2021年10月29-31日，陕西 咸阳

为促进中药药理学科的学术交流与发展，提高中药药理学及中药新药研发水平，由中国药理学会中药与天然药物药理专业委员会与陕西中医药大学联合举办的“第十三届全国中药与天然药物药理学术交流会”于2021年10月29-31日在陕西省咸阳市举行。本次会议展示我国中药、天然药物和传统药物的基础药理学和临床药理学的最新研究进展，研讨热点问题，旨在促进交流与合作，提高研究水平。

会议议题为中药和天然药物的基础药理学、临床药理学和毒理学，基于现代生物医药科学的新理念、新策略和新技术的中药和天然药物药理学研究，中药和天然药物的新药研究与开发和中药和天然药物抗重大传染病研究。会议主要包括三方面内容：一是学术交流，形式为大会报告、专题报告、青年学术论坛及壁报展讲；二是举办“中医药治未病相关药理学研究及新药研发”专题研讨会，针对《中医药发展战略规划纲要（2016-2030年）》提出的中医药在治未病中的主导作用是未来中医药发展的战略定位之一，对相关重大科学和技术问题进行研讨，为提高当代健康理念及重大疾病防控水平提供参考（全体与会代表均可参加）；三是召开中国药理学会中药与天然药物药理专业委员会会议。学术交流形式为大会报告、专题报告、青年学术论坛和壁报展讲。

会议报告

Progress in anti-inflammatory effects of escin

FU Feng-hua1,2,WANG Tian1,2

（1.School of Pharmacy,2.Key Laboratory of Molecular Pharmacology and Drug Evaluation of Ministry of Education,Yantai University,Yantai 264005,China）

Abstract：The fraction of horse chestnut seeds was named escins,which mainly consists of A,B,C,and D escin.Accumulating evidence suggests that escin exerts potent anti-inflammatory and anti-edematous effects.The effects of escin on inflammation and edema have been confirmed in various models.In a study in 1961,intravenous administration of escin was found to reduce acute edema in a rat paw.In the same study,escin was found to inhibit the increase in vascular permeability induced by egg white injection.Escin dose-dependently reduced the capillary permeability in chlo⁃roform-induced local inflammation in the abdominal skin surface of rabbits.The anti-inflammatory and anti-edematous effects of external use of escin were studied in carrageenan-induced paw edema and histamine-induced capillary perme⁃ability in rats.Escin gel decreased the contents of PGE2,TNF-α,and IL-1β,and reduced the raw edema and capillary permeability.The carrageenan-induced paw edema and pleuritis in bilaterally adrenalectomized rats were used to inves⁃tigate the anti-inflammatory effects of escin and glucocorticoid alone or combined.Co-administration of escin with corti⁃sone significantly reduced the volume of exudates and the number of white blood cells of exudates.The findings sug⁃gest escin can synergize with glucocorticoids to enhance their anti-inflammatory effect.The anti-inflammatory effect of escin was investigated in carrageenan-induced paw edema and acetic acid-induced capillary permeability in mice.Escin showed an anti-inflammatory effect,which is similar to that seen with dexamethasone treatment.However,escin showed a longer duration of the anti-inflammatory response than that of dexamethasone.Furthermore,escin had no signif⁃icant effects on spleen index,thymus index,proliferative capacity of splenocytes,lymphocyte count,and phagocytic rate.The findings suggest that escin is a potent anti-inflammatory drug with long-lasting anti-inflammatory effects without any immunosuppressive effects.Traditionally the mechanism of anti-inflammatory effect of escin is supposed to be rela⁃tive to release of PGF2α and corticosterone.The early studies showed that escin might promote the release of PGF2α and affect the pituitary adrenal system,stimulate the release of adrenocorticotropic hormone（ACTH）and glucocorticoid,which may explain its anti-inflammatory and anti-edema effects.Escin has glucocorticoid-like anti-inflammatory effect.However,escin did not exhibit an anti-inflammatory effect in low dose.Combination of suboptimal concentrations of escin with corticosterone inhibited the release of inflammatory factors including NO,TNF-α and IL-1β in the LPS-stimulated macrophage cells.Previous studies demonstrate that escin combined with glucocorticoid produced synergistic antiinflammatory effects.The potential synergistic mechanisms may be associated with the property which escin regulates the glucocorticoid receptor（GR）signaling pathway.Escin can upregulate the expression of GR,promote the combina⁃tion of glucocorticoid and GR,then promote the activated GR transfer into the nucleus.Activated GR will inhibit the acti⁃vation of NF-κB directly,thus further inhibiting the expression of TNF-α and IL-1β and other inflammatory factors.Escin could inhibit 11β-HSD2 but not 11β-HSD1,thus decrease the metabolism of glucocorticoid.Escin and glucocorticoids have similar chemical structures.This indicate that one of the anti-inflammatory mechanisms of escin may be due to its stimulating GR by binding to it.Eacin might be a partial agonist of GR.A good many of researches have demonstrated the anti-inflammatory properties of escin,and shed light on the underlying mechanisms by which escin exerts these effects.Escin,as an oral or intravenous formulation,or a topical gel,inhibits inflammation,producing measurable improve⁃ments in edema and acute lung injury.Further clinical studies of escin are needed to demonstrate these properties in larger patient populations.

