Huopo Xialingtang is a famous classical formula for treating dampness and warmth， which is included in the Catalogue of Ancient Famous Classical Formulas（The First Batch）. In this paper， bibliometric methods was used to collect the literature related to Huopo Xialingtang， and 16 items of related literature were retrieved， involving five medical books， which were used to textual research on the origin， name， composition， drug dosage， preparation method， processing and main treatment symptoms of this formula. The results indicated that Huopo Xialingtang was originated from Yiyuan written by Shi Funan in the Qing dynasty， and and was later named and extended by He Lianchen. The composition of the proposed formula was consistent with the record of Yiyuan， and the origin of each Chinese materia medica was basically clear. Houpo was the dried bark and root bark of Magnolia officinalis， Zexie was the dried tubers of Alisma orientale， Kuxingren was the dried mature seeds of Prunus armeniaca， Doukou was the dried mature fruits of Amomum kravanh， the origin of Tuhuoxiang was consistent with the 2018 edition of Shanghai Standards of Processing Chinese Crud Drugs， and the origins of the remaining Chinese medicines were consistent with the 2020 edition of Chinese Pharmacopoeia. The converted dose of each Chinese medicine was 7.46 g for Agastache rugosa， 3.73 g for Magnoliae Officinalis Cortex， 8.39 g for Pinelliae Rhizoma Praeparatum cum Zingibere et Alumine， 11.19 g for Poria， 11.19 g for Armeniacae Semen Amarum， 14.92 g for Coicis Semen， 2.61 g for Amomi Fructus Rotundus， 5.60 g for Polyporus， 5.60 g for Alismatis Rhizoma， 14.92 g for Tetrapanacis Medulla. Huopo Xialingtang was initially used for the treatment of dampness and warmth at the beginning of the disease， and was later expanded to treat dampness obstruction， dampness-warming dysentery and so on， but always with the dampness-heat in the lungs and spleen as the pathogenesis. In modern times， the clinical application is more extensive， used in digestive， respiratory， endocrine， nervous system and other types of diseases， especially for chronic gastritis， stomach pain and fever. By combing the ancient literature of Huopo Xialingtang， we verified the origin of the formula and determined the key information of the prescription， which can provide literature reference for the clinical application and drug development of this formula.

