To summarize the clinical experience of Professor LIU Shangyi in treating pruritus vulvae. It is believed that women have the physiological characteristics of liver and kidney as the root， and their pubic area is easily attacked by wind-dampness pathogenic qi， so the core mechanism of pruritus vulvae is proposed as wind-dampness accumulation and deficiency of liver and kidney. The core treatment method is to dispel wind-dampness and nourish the liver and kidneys， and modify the Danggui Decoction （当归饮子） to form a self-prescribed Yinyang Formula （阴痒方） as the basic prescription to treat pruritus vulvaen.

Nonalcoholic steatohepatitis （NASH） is a chronic metabolic disease characterized by hepatocyte fatty degeneration and ballooning degeneration， and it plays an important role in the progression of hepatic steatosis. Recent studies have shown that immune homeostasis imbalance between T helper 17 （Th17） and regulatory T （Treg） cells are closely associated with the pathological process of NASH. Transforming growth factor-β1 （TGF-β1） is a key cytokine for regulating the differentiation and proliferation of Th17/Treg cells， and TGF-β1 binds to its receptor and activates the Smad signaling pathway， thereby regulating the immune balance of Th17/Treg cells and the expression of inflammatory factors and participating in the repair of liver inflammation. This article systematically reviews the molecular mechanism of the TGF-β1/Smad signaling pathway in affecting NASH by regulating the immune balance of Th17/Treg cells， in order to provide a theoretical basis for the research on the pathogenesis of NASH and related treatment strategies.

Nonalcoholic steatohepatitis(NASH)is a liver disease closely associated with metabolic syndrome,and its pathogenesis includes insulin resistance,lipid metabolism disorders,and inflammatory response.This article briefly describes how CD8+T cells exert a cytotoxic effect through the three pathways of the Fas-Fas ligand signaling pathway,the release of perforin and granzymes,and the secretion of tumor necrosis factor-α and other cytokines,and these mechanisms allow CD8+T cells to specifically kill virus-infected cells and tumor target cells,thereby participating in immune regulation.At the same time,this article summarizes that CD8+T cells promote the recruitment of macrophages cooperate with natural killer T cells to participate in the development of adipose tissue inflammation,and lead to liver injury through automatic attack and epigenetic mechanisms,finally promoting the pathogenesis of NASH.It is concluded that CD8+T cells may become a new therapeutic target for NASH,and in-depth research on the specific mechanism of CD8+T cells affecting the pathogenesis in NASH in the future may help to further guide clinical treatment.

Objective To explore the effects of Jianpi Yichang Powder on the expressions of interleukin(IL)-1β and IL-18 of NLRP3 signaling pathway in ulcerative colitis(UC)model rats.Methods Ten rats were randomly selected from 40 SD rats as the normal group,and the other rats freely drank 5%dextran sulfate solution for 7 days to replicate UC rats model.The model rats were randomly divided into model group,sulfasalazine group and Jianpi Yichang Powder group,with 10 rats in each group.Jianpi Yichang Powder group and sulfasalazine group were given corresponding liquid medicine for gavage,and the normal and model groups were given equivalent volume distilled water for gavage for consecutive 14 d.The general status was observed,and the disease activity index(DAI)was scored,the contents of NLRP3,apoptosis-associated spotted proteins(ASC),and Caspase-1 in serum were detected by ELISA,the expressions of IL-1β and IL-18 protein and mRNA in colon tissue were detected by immunohistochemistry,Western blot and RT-PCR respectively.Results Compared with the normal group,the general status of the rats in model group was relatively worse,and DAI score significantly increased(P<0.01),the contents of NLRP3,ASC and Caspase-l in serum were significantly increased(P<0.01),the expressions of IL-1β and IL-18 protein and mRNA in colon tissue were significantly increased(P<0.01).Compared with the model group,the general status of the rats in Jianpi Yichang Powder group and sulfasalazine group were significantly improved,DAI score significantly decreased(P<0.01),the contents of NLRP3,ASC and Caspase-l in serum significantly reduced(P<0.05,P<0.01),and the expressions of IL-1β and IL-18 protein and mRNA in colon tissue significantly decreased(P<0.05,P<0.01).Conclusion Jianpi Yichang Powder can inhibit IL-1β and IL-18 expression of NLRP3 signaling pathway to reduce colon immune inflammatory damage,thus play a role in treating UC.

Sishen Pills is a classic prescription for the treatment of spleen and kidney diarrhea,which has the effect of warming the kidney and the spleen,astringent intestine and antidiarrheal.In modern clinical application,the modified prescriptions based on Sishen Pills,combined with other treatments of TCM and integrated traditional Chinese and Western medicine are often used to treat ulcerative colitis with spleen-kidney yang deficiency syndrome,and the curative effect is remarkable.Experimental pharmacological studies have shown that Sishen Pills may achieve the purpose of ulcerative colitis by regulating the expression of related signaling pathway proteins,regulating inflammatory factors,inhibiting inflammatory response,regulating autophagy,regulating intestinal flora,improving intestinal mucosal permeability,repairing intestinal mucosal barrier,regulating cellular energy metabolism,anti-oxidative stress,regulating cellular immune function,etc.In this article,the research status of Sishen Pills in the treatment of ulcerative colitis was sorted out and summarized,in order to provide reference for further study of its mechanism and clinical application.

Objective To explore the predictive value of novel anthropometric indicators for the long-term prognosis in patients with acute myocardial infarction(AMI).Methods A total of 712 patients diagnosed with AMI in the People's Hospital of Xinjiang Uygur Autonomous Region from January 2018 to December 2019 were selected as research subjects,and divided into an event group and a non-event group according to whether major cardiovascular adverse events(MACEs)occurred during the period of follow-up.Gensini score was used to quanti-tatively assess the degree of coronary artery stenosis.Spearman correlation analysis was used to explore the correla-tion between the new anthropometric indicators and Gensini score.Receiver operating characteristic(ROC)curve was used to evaluate the ability of new anthropometric indicators to predict MACEs,and the patients were grouped according to the optimal cut-off value.Kaplan-Meier curve was used to analyze the survival difference between the groups.Multivariate Cox regression was used to analyze the independent risk factors of MACEs.Results During a median follow-up of 27(20,39)months,a total of 125 patients developed MACEs.As compared with those in the non-event group,the patients in the event group had a higher proportion of hypertension,diabetes and abdominal obesity,higher HbA1c and FBG levels,and longer body weight and waist circumference.The LAP index,CMI index,BRI index and Gensini score were significantly increased,and the differences were statistically significant(P＜0.05).Spearman correlation analysis showed that LAP index,CMI index and BRI index were positively corre-lated with Gensini score(r=0.233,0.126,0.272,P<0.001).ROC curve analysis showed that the AUC of LAP index,CMI index,VAI index,BRI index and ABSI index were 0.745,0.640,0.490,0.874 and 0.506 respec-tively;Kaplan-Meier curve analysis showed that the cumulative incidence of MACEs in LAP index,CMI index and BRI index was significantly increased in the high-value group(Log-rank test,P＜0.05).The results of multivariate Cox regression analysis after adjusting confounding showed that CMI index(HR=1.430,95%CI:1.049～1.952,P=0.024)and BRI index(HR=1.332,95%CI:1.234～1.439,P＜0.001)were independent risk factors for MACEs.Conclusions CMI index and BRI index of new anthropometric indicators are independent risk factors for long-term prognosis in patients with AMI.

