OBJECTIVETo study the chemical constituents in roots of Caragana microphylla.

METHODThe constituents were isolated by silica gel column chromatography, and their structures were identified by spectroscopic methods and chemical evidence.

RESULTEight compounds were identified as beta-sitosterol (1), pseudobaptigenin (2), pentacosanylferulates (3), heptadecanylferulates (4), ferulic acid (5), daucosterol (6), trifolirhizin (7), ononin (8) respectively.

CONCLUSIONCompounds 1, 3-7 were obtained from the plant for the first time, and 3, 4, 5 and 7 were obtained from the genus Caragana for the first time.

Caragana ; chemistry ; Coumaric Acids ; analysis ; chemistry ; isolation & purification ; Glucosides ; analysis ; chemistry ; isolation & purification ; Heterocyclic Compounds, 4 or More Rings ; analysis ; chemistry ; isolation & purification ; Plant Roots ; chemistry ; Plants, Medicinal ; chemistry ; Sitosterols ; analysis ; chemistry ; isolation & purification

Background/Aims: Accumulating evidence indicates that L-carnitine (LC) protects against multiorgan damage through its antioxidant properties and preservation of the mitochondria. Little information is available about the effects of LC on renal fibrosis. This study examined whether LC treatment would provide renoprotection in a rat model of unilateral ureteral obstruction (UUO) and in vitro. Methods: Sprague-Dawley rats that underwent UUO were treated daily with LC for 7 or 14 days. The influence of LC on renal injury caused by UUO was evaluated by histopathology, and analysis of gene expression, oxidative stress, mitochondrial function, programmed cell death, and phosphatidylinositol 3-kinase (PI3K)/ AKT/forkhead box protein O 1a (FoxO1a) signaling. In addition, H2O2-exposed human kidney cells (HK-2) were treated with LC. Results: LC treatment inhibited expression of proinflammatory and profibrotic cytokines, and was followed by a significant attenuation of tubulointerstitial inflammation and fibrosis. The increased oxidative stress caused by UUO was associated with mitochondrial dysfunction and excessive apoptosis and autophagy via PI3K/AKT/FoxO1a-dependent signaling, and this was abrogated by administration of LC. In H2O2-exposed HK-2 cells, LC decreased intracellular production of reactive oxygen species, and suppressed expression of profibrotic cytokines and reduced the number of apoptotic cells. Conclusions LC protects against the progression of tubulointerstitial fibrosis in an obstructed kidney.