OBJECTIVE To optimize the preparation process of sinomenine microemulsion and evaluate its pharmacodynamics.METHODS HPLC method for sinomenine content determination was established,and sinomenine microemulsion prescription was in-itially screened by solubility test and pseudo-ternary phase diagram.D-optimal mixing experimental design method was used to optimize sinomenine microemulsion prescription with particle size and drug load as investigation indexes,and its particle size,drug load and sta-bility were evaluated.Transdermal absorption was investigated by transdermal test in vitro,and the anti-inflammatory effect was evalua-ted by ear swelling test.RESULTS With methanol:0.1%phosphoric acid(40 ∶ 60)as the mobile phase,the detection wavelength was 262 nm,and the method was suitable for the determination of sinomenine.The optimal formula of microemulsion was obtained as castor oil(7.0%),PEG40 hydrogenated castor oil/anhydrous ethanol(69.0%),the optimal Km value was 3∶1,and distilled water(24.0%).The average particle size of the microemulsion was 18.76 nm,the PDI was 0.072 and the drug loading was 5.225%.The cumulative permeability of 1.0%sinomenine microemulsion at 12 h was 1.223 4 μg·cm-2,and the steady permeability rate was 0.0649 μg·cm-2·h-1,which was better than sinomenine solution.The inhibitory rate of sinomenine microemulsion was 65.07%,which was similar to dexamethasone.CONCLUSION The preparation of sinomenine microemulsion has the advantages of stable process,high drug loading,good transdermal absorption and anti-inflammatory effect,which can provide reference for the development of sinomenine transdermal drug delivery preparation.

OBJECTIVE To investigate the inhibitory effects of Ginkgo biloba extract （GBE） on renal inflammation in diabetic nephropathy （DN） model mice， and its potential mechanism. METHODS KK/Ay mice were fed with high fat and high sugar to induce DN model. They were divided into model group， positive control group [metformin 200 mg/（kg·d）]， GBE low-dose and high-dose groups [100， 200 mg/（kg·d）]， with 6 mice in each group. Six C57BL/6J mice were fed with a regular diet as the control group. Administration groups were given relevant liquid intragastrically， control group and model group were given constant volume of normal saline intragastrically， once a day， for 8 consecutive weeks. The body weight， fasting blood glucose， 24-hour food intake， 24-hour urine output， monocyte chemoattractant protein-1 （MCP-1）， interleukin-12 （IL-12）， IL-10， advanced glycation end products （AGEs）， blood urea nitrogen （BUN） and serum creatinine （Scr） of mice were measured， and the ratio of bilateral kidneys to body weight was also calculated. The pathological injury and fibrotic changes of the renal cortex were observed， and the expressions of macrophage polarization marker proteins [type M1： inducible nitric oxide synthase （iNOS）； type M2： arginase-1 （Arg-1）] and AGEs-the receptor of advanced glycation end products （RAGE）/Ras homolog gene pharm_chenjing@163.com family member A （RhoA）/Rho-associated coiled-coil forming protein kinase （ROCK） signaling pathway-related proteins were determined in renal cortex. RESULTS Compared with the model group， the symptoms such as renal cortical hyperplasia， vacuoles， infiltration of inflammatory cells， and renal cortical fibrosis had been improved in GBE low-dose and high-dose groups； body weight， serum level of IL-10， the expression of Arg-1 in the renal cortex were significantly higher than model group （P＜ 0.01）； fasting blood glucose， 24-hour food intake， 24-hour urine output， serum levels of MCP-1， IL-12， BUN， Scr and AGEs， the ratio of bilateral kidneys to body weight， renal injury score， the proportion of renal interstitial fibrosis， the protein expressions of iNOS， RAGE， RhoA and ROCK1 （except for GBE low-dose group） in renal cortex were significantly lower than model group （P＜0.01）. CONCLUSIONS GBE could improve kidney damage and alleviate inflammatory response in DN model mice， the mechanism of which may be related to inhibiting the AGEs-RAGE/RhoA/ROCK signaling pathway and regulating macrophage polarization.