[Identification of quality markers for Pudilan Xiaoyan Oral Liquid].

On the basis of anti-inflammatory activity, combined with multiple indicators, the quality markers of Pudilan Xiaoyan Oral Liquid were screened and determined for quality control. Lipopolysaccharide(LPS) was used to induce normal human bronchial epithelial cell(NHBE) inflammation model. The anti-inflammatory effects of the main chemical components in Pudilan Xiaoyan Oral Liquid were examined one by one, and the pharmacodynamic basis for the overall anti-inflammatory efficacy of Pudilan Xiaoyan Oral Liquid was clarified to identify the quality markers of Pudilan Xiaoyan Oral Liquid and the contents of the quality markers were determined by high performance liquid chromatography(HPLC).

The structural composition of components contributes to the superiority of the geoherb for "diuresis and diffusing dampness".

The purpose of this study is to explore the intrinsic reasons for the superiority of the salt-made geoherb comparing the content of various components of the salt-made geoherb . The effects of "diuresis and diffusing dampness" using salt-made from seven different origins were investigated through pharmacodynamic experiments and . The results indicated that salt-made from different origins had diuretic efficacy; this was demonstrated by the significant increase in the volume of rat urine, the concentration of Na, K, and Cl in the urine, and the significant decrease in the levels of AQP-2 in rat renal medulla and HK-2 cells.

β-elemene regulates endoplasmic reticulum stress to induce the apoptosis of NSCLC cells through PERK/IRE1α/ATF6 pathway.

Endoplasmic reticulum stress (ERs) has been regarded as an important cause for the pathogenesis of non-small-cell lung cancer (NSCLC). β-elemene is an active component in the essential oil extracted from a medicinal herb, Curcuma wenyujin, and has been reported to be effective against non-small-cell lung cancer (NSCLC). However, the potential effect and underlying mechanisms of β-elemene on regulating ERs to inhibit NSCLC are still unclear.

Effect of Human Breast Milk on the Expression of Proinflammatory Cytokines in Caco-2 Cells after Hypoxia/Re-Oxygenation.

Background: Neonatal necrotizing enterocolitis is a common and often fatal gastrointestinal disease, especially in premature infants. To study potential mechanisms underlying the protective effect of breast milk on neonatal necrotizing enterocolitis, we induced intestinal inflammation in a Caco-2 cell model of neonatal necrotizing enterocolitis by hypoxia/re-oxygenation to investigate whether breast milk supernatant fluid inhibited the expression of proinflammatory cytokines interleukin-1β, interleukin-6, and tumor necrosis factor-α.

Methods: Caco-2 cells were divided into normal (control) and neonatal necrotizing enterocolitis groups.

Protection of tauroursodeoxycholic acid on high glucose-induced human retinal microvascular endothelial cells dysfunction and streptozotocin-induced diabetic retinopathy rats.

Ethnopharmacological Relevance: Tauroursodeoxycholic acid (TUDCA), one of the main ingredients from bear gall which hold "Clearing heat and detoxification, Removing liver fire for improving eyesight" functions, is formed by the conjugation of ursodeoxycholic acid (UDCA) with taurine. However, the limited information of TUDCA on protecting diabetic retinopathy (DR) has been known. The present study was conducted to evaluate the protection of TUDCA on high glucose-induced human retinal microvascular endothelial cells (HRMECs) dysfunction and streptozotocin (STZ)-induced diabetic retinopathy (DR) rats and the possible mechanism underlying was also explored.

The C-terminal tails of 4,4'-diphenylmethane-bis(methyl) carbamate are essential for binding to receptor for advanced glycation end products to attenuate advanced glycation end products-induced inflammation and apoptosis responses in human umbilical vein endothelial cells.

Objectives: A novel compound 4,4'-diphenylmethane-bis(methyl) carbamate (CM1) was shown to possess preventive activity on AGEs-induced human umbilical vein endothelial cells (HUVECs) damage via binding to RAGE. However, the underlying structural basis of CM1 on binding to RAGE was not fully understood.

Methods: In the present study, CM1 analogues were designed and synthesized to compare the activity differences on inhibiting AGEs-induced inflammatory response including TGF-β1, RAGE protein expression in HUVECs, and macrophages migration and adhesion to HUVECs.