Abstract. Objective: To study the changes of the traditional Chinese medicine Aster tataricus Linn's main chemical compositions before and after honey-roasted, and analyze the main chemical compositions of its two different processed products which includes crude or Honey-roasted. Methods: Using ultraviolet spectrophotometry to measure the content of total triterpenoids and total flavonoids in crude and honey-roasted Aster tataricus L.; The Thin Layer Chromatography (TLC) was employed to compare the changes of petroleum ether, acetic ether and n-butanol between the crude Aster tataricus and the one processed with honey. Results: The amount of flavonoids and total triterpenoids in Aster tataricus L after honey-roasted are significantly higher than those in the crude ones. The TLC showed that flavonoids ingredients significantly increased. Conclusion: The reason why honey-roasted Aster tataricus L. can enhance cough-expectoranting curative effect is due to its change of main effective component, including the increased dissolution of total flavonoids and total triterpenoids, and the synergy of refined honey.

Background: Patients with acute kidney injury (AKI) have higher risks of developing chronic kidney disease (CKD). The basis for the AKI-to-CKD transition remains poorly understood, but studies in animal models suggest a linkage between the inflammatory response to injury and subsequent nephron loss and interstitial fibrosis. The proximal tubule is the primary venue of injury and progression of disease during this process. Methods: Mouse unilateral ischemia/reperfusion injury (U-IRI) model was used to study the kinetics of proximal injury marker expression during AKI-to-CKD transition. Immortalized MPT cells and primary cultured renal cells were used to study factor(s) that induce vascular cell adhesion protein-1 (VCAM-1) expression in proximal tubule cells. Results: Kidney injury molecule-1 (KIM-1) was rapidly upregulated on day 1 after injury and gradually reduced close to the baseline; whereas VCAM-1 was not upregulated on day 1 but markedly increased afterwards during AKI-to-CKD transition. The proximal tubular VCAM-1 expression is induced by proinflammatory cytokines including TNFα and IL-1β. Blockade of these signaling pathways by using NF-κB inhibitor or by using double null mutant Myd88 and Trif derived PCRC in vitro or decrease of immune cell recruitment using Ccr2 null mouse in vivo significantly suppressed VCAM-1 expression. Human single cell transcriptome analysis identified a distinct cluster of injured proximal tubules that highly expressed VCAM1 but not HAVCR1 (KIM1), and the population of these VCAM1-positive proximal tubule cells was associated with CKD progression and VCAM-1 levels were significantly higher in the patients with Stage 3 CKD as compared to the healthy references. Conclusions: Proximal tubule cells upregulated KIM-1 and VCAM-1 in an orchestrated fashion after injury. Upregulation of VCAM-1 associated with chronic tubular injury and interstitial fibrosis and may mark the earliest molecular event during AKI-to-CKD transition.