invariance.

Fibrosis is the major pathological feature of diabetic kidney disease (DKD). Autophagy, a process to maintain metabolic homeostasis, is obviously inhibited in DKD. Triptolide (TP) is a traditional Chinese medicine extract known for immune suppression and anti-inflammatory and anti-cancer activities. In this study, we investigated the effects of TP on autophagy and fibrosis in DKD. TP restored autophagy and alleviated fibrosis in DKD rats and high-glucose-incubated human mesangial cells. After we applied 3-methyladenine (an autophagy inhibitor) and autophagy-related gene 5-small interfering RNA (siRNA), we found that the improvement of fibrosis on TP was related to the restoration of autophagy. In addition, miR-141-3p levels were increased under high glucose but reduced after TP treatment. miR-141-3p overexpression aggravated the fibrosis and restrained the autophagy further, while miR-141-3p inhibition imitated the effects of TP. As an action target, phosphatase and tensin homolog (PTEN) showed corresponding opposite changes. After PTEN-siRNA transfection, the effects of TP on autophagy and fibrosis were inhibited. PTEN levels were downregulated, with downstream phosphorylated protein kinase B (Akt) and the mammalian target of rapamycin (mTOR) upregulated in high glucose, which were reversed by TP treatment. These findings indicate that TP alleviates fibrosis by restoring autophagy through the miR-141-3p/PTEN/Akt/mTOR pathway and is a novel therapeutic option for DKD.

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Tissue regeneration following injury from disease or medical treatment still represents a challenge in regeneration medicine. Prostaglandin E2 (PGE2), which involves diverse physiological processes via E-type prostanoid (EP) receptor family, favors the regeneration of various organ systems following injury for its capabilities such as activation of endogenous stem cells, immune regulation, and angiogenesis. Understanding how PGE2 modulates tissue regeneration and then exploring how to elevate the regenerative efficiency of PGE2 will provide key insights into the tissue repair and regeneration processes by PGE2. In this review, we summarized the application of PGE2 to guide the regeneration of different tissues, including skin, heart, liver, kidney, intestine, bone, skeletal muscle, and hematopoietic stem cell regeneration. Moreover, we introduced PGE2-based therapeutic strategies to accelerate the recovery of impaired tissue or organs, including 15-hydroxyprostaglandin dehydrogenase (15-PGDH) inhibitors boosting endogenous PGE2 levels and biomaterial scaffolds to control PGE2 release.