ObjectiveTo explore the potential mechanism of Banxia Xiexin Decoction （半夏泻心汤， BXD） in the treatment of diabetic gastroparesis （DGP）. MethodsA total of 29 SD rats were randomly divided into four groups， blank group （5 rats） and model group， BXD group and metformin group （8 rats in each group）. Except for the blank group， rats were administered intraperitoneally with 1% streptozotocin （STZ） solution and were fed a high-sugar， high-fat diet to establish the DGP rat model. After successful modeling， the BXD group was treated with BXD at 6.68 g/（kg·d） by gavage， the metformin group was treated with metformin hydrochloride at 105 mg/（kg·d） by gavage， and the blank group and the model group were treated with normal saline at 6.68 ml/（kg·d） by gavage， for 8 weeks. After the last administration， fasting blood glucose （FBG）， glycated hemoglobin （HbA1c）， total cholesterol （TC）， triglycerides （TG） were measured and gastric emptying rate was calculated. ELISA was used to detect the levels of gastrointestinal hormones motilin （MTL） and gastrin （GAS）， as well as inflammatory factors including tumor necrosis factor-α （TNF-α）， interleukin-6 （IL-6）， interleukin-1β （IL-1β） and interleukin-10 （IL-10） in gastric tissue. Oil red O staining was performed to observe liver pathological morphology. Hematoxylin and eosin （HE） staining was used to observe gastric antrum tissue morphology. Immunofluorescence staining was used to detect liver X receptor α （LXRα） levels in the liver. Western Blot was used to detect the protein levels of LXRα in liver tissue， and of janus kinase 2 （JAK2）， phospho-janus kinase 2 （p-JAK2）， signal transducer and activator of transcription 3 （STAT3） and phospho-signal transducer and activator of transcription 3 （p-STAT3） in gastric antrum tissue. Quantitative real-time polymerase chain reaction （qPCR） was used to measure the mRNA expression of LXRα in liver tissue and JAK2， STAT3 in gastric antrum tissue. ResultsCompared with the blank group， the model group showed significant hepatic fatty degeneration， gastric antrum tissue structure destruction， and increases in FBG， HbA1c， TC， and TG levels； the average fluorescence intensity， protein level， and mRNA expression of LXRα in liver tissue were reduced； the gastric emptying rate and gastric tissue GAS and MTL levels decreased； inflammatory factors including TNF-α， IL-6， IL-1β in gastric tissue increased， IL-10 decreased； in gastric antrum tissue， the mRNA expression of p-JAK2/JAK2， p-STAT3/STAT3， and JAK2 and STAT3 increased （P＜0.01）. Compared with the model group， both the BXD group and the metformin group showed improved liver and gastric antrum tissue pathology； FBG， HbA1c， TC， and TG levels decreased， while LXRα fluorescence intensity， protein level， and mRNA expression in liver tissue significantly increased； the gastric emptying rate and the levels of GAS and MTL in gastric tissue were markedly higher； the levels of TNF-α， IL-6， and IL-1β decreased， whereas IL-10 levels increased， p-JAK2/JAK2， p-STAT3/STAT3， and the mRNA expression of JAK2 and STAT3 in gastric antrum tissue decreased （P＜0.05 or P＜0.01）. The BXD group showed higher level than the metformin group in FBG， HbA1c， and TG levels， lower level in gastric emptying rate and gastric tissue GAS content， and higher level in gastric tissue TNF-α， IL-6， IL-1β levels； there was also a decrease in IL-10 levels， and a reduction in LXRα fluorescence intensity and mRNA expression in liver tissue， as well as in p-JAK2/JAK2 levels in gastric antrum tissue （P＜0.05 or P＜0.01）. ConclusionBXD can reduce blood glucose and lipid levels in DGP model rats while improving gastric function and alleviating gastric tissue inflammation. Its mechanism may be related to the regulation of LXRα expression in liver tissue and the JAK2/STAT3 pathway in gastric antrum tissue.

ObjectiveTo evaluate the safety/efficacy of compound Kushen injection （CKI） by zebrafish model and explore the possible mechanism. MethodsZebrafish were exposed to different concentrations of CKI solution， and the mortality rate after 24 h was calculated. After exposure to sublethal concentration （10） and safe dose concentration （0） for 24 h， the safety of CKI was evaluated based on acridine orange staining for the liver， liver area changes， and liver histological sections. The inflammatory bowel disease （IBD） model of zebrafish was established with 2，4，6-trinitrobenzenesulfonic acid sol （TNBS）. The efficacy of CKI in the treatment of IBD was evaluated by the changes in the area of neutral red staining， the number of neutrophils， the area of alcian blue staining， and the contents of tight junction protein （Occludin）， zonula occludens-1 （ZO-1）， tumor necrosis factor（TNF）-α， and prostaglandin E₂（PGE₂） in the intestine of zebrafish. The mechanism of CKI in the treatment of IBD was predicted by network pharmacology and verified by real-time polymerase chain reaction（Real-time PCR）. ResultsIn the safety evaluation， compared with the blank group， the sublethal concentration of CKI could cause liver cell apoptosis， liver area reduction， loose and disordered arrangement of liver cell structure， obvious vacuolation， and other pathological characteristics of zebrafish， while these indicators showed no significant changes under safe dose conditions. In the effectiveness evaluation， compared with the model group， the safe dose of CKI could increase the neutral red staining area of the intestine in a dose-dependent manner and improve the intestinal phagocytosis function. It could reduce the accumulation of intestinal neutrophils， increase the alcian blue staining area， enhance intestinal goblet cell secretion， improve the contents of Occludin and ZO-1， and decrease the contents of TNF-α and PGE₂. Network pharmacology analysis identified 288 potential targets for CKI treatment of IBD. The top five targets obtained by protein-protein interaction （PPI） network analysis were epidermal growth factor receptor A（EGFRA）， protein kinase B1（Akt1）， heat shock protein 90（HSP90AA1）， homologous oncogene of avian sarcoma virus（SRC）， and protooncogene （JUN）. Kyoto encyclopedia of genes and genomes（KEGG） results showed that CKI may be related to the Wnt signaling pathway and cholinergic synaptic pathway in the treatment of IBD， and Real-time PCR results verified the above pathways. ConclusionExcessive use of CKI can induce obvious liver injury in zebrafish， while the rational use of CKI does not cause obvious toxic reactions and can achieve a therapeutic effect on IBD by regulating the Wnt pathway.

Alzheimer's disease （AD）， a degenerative disease of the central nervous system， is characterized by progressive degradation of learning， memory， and cognitive functions. Currently， few drugs are available for treating AD， and their effects are limited. Berberine （BBR） is a natural isoquinoline （quaternary ammonium-like） with a wide range of pharmacological effects. Studies have proven that BBR has good potential in the treatment of AD. Specifically， BBR can inhibit the generation， aggregation， and neurotoxicity of amyloid-β and the hyperphosphorylation of Tau protein， promote the clearance of phosphorylated Tau protein， reduce the cholinesterase activity， neuroinflammation， and oxidative stress， regulate neuronal apoptosis， improve the mitochondrial function and glucose and lipid metabolism， suppress the monoamine oxidase activity， and modulate gut microbiota. In addition， researchers have ameliorated the low bioavailability of BBR. Probing into the potential targets is hoped to provide a reference for further research on the prevention and treatment of AD by BBR.

Depression is a common psychiatric disorder characterized by persistent low mood or mental disorders. Current treatments primarily focus on regulating neurotransmitter levels， but their effectiveness is limited. The mechanisms underlying its onset are complex， and there is no unified consensus. Abnormal signaling pathway transmission plays a crucial role in the development of depression， involving multiple pathways， including Toll-like receptor 4/nucleotide-binding oligomerization domain-like receptor protein 3 （TLR4/NLRP3）， nuclear factor-κB （NF-κB）， Janus kinase/signal transducer and activator of transcription （JAK/STAT）， mitogen-activated protein kinase/extracellular signal-regulated kinase （MAPK/ERK）， brain-derived neurotrophic factor/tyrosine kinase receptor B （BDNF/TrkB）， cyclic AMP/protein kinase A/cAMP response element-binding protein （cAMP/PKA/CREB）， and others. Traditional Chinese medicine（TCM） is based on a holistic approach and the principle of treatment based on the differentiation of syndromes， regulating the balance of multiple systems and organ functions from a macroscopic perspective. This approach has shown unique advantages in the treatment of depression. TCM attributes the onset of depression to dysfunction of the organ systems， involving liver Qi stagnation， heart spirit deficiency， kidney essence depletion， and spleen dysfunction. TCM compound treatments focus on soothing the liver， strengthening the spleen， calming the heart， and replenishing essence， with formulas such as Xiaoyaosan， Zishui Qinggan Yin， and Chahu Jia Guizhi Longgu Muli Tang. The active components of Chinese herbs mainly aim to tonify and regulate Qi， such as salidroside， ginsenoside Rb₁， astragaloside， and muscone. External TCM treatments， primarily acupuncture， aim to open the orifices and invigorate the spirit. Acupoints such as Baihui， Shenting， and Yintang are commonly used. Additionally， massage and moxibustion therapy can intervene in depression by regulating signaling pathways. This article reviews the core role of signaling pathways in the development of depression and the mechanism of TCM regulation of signaling pathways to intervene in depression， aiming to discover new therapeutic approaches that can improve the symptoms of depressed patients.

OBJECTIVE To provide a reference for the pharmaceutical care of a patient with type 2 diabetes mellitus （T2DM） and limb-girdle muscular dystrophy （LGMD） who developed euglycemic diabetic ketoacidosis （euDKA） after taking empagliflozin. METHODS Clinical pharmacists provided pharmaceutical care for a patient with T2DM and LGMD who developed euDKA after taking empagliflozin. According to the patient’s recent use of medications and his conditions， clinical pharmacists assessed the correlation between euDKA and empagliflozin as “very likely”. As to euDKA， clinical pharmacