Arsenic (organoarsenic) compound is one of the oldest drugs used by humans to treat various diseases. From its initial application in treating various skin diseases to the 1970s when arsenic trioxide (ATO) was proven to be able to significantly relieve acute promyelocytic leukemia (APL), arsenic (organoarsenic) compounds gradually occupied an important position in the history of medical development. This article reviews the pharmaceutical research progress of inorganic arsenic compounds and organic arsine compounds, covering anticancer, antiparasitic, antiviral and antibiotic aspects. It further explores the potential for developing new arsenic (organoarsenic) drugs with higher efficacy and lower toxicity, aiming to provide new research directions and ideas for the application of arsenic (organoarsenic) compounds in disease treatment.

Objective:To investigate the role of Platycoside E(PE)in a mouse model of bleomycin(BLM)-induced pulmonary fibrosis by targeting the JAK/STAT signaling pathway to suppress macrophage M2 polarization.Methods:Forty BALB/c mice were randomly assigned to five experimental groups:blank control group,model group,pirfenidone(PDF)experimental group,PE high-dose group and PE low-dose experimental group,each with eight mice.After adaptive feeding,except for blank control group,all mice were used in the model of BLM nasal drip-induced pulmonary fibrosis.HE and Masson staining were employed to examine pathological alterations of lung tissue in mice;ELISA to detect concentrations of IL-10,IL-4,IL-17A and TNF-α in mice serum;expressions of CD206 and CD11b in lung tissue were detected by immunofluorescence.Western blot to detect protein expressions of JAK1,p-JAK1,STAT6 and p-STAT6 in lung tissues.Results:Compared with blank control group,tissues in model group showed distorted structure and thickened alveolar walls,fibrotic foci were formed,and alveolar inflammatory fraction and collagen volume fraction were significantly increased(P<0.01).ELISA showed that concentrations of IL-4,IL-10,IL-6 and TNF-α in serum were significantly reduced compared to those of model group.Immunofluorescence showed that fluorescence intensity of CD11b and CD206 treated by PE were decreased significantly.Western blot showed that expressions of JAK1,p-JAK,STAT6 and p-STAT6 proteins were significantly elevated in lung tissues of model mice.Following PE treatment,levels of the above proteins were diminished.Conclusion:PE can effectively improve lung fibrosis induced by BLM in mice,the mechanism may be related to the inhibition of JAK/STAT pathway to block macrophage M2 polarization.

AIM:To elucidate the intervention and mechanism of 4'-hydroxychalcone(4-HC)in colitis mice through the regulation of Th17/Treg homeostasis.METHODS:Using a dextran sodium sulfate(DSS)-induced colitis model in mice,we meticulously observed the pathological characteristics of colon tissue via HE staining.Additionally,we employed immunohistochemical analysis and Western blot techniques to assess the expression levels of proteins associated with the JAK/STAT signaling pathway,as well as the specific content of tight junction proteins such as ZO-1 and occludin.The differentiation of Th17 and Treg cells was analyzed through flow cytometry.RESULTS:Compared to the normal group,the DSS group exhibited a consistent decline in body weight,coupled with symptoms of diarrhea and hematochezia,an increase in the DAI score,and a notable reduction in colon length.In contrast,the body weight of the 4-HC group dis-played an upward trend following an initial decrease,with improvements in diarrhea and hematochezia symptoms,a reduc-tion in the DAI score,and a restoration of colon length relative to the model group.The integrity of colon tissue in the 4-HC group was significantly better than that in the DSS group,evidenced by a marked increase in the number of goblet cells and an enhancement in crypt integrity,while the average histology score showed a decrease.Western blot analysis re-vealed substantial increase in ZO-1 and occludin expression after 4-HC treatment.Flow cytometry results indicated a dra-matic decrease in the differentiation rate of Th17 cells in spleen lymphocytes and mesenteric lymph nodes,while the dif-ferentiation rate of Treg cells was significantly elevated.Immunohistochemical and Western blot analyses demonstrated that 4-HC markedly reduced the phosphorylation of STAT1 and STAT3,while up-regulating the phosphorylation of STAT6,suggesting that 4-HC modulates CD4+T cell activity through the JAK-STAT pathway.CONCLUSION:The 4-HC may enhance the course of DSS-induced colitis in mice,alleviate colonic tissue damage,and modulate the balance be-tween Th17 and Treg cells,potentially involving the JAK/STAT signaling pathway.

Objective:To investigate the role of Platycoside E(PE)in a mouse model of bleomycin(BLM)-induced pulmonary fibrosis by targeting the JAK/STAT signaling pathway to suppress macrophage M2 polarization.Methods:Forty BALB/c mice were randomly assigned to five experimental groups:blank control group,model group,pirfenidone(PDF)experimental group,PE high-dose group and PE low-dose experimental group,each with eight mice.After adaptive feeding,except for blank control group,all mice were used in the model of BLM nasal drip-induced pulmonary fibrosis.HE and Masson staining were employed to examine pathological alterations of lung tissue in mice;ELISA to detect concentrations of IL-10,IL-4,IL-17A and TNF-α in mice serum;expressions of CD206 and CD11b in lung tissue were detected by immunofluorescence.Western blot to detect protein expressions of JAK1,p-JAK1,STAT6 and p-STAT6 in lung tissues.Results:Compared with blank control group,tissues in model group showed distorted structure and thickened alveolar walls,fibrotic foci were formed,and alveolar inflammatory fraction and collagen volume fraction were significantly increased(P<0.01).ELISA showed that concentrations of IL-4,IL-10,IL-6 and TNF-α in serum were significantly reduced compared to those of model group.Immunofluorescence showed that fluorescence intensity of CD11b and CD206 treated by PE were decreased significantly.Western blot showed that expressions of JAK1,p-JAK,STAT6 and p-STAT6 proteins were significantly elevated in lung tissues of model mice.Following PE treatment,levels of the above proteins were diminished.Conclusion:PE can effectively improve lung fibrosis induced by BLM in mice,the mechanism may be related to the inhibition of JAK/STAT pathway to block macrophage M2 polarization.

AIM:To elucidate the intervention and mechanism of 4'-hydroxychalcone(4-HC)in colitis mice through the regulation of Th17/Treg homeostasis.METHODS:Using a dextran sodium sulfate(DSS)-induced colitis model in mice,we meticulously observed the pathological characteristics of colon tissue via HE staining.Additionally,we employed immunohistochemical analysis and Western blot techniques to assess the expression levels of proteins associated with the JAK/STAT signaling pathway,as well as the specific content of tight junction proteins such as ZO-1 and occludin.The differentiation of Th17 and Treg cells was analyzed through flow cytometry.RESULTS:Compared to the normal group,the DSS group exhibited a consistent decline in body weight,coupled with symptoms of diarrhea and hematochezia,an increase in the DAI score,and a notable reduction in colon length.In contrast,the body weight of the 4-HC group dis-played an upward trend following an initial decrease,with improvements in diarrhea and hematochezia symptoms,a reduc-tion in the DAI score,and a restoration of colon length relative to the model group.The integrity of colon tissue in the 4-HC group was significantly better than that in the DSS group,evidenced by a marked increase in the number of goblet cells and an enhancement in crypt integrity,while the average histology score showed a decrease.Western blot analysis re-vealed substantial increase in ZO-1 and occludin expression after 4-HC treatment.Flow cytometry results indicated a dra-matic decrease in the differentiation rate of Th17 cells in spleen lymphocytes and mesenteric lymph nodes,while the dif-ferentiation rate of Treg cells was significantly elevated.Immunohistochemical and Western blot analyses demonstrated that 4-HC markedly reduced the phosphorylation of STAT1 and STAT3,while up-regulating the phosphorylation of STAT6,suggesting that 4-HC modulates CD4+T cell activity through the JAK-STAT pathway.CONCLUSION:The 4-HC may enhance the course of DSS-induced colitis in mice,alleviate colonic tissue damage,and modulate the balance be-tween Th17 and Treg cells,potentially involving the JAK/STAT signaling pathway.

Arsenic (organoarsenic) compound is one of the oldest drugs used by humans to treat various diseases. From its initial application in treating various skin diseases to the 1970s when arsenic trioxide (ATO) was proven to be able to significantly relieve acute promyelocytic leukemia (APL), arsenic (organoarsenic) compounds gradually occupied an important position in the history of medical development. This article reviews the pharmaceutical research progress of inorganic arsenic compounds and organic arsine compounds, covering anticancer, antiparasitic, antiviral and antibiotic aspects. It further explores the potential for developing new arsenic (organoarsenic) drugs with higher efficacy and lower toxicity, aiming to provide new research directions and ideas for the application of arsenic (organoarsenic) compounds in disease treatment.

AIM:To explore the effect and mechanism of action of the aqueous extract of Fritillaria ussuriensis(FU-AE)against nonalcoholic fatty liver disease(NAFLD).METHODS:The association between Fritillaria ussuriensis Maxir.(FU)and NAFLD was analyzed by network pharmacology.A mouse model of NAFLD was induced in mice by high fat diet(HFD)+10%fructose drinking water,and three doses of Fritillaria ussuriensis aqueous extract were given to the mice for intervention.Colorimetric assay was used for detection of aspartate aminotransferase(AST),alanine aminotrans-ferase(ALT),triglyceride(TG),total cholesterol(TC),high-density lipoprotein cholesterol(HDL-C),and low-density lipoprotein cholesterol(LDL-C)levels in the serum of experimental mice.Hematoxylin and eosin staining was used to as-sess the pathological and histological changes in the liver of mice and to clarify the anti-NAFLD effect of aqueous extracts of Fritillaria ussuriensis.Liver tissue proteins were extracted,and expression of proteins related to the AMP-activated pro-tein kinase(AMPK)/acetyl-CoA carboxylase(ACC)pathway was detected by Western blot to clarify the mechanism of an-ti-NAFLD action of Fritillaria ussuriensis.The microbial composition of cecum contents was explored using 16S rRNA se-quencing to reveal the modulatory effect of the aqueous extract of Fritillaria ussuriensis on the structure of intestinal flora in mice with nonalcoholic fatty liver disease.RESULTS:Aqueous extract of Fritillaria ussuriensis(high dose)ameliorated exogenous adipocyte infiltration in the liver of mice with NAFLD(P<0.05).AST,ALT,TG,TC and LDL-C levels were significantly decreased(P<0.05)and HDL-C levels were significantly increased(P<0.05)in the high-dose group.Aque-ous extract of Fritillaria ussuriensis(high dose)significantly increased expression of phosphorylated AMPKα,AMPKα,and phosphorylated ACC in the livers of the model mice(P<0.05),significantly reduced expression of ACC(P<0.05),and significantly increased the relative abundance of the potentially beneficial bacteria Faecalibaculum rodentium,Lacto-bacillus johnsonii,Akkermansia muciniphila(P<0.05).CONCLUSION:Aqueous extract of Fritillaria ussuriensis may ameliorate NAFLD in mice by activating the AMPK/ACC pathway and modulating the structure of intestinal flora.

AIM:To investigate the potential of atractylenolide Ⅲ(AⅢ)in mitigating dextran sulfate sodium(DSS)-induced injury in a mouse model of chronic inflammatory bowel disease(IBD),and to explore the mechanisms in-volved,particularly the modulation of signal transducer and activator of transcription 3(STAT3)signaling,which plays a crucial role in the homeostasis of T helper 17(Th17)and regulatory T(Treg)cells.METHODS:A mouse model of DSS-induced chronic IBD was established,and the mice were divided into 4 groups:control,model(DSS),high-dose(50 mg/kg)AⅢ,and low-dose(30 mg/kg)AⅢ.The disease activity index(DAI)was utilized to assess disease severity.Histo-pathological damage in the colons of IBD mice was evaluated by hematoxylin-eosin(HE)staining.The protein levels of phosphorylated STAT3,occludin and zonula occludens-1(ZO-1)were analyzed using immunohistochemical staining and Western blot.Flow cytometry was employed to examine the differentiation of splenic lymphocytes into Th17/Treg cells.RESULTS:Both DAI assessments and HE staining indicated that AⅢ significantly alleviated inflammatory injury in mice with DSS-induced chronic IBD.Immunohistochemical analysis demonstrated that AⅢ enhanced the expression of ZO-1 and occludin in colonic tissues.Flow cytometry results revealed that AⅢ helped maintain the balance between splenic Th17 and Treg cells.Furthermore,immunohistochemical staining and Western blot showed that AⅢ inhibited the phos-phorylation of STAT3.CONCLUSION:Treatment with AⅢ effectively reduced inflammatory injury in a mouse model of chronic IBD by preserving Th17/Treg homeostasis through the inhibition of STAT3 phosphorylation.As a natural com-pound,AⅢ exhibits significant therapeutic potential for the treatment of chronic IBD.

AIM:To investigate the potential of atractylenolide Ⅲ(AⅢ)in mitigating dextran sulfate sodium(DSS)-induced injury in a mouse model of chronic inflammatory bowel disease(IBD),and to explore the mechanisms in-volved,particularly the modulation of signal transducer and activator of transcription 3(STAT3)signaling,which plays a crucial role in the homeostasis of T helper 17(Th17)and regulatory T(Treg)cells.METHODS:A mouse model of DSS-induced chronic IBD was established,and the mice were divided into 4 groups:control,model(DSS),high-dose(50 mg/kg)AⅢ,and low-dose(30 mg/kg)AⅢ.The disease activity index(DAI)was utilized to assess disease severity.Histo-pathological damage in the colons of IBD mice was evaluated by hematoxylin-eosin(HE)staining.The protein levels of phosphorylated STAT3,occludin and zonula occludens-1(ZO-1)were analyzed using immunohistochemical staining and Western blot.Flow cytometry was employed to examine the differentiation of splenic lymphocytes into Th17/Treg cells.RESULTS:Both DAI assessments and HE staining indicated that AⅢ significantly alleviated inflammatory injury in mice with DSS-induced chronic IBD.Immunohistochemical analysis demonstrated that AⅢ enhanced the expression of ZO-1 and occludin in colonic tissues.Flow cytometry results revealed that AⅢ helped maintain the balance between splenic Th17 and Treg cells.Furthermore,immunohistochemical staining and Western blot showed that AⅢ inhibited the phos-phorylation of STAT3.CONCLUSION:Treatment with AⅢ effectively reduced inflammatory injury in a mouse model of chronic IBD by preserving Th17/Treg homeostasis through the inhibition of STAT3 phosphorylation.As a natural com-pound,AⅢ exhibits significant therapeutic potential for the treatment of chronic IBD.

ObjectiveTo study the characteristics and explore risk factors of traffic injuries in Wenzhou part of the Ningbo-Taizhou-Wenzhou (Yong-tai-wen for short) highway during 2005-2009 so as to provide scientific evidence for promoting prevention and cure level of highway traffic injury.Methods The original data of traffic accident in Wenzhou part of the Yong-tai-wen highway during 2005-2009 were collected to carry out the descriptive epidemiological investigation of the injury characteristics.Simultaneously,multi-factor analysis was conducted to screen out the risk factors for traffic accidents.Results A total of 308 traffic accidents involving 603 casualties (157 deaths) were interviewed during 2005-2009.The casualties from expressway traffic accidents declined yearly,but annual death rate was still very high (26.04％).Meanwhile,the males were more likely subjected to traffic injuries than females.The most common injury sites were the head and limb and the main fatal injuries were the head and pelvic injuries.Accident-prone period was from 0:00 to 8:00 in the morning and traffic scenarios were mainly characterized by rear collision (39％).Risk factors for traffic accidents included poor lighting conditions,overloaded vehicles on the road sections,male drivers,driving without a license,fatigue driving and speeding.ConclusionsTraffic accidents present high incidence and casualty rates,and are mainly resulted from overloaded and fatigue driving.Therefore,the training and education on safe driving should be done particularly for the males and low driving age drivers to strictly forbid the overload driving,fatigue driving or overspeed driving.