Metabolic associated fatty liver disease has become the most important chronic liver disease in China.Its mechanism is not completely clear.Professor Sheng Guoguang examines the symptoms and seek the cause,treats the disease by stages from the perspective of"earth-obstructing and wood-stagnation,phlegm and blood stasis",summarizes the core pathogenesis of each stage,and prescribes drugs for the pathogenesis.In the early stage,the disease is mainly caused by earth-obstructing and wood-stagnation and phlegm and blood stasis and the corresponding treatment method should be activating spleen to eliminate depression,relieving phlegm and promoting blood circulation,with common use of modified Sizhu Decoction combined with Erchen Decoction.In the middle stage,phlegm and blood stasis transform into heat are the main pathogenesis,and the appropriate treatment is clearing liver and purging fire,and relieving phlegm and promoting blood circulation,with common use of modified Xiaochaihu Decoction combined with Erchen Decoction.In the late stage,weakness of the internal organs is the main pathogenesis,and it is appropriate to nourish liver and fortify the spleen,tonifying the kidney and consolidate the root,supplementing with reducing phlegm and activating blood circulation,with common use of modified Yiguan Decoction combined with Liujunzi Decoction in modification,which has achieved confirmed clinical efficacy.

Objective:To discuss the effect of the small ubiquitin-like modifier-specific protease 1(SENP-1)/hypoxia-inducible factor 1α(HIF-1α)pathway on chronic intermittent hypoxia(CIH)-induced vascular endothelial injury in the rats,and to clarify the related mechanism.Methods:The SD rats were randomly divided into control group and CIH group,and then the rats in each group were further divided into 2,4,and 6-week subgroups,and there were 8 rats in each subgroup.The rats in CIH group were exposed to CIH in a CIH chamber to induce CIH and create the obstructive sleep apnea hypopnea syndrome(OSAHS)models,while the rats in control group were exposed to normoxic conditions.The serum and thoracic aorta tissue of the rats in various groups were collected at each time point.HE staining was used to observe the thoracic aorta vascular injury of the rats in various groups;ELISA method was used to detect the levels of nitric oxide(NO),endothelin-1(ET-1),von Willebrand factor(vWF),and thrombomodulin(TM)in serum of the rats in various groups;Western blotting method was used to detect the expression levels of SENP-1,HIF-1α,and vascular endothelial growth factor A(VEGFA)proteins in thoracic aorta tissue of the rats in various groups.In vitro,the aortic endothelial cells(rAECs)of the rats were cultured and infected with SENP-1 shRNA adenovirus(sh-SENP-1)to construct the cell line with low expression of SENP-1.The CIH was used to induce the vascular endothelial cell injury,and the cells were divided into CIH group,CIH+sh-NC group,and CIH+sh-SENP-1 group;control group was set up separately.CCK-8 method was used to detect the proliferation activities of the cells in various groups;ELISA method was used to detect the activities of lactate dehydrogenase(LDH)in the supernatant and the levels of NO,ET-1,malondialdehyde(MDA),and activities of superoxide dismutase(SOD)in the cells in various groups;flow cytometry was used to detect the apoptotic rates of the cells in various groups;Western blotting method was used to detect the expression levels of SENP-1,HIF-1α,and VEGFA proteins in the cells in various groups.Results:With the extension of CIH induction time,compared with control group,the thoracic aorta endothelium in CIH group gradually became rough and significantly thickened,the level of serum NO of the rats in CIH group was decreased(P＜0.05),and the levels of serum ET-1,vWF,and TM,and the expression levels of SENP-1,HIF-1α,and VEGFA proteins in thoracic aorta tissue were increased(P＜0.05).Compared with control group,the proliferation activity of the cells in CIH group was decreased(P＜0.05),the LDH activity in the supernatant,the levels of ET-1,MDA,and the apoptotic rate in the cells were increased(P＜0.05),while the levels of NO and activity of SOD in the cells were decreased(P＜0.05),and the expression levels of SENP-1,HIF-1α,and VEGFA proteins in the cells were increased(P＜0.05).Compared with CIH group,the proliferation activity of cells in CIH+sh-SENP-1 group was increased(P＜0.05),the activity of LDH in the supernatant,the levels of ET-1,MDA,and the apoptotic rate of the cells were decreased(P＜0.05),while the level of NO and activity of SOD in the cells were increased(P＜0.05),and the expression levels of SENP-1,HIF-1α,and VEGFA proteins were decreased(P＜0.05).Conclusion:The SENP-1/HIF-1α pathway is highly activated in the thoracic aorta injury tissue of the rats induced by CIH.Silencing SENP-1 expression can reduce CIH-induced vascular endothelial cell injury,and its mechanism may be related to downregulating the activation level of SENP-1/HIF-1α pathway.

ObjectiveTo systematically review the ancient and modern literature about Maimendongtang, so as to provide a scientific basis for the modern clinical application and preparation research and development of Maimendongtang. MethodThe Chinese Medical Code (version 5) was searched with "Maimendongtang" as the keyword. The modern clinical studies of Maimendongtang were retrieved from CNKI with “Maimendongtang” as the keyword and the time interval from January 1, 1975 to December 31, 2022. The articles involving the main symptoms, herb composition, dosage, and decocting and medication methods of Maimendongtang were selected and screened according to the inclusion and exclusion criteria. Finally, the information including the book name, indications, herbs, dosage, and decocting and medication methods were included to summarize the ancient and modern application of Maimendongtang. ResultA total of 357 publications of Maimendongtang were included, involving 115 ancient books. Maimendongtang was first published in the Synopsis of the Golden Chamber by ZHANG Zhongjing in the Han dynasty. It is composed of Ophiopogonis Radix, Pinelliae Rhizoma, Ginseng Radix et Rhizoma, Semen Oryzae Sativae, Jujubae Fructus, and Glycyrrhizae Radix et Rhizoma. Despite the slight changes during the inheritance by later generations, the indications, herb composition, dosage, and decocting and medication methods of this formula were generally consistent with those in the Synopsis of the Golden Chamber. A total of 182 modern articles were included to analyze the clinical application of Maimendongtang. This formula was mainly used to treat respiratory system diseases, digestive system diseases, tumor-related diseases, etc. ConclusionAccording to the textual research on the ancient and modern literature, the composition, dosage, indications, and decocting and medication methods of Maimendongtang are basically consistent with those recorded in the Synopsis of the Golden Chamber. The modern clinical application not only follows the main indications but also expands the clinical application scope of this formula, which is mainly used to treat patients with the syndrome of yin deficiency of lung and stomach. The modern clinical application of Maimendongtang has promoted the inheritance and innovation of classic famous prescriptions and provided a scientific basis for the drug research and development.

This article provides a systematic review of the research progress in the mechanisms related to lung cancer and ferroptosis， ferroptosis-related lung cancer biomarkers and gene mutation targets， and ferroptosis-targeted regulation of Chinese medicine in treating lung cancer in the past five years， providing a feasible and effective basis for the prevention and treatment of lung cancer with Chinese medicine and the development of new drugs. According to the available studies， ferroptosis is widely suppressed in lung cancer， while the specific regulatory mechanisms have not been fully elucidated. The suppression is related to lipid metabolism， iron metabolism， cystine/glutamate antiporter system Xc^- （System Xc^-）/glutathione （GSH）/glutathione peroxidase 4 （GPX4）， ferroptosis suppressor protein 1 （FSP1）/coenzyme Q10 （CoQ10）/nicotinamide adenine dinucleotide phosphate ［NAD（P）H］， long non-coding RNA （lncRNA）， nuclear factor E₂-related factor 2 （Nrf2）， and p53. In modern times， traditional Chinese medicine is widely used in the comprehensive treatment of lung cancer， and it has gradually become a hot research topic due to its obvious advantages of anti-tumor activity， high efficacy， and low toxicity. Traditional Chinese medicine plays an important role in the treatment of lung cancer. Studies have shown that the active components， extracts， and prescriptions of Chinese medicine can induce ferroptosis in lung cancer cells through targeted regulation of iron metabolism， lipid metabolism， and p53， Nrf2， LncRNA， and GPX4 pathways to inhibit the growth and proliferation of lung cancer， thus exerting anti-tumor effects. Therefore， regulating ferroptosis is expected to become a new direction for preventing lung cancer. Basic research has shown that Chinese medicine can regulate ferroptosis via multiple targets and pathways in the treatment of lung cancer. At present， Chinese medicine demonstrates great research prospects in regulating ferroptosis to treat lung cancer， which， howeve， still faces challenges to achieve clinical transformation.

