Objective:To optimize the extraction process of Shangke Zhitong oil. Methods:Taking the comprehensive score of extracting amounts of acteoside and garlic acid as the index, L9(34)orthogonal test was used to observe the effects of alcohol concentration,soaking time, extraction times and extraction duration on the extraction results. Results:The best extraction process was as follows:the herbs were soaked for 1 h in 65% alcohol,and then refluxed and extracted for three times with 1.5 h for the first time,1 hour for the second time and the third time. The extraction capacity of acteoside and garlic acid was 0.870 8 and 0.717 8 mg·ml-1,respectively. Conclusion:The extraction process is simple,feasible,scientific and reasonable.

Objective To explore the effects of C/EBPα knockout in podocyte on diabetic nephropathy and its mechanisms.Methods C/EBPαloxp/loxp mice were crossed with podocin-cre mice to obtain F1 hybrids and then propagated until homozygous mice (C/EBPαf/f) were obtained.Diabetic nephropathy (DN) models were established by low-dose streptozotocin (STZ,100 mg/kg) administration after 25 weeks of normal diet or 45％ high-fat diet treatment,and biochemical indicators of blood and urea were measured.The morphological characteristics and the proteins regulating oxidative stress and mitochondrial function were detected.Results The type 2 DN models were successfully constructed based on transgenic mice.The kidneys of 8-month-old C/EBPαf/f mice did not show obvious morphological changes,but after constructing DN models,they showed obvious renal impairment,inflammation and oxidative stress.Compared with wild-type DN mice,the protein levels of nephrin and E-cadherin in DN C/EBPαf/f mice with DN were significantly decreased (P ＜ 0.01);fibronectin and Nrf2 protein levels were all increased (all P ＜ 0.05).Keap1,phospho-AMPK and mitochondrial function related genes Pgc-1α protein levels were all decreased (all P ＜ 0.05).Conclusion Podocyte C/EBPα knockout exacerbates diabetic nephropathy by promoting fibrosis and inhibiting Pgc-1α-mediated mitochondrial antioxidant function.