Key words：escin;inflammation;edema;capillary permeability;acute lung injury

Corresponding author：FU Feng-hua,E-mail：fufh@ytu.edu.cn

Naringenin prevented nonalcoholic steatohepatitis fibrosis via regulating MAPK/FoxO3a pathway and promoting apoptosis of activated hepatic stellate cells

YUE Shan-shan,QI Rong

（Department of Pharmacology,School of Basic Medical Sciences,Peking University Health Science Center,Beijing 100191,China）

Abstract：OBJECTIVEThe pathological characteristics of nonalcoholic steatohepatitis（NASH）include liver steato⁃sis,inflammation,and fibrosis.Fibrosis is the most severe and significant pathological feature in NASH.Effective drug treatment could reverse early liver fibrosis and is of significance to prevent NASH from progressing into cirrhosis and liver cancer.Identification of drug targets for NASH treatment has been an active research area and is essential for the development of anti-NASH medications.Naringenin（NGN）is a flavonoid compound rich in citrus fruits.Our preliminary data demonstrated that NGN reduced diet-induced lipid accumulation and inflammation in the mouse liver,but whether NGN can attenuate liver fibrosis of NASH is not known.METHODSTo study the effect of NGN on NASH fibrosis.WT mice were fed with high fat diet（HFD）and injected intraperitoneally 20%carbon tetrachloride at the same time for 8 weeks to induce NASH,and NGN was administrated by gavage in the meantime.In vitro,LO2 cells and LX2 cells were stimulated by oleic acid（OA）combined with lipopolysaccharide（LPS）,respectively.RESULTSTreating the WT mice with NGN 100 mg·kg-1·d-1significantly attenuated hepatic lipid accumulation,hepatic fibrosis,plasma ALT and AST levels,inhibited protein expression of p-ERK,p-FoxO3a in the mouse livers.In vitro,on OA and LPS stimulated LO2 or LX2 cells,NGN significantly promoted apoptosis of activated hepatic stellate cells while inhibited apoptosis of hepatocytes.Mechanism study indicated that NGN inhibited MAPK pathway and promoted activation of FoxO3a,conse⁃quently promoted apoptosis of the activated LX2 cells and inhibited liver fibrosis.CONCLUSIONNGN preventes NASH fibrosis via regulating MAPK/FoxO3a pathway,thus promoting apoptosis of the activated hepatic stellate cells.

Key words：nonalcoholic steatohepatitis;liver fibrosis;hepatic stellate cells;apoptosis;MAPK;FoxO3a

Corresponding author：QI Rong,E-mail：qirong0311@163.com

近十年中国国家自然科学基金会中药药理学与药物药理学申请……