Objective : To investigate the effects and mechanism of small ubiquitin-like modifier ( SUMO) specific proteinase-1 (SENP-1) on chronic intermittent hypoxia ( CIH) induced myocardial injury in rats． Methods : 32 male SD rats were randomly divided into : control group，CIH group，negative control adeno-associated virus interven- tion group (AAV-shNC) and SENP-1 shRNA adeno-associated virus intervention group (AAV-shSENP-1) ，with 8 rats in each group．After 6 weeks of CIH induction，echocardiography was performed．The levels of cardiac troponin I (cTNI) ，creatine kinase MB isoenzyme ( CKMB) ，myoglobin (Mb) ，lactate dehydrogenase (LDH) in serum and malondialdehyde (MDA) ，uperoxide dismutases ( SOD) ，glutathione ( GSH) ，interleukin( IL) -1 β , IL-6 and tumor necrosis factor-α(TNF-α) in myocardial tissue were detected by ELISA．The pathological changes of myocardial tis- sue was observed by HE staining．The reactive oxygen species ( ROS) level in myocardial tissue was detected by DCFH-DA fluorescence probe labeling．The small ubiquitin-like modifier (SUMO) level of hypoxia inducible factor- 1 α (HIF-1 α) protein in myocardial tissue was detected by kit．The mRNA and protein levels of SENP-1 and HIF- 1 α in myocardial tissue were detected by qRT-PCR and Western blot. Results : Compared with the control group， the pathological damage of myocardial tissue in CIH group was serious，the levels of left ventricular end diastolic diameter (LVEDD) ，left ventricular end systolic dimension (LVESD) and serum cTNI，CKMB，Mb and LDH signif- icantly increased (P＜0. 05) ，and the levels of ROS，MDA，IL-1 β , IL-6，TNF-α and the mRNA and protein levels of SENP-1 and HIF-1α in myocardial tissue also significantly increased (P ＜0. 05 ) ，while the levels of LVEF， LVFS，serum GSH and SOD significantly decreased (P ＜0. 05) ，and the SUMOylates level of HIF-1α protein in myocardial tissue also significantly decreased (P ＜0. 05 ) ．Compared with CIH group，AAV-shSENP-1 group had less myocardial pathological damage，the levels of LVEDD，LVESD and serum cTNI，CKMB，Mb and LDH signifi- cantly decreased (P＜0. 05) ，and the levels of ROS，MDA，IL-1 β, IL-6，TNF-α and the mRNA and protein levels of SENP-1 and HIF-1α in myocardial tissue also significantly decreased (P＜0. 05) ，the levels of LVEF，LVFS，serum GSH and SOD significantly increased (P＜0. 05) ，and the SUMOylates level of HIF-1α protein in myocardial tissue also significantly decreased (P＜0. 05) ． Conclusion Inhibition of SENP-1 expression can alleviate CIH induced myocarditis and oxidative stress in rats，improve myocardial injury and cardiac dysfunction，and its mechanism may be related to the improvement of HIF-1α SUMOylates level，thus inhibiting HIF-1α expression.