Objective:To explore the role and mechanism of Vγ4 T cell depletion in epidermal tissue repair after ultraviolet damage to mouse skin.Methods:The study was an experimental study. Fifty-four female C57BL/6J wild-type mice aged 6 to 8 weeks were divided into Vγ4 T cell depletion group and control group (27 mice in each group) according to the random number table, and the Armenian hamster anti-mouse Vγ4 T cell receptor (TCR) monoclonal antibody of 200 μg and an equal amount of homologous control IgG antibody were intraperitoneally injected, respectively. At one week after injection (the same time point to harvest mice below), dermal cells and lymph node cells were respectively extracted from the back skin tissue, armpit and inguinal lymph nodes of 3 mice in each group (mice in following study were all taken from these 2 groups), and the proportions of Vγ4 T cells in dermal cells and lymph node cells were detected by flow cytometry. Five mice from each group were harvested for observation of skin on the back and skin tissue structure was observed and the epidermal tissue thickness was measured after hematoxylin-eosin (HE) staining. Five mice from each group were harvested for detection of proportion of dendritic epidermal T cells (DETCs) in epidermal cells by flow cytometry after extracted. Three mice were taken from each group and recruited in Vγ4 T cell depletion+5 times ultraviolet irradiation (UVR) group and control+5 times UVR group, respectively, then UVR was administered once per day for 5 times, and the condition of skin on the back was observed immediately after daily irradiation. Five mice were taken from each group and divided into Vγ4 T cell depletion+1 UVR group and control+1 UVR group, respectively. Immediately after one UVR treatment, the epidermal tissue thickness was measured after HE staining. Three mice from each group were selected and recruited in Vγ4 T cell depletion alone group and control alone group, then 3 mice from each group rwere recruited in Vγ4 T cell depletion+1 time UVR group and control+1 time UVR group, respectively, and were treated as before. The mRNA expressions of insulin-like growth factor-Ⅰ (IGF-Ⅰ), keratinocyte growth factor (KGF), Vγ5 TCR, interleukin-15 (IL-15), IL-1β, IL-23, natural killer group 2 member D (NKG2D), histocompatibility antigen 60 (H60), mouse UL16-binding protein-like transcript 1 (Mult1), and retinoic acid early inducible protein 1 (Rae1) in the epidermal tissue were detected by real-time fluorescent quantitative reverse transcription polymerase chain reaction.Results:At one week after injection, the proportions of Vγ4 T cells in dermal cells and lymph node cells of mice in Vγ4 T cell depletion group were significantly lower than those in control group (with t values of 27.99 and 13.12, respectively, P<0.05); there were no statistically significant differences in the skin general condition and tissue structure of mice between Vγ4 T cell depletion group and control group; the epidermal tissue thickness of mice between Vγ4 T cell depletion group and control group was similar ( P>0.05); the proportion of DETCs in epidermal cells of mice in Vγ4 T cell depletion group was (3.9±0.8)%, which was significantly higher than (1.6±0.5)% in control group ( t=4.84, P<0.05). Compared with that in control+5 times UVR group, the skin scale increased after one UVR treatment, scaly scab appeared after 2 times of irradiation, and scaly scab increased significantly after 3 to 5 times of irradiation in Vγ4 T cell depletion+5 times UVR group. Immediately after UVR treatment, the epidermal tissue thickness of mice in Vγ4 T cell depletion+1 time UVR group was significantly increased compared with that in control+1 time UVR group ( t=11.50, P<0.05). Compared with those in control alone group, the mRNA expression of Vγ5 TCR in the epidermal tissue of mice in Vγ4 T cell depletion alone group was up-regulated ( t=41.16, P<0.05), while the mRNA expression of IL-23 was down-regulated ( t=6.52, P<0.05); compared with those in control alone group, the mRNA expressions of Vγ5 TCR and KGF in the epidermal tissue of mice in control+1 time UVR group were significantly up-regulated (with t values of 15.22 and 13.22, respectively, P<0.05), while the mRNA expressions of IGF-Ⅰ and IL-23 were significantly down-regulated (with t values of 3.71 and 4.95, respectively, P<0.05); compared with those in Vγ4 T cell depletion alone group, the mRNA expressions of IGF-Ⅰ and KGF in the epidermal tissue of mice in Vγ4 T cell depletion+1 time UVR group were significantly up-regulated (with t values of 11.40 and 18.88, respectively, P<0.05), while the mRNA expression of IL-1β was significantly down-regulated ( t=4.42, P<0.05); compared with those in control+1 time UVR group, the mRNA expressions of Vγ5 TCR, IGF-Ⅰ, and KGF in the epidermal tissue of mice in Vγ4 T cell depletion+1 time UVR group were significantly up-regulated (with t values of 4.52, 15.24, and 9.43, respectively, P<0.05); the mRNA expression of IL-15 in the epidermal tissue of mice in these 4 groups was generally similar ( P>0.05). Compared with those in control alone group, the mRNA expressions of NKG2D and Rae1 in the epidermal tissue of mice in Vγ4 T cell depletion alone group were significantly up-regulated (with t values of 3.67 and 47.40, respectively, P<0.05), the mRNA expressions of NKG2D, Mult1, and Rae1 in the epidermal tissue of mice in control+1 time UVR group were significantly up-regulated (with t values of 5.30, 6.50, and 9.16, respectively, P<0.05); compared with those in Vγ4 T cell depletion alone group, the mRNA expressions of NKG2D, H60, Mult1, and Rae1 in the epidermal tissue of mice in Vγ4 T cell depletion+1 time UVR group were significantly down-regulated (with t values of 4.57, 4.13, 4.67, and 27.36, respectively, P<0.05); compared with those in control group+1 time UVR group, the mRNA expressions of NKG2D, H60, Mult1, and Rae1 in the epidermal tissue of mice in Vγ4 T cell depletion+1 time UVR group were significantly down-regulated (with t values of 5.77, 8.18, 12.90, and 8.08, respectively, P<0.05). Conclusions:The clearance of Vγ4 T cells is conducive to the proliferation and down-regulation of cytotoxicity of DETCs, and may promote the repair of mouse epidermal damage after UVR.

Non-alcoholic fatty liver disease(NAFLD)is one of the common chronic liver diseases in the world.The molecular mechanism of NAFLD is complex,involving many signal molecules,and the vitamin D(VD)/VDBP/vitamin D receptor(VDR)axis is also involved.VD is a lipid-soluble steroid,which can participate in the regula-tion of lipid metabolism,insulin secretion,immune function,inflammatory response and other biological processes.Stud-ies have shown that VD deficiency is closely related to liver lipid accumulation,inflammation,insulin resistance,oxida-tive stress,intestinal flora imbalance,autophagy,apoptosis,pyroptosis and fibrosis,and plays an important role in the oc-currence and development of NAFLD.This paper reviews the research progress on Vitamin D in recent years in the field of NAFLD,including the physiological characteristics of VD and its role in the NAFLD mechanism,so as to provide referenc-es for the prevention and treatment of NAFLD.

TGF-β1 is considered a key mediator in the formation of hepatic fibrosis and mainly acts by activating the downstream Smad signaling pathway.Smad2 and Smad3 are two major downstream regulators that promote TGF-β1-mediated tissue fibrosis,while Smad7 is a negative-feedback regulator of the TGF-β1/Smad pathway and inhibits TGF-β1-mediated hepatic fibrosis.A growing number of studies are showing that natural products can delay the progression of hepatic fibrosis by regulating the TGF-β1/Smad pathway,inhibiting HSC activation,and reducing ECM deposition.This article reviews the molecular mechanism of the TGF-β1/Smad signaling pathway in hepatic fibrosis,and summarizes the natural products that target the regulation of this pathway,providing a reference for research into the treatment of hepatic fibrosis.

Pathological mechanism of ulcerative colitis(UC)is not fully clear,which may be the result of Th17/Treg immune imbalance and the interaction of multiple complex factors.Numerous studies have found that classical TCM prescriptions,experienced formulas and TCM active components could regulate Th17/Treg balance by intervening in cytokines,transcription factors,and signaling pathways,restore intestinal mucosal immune function,suppress intestinal mucosal inflammatory response,and repair intestinal mucosal barrier damage.Based on the research status of UC,Th17/Treg balance and TCM treatment,this article reviewed the relationship between Th17/Treg balance and UC,and explained the key role of Th17/Treg balance in the occurrence and development of UC.At the same time,the Chinese materia medica targeting to regulate the balance of Th17/Treg in the treatment of UC in recent years was summarized,in order to provide reference for the treatment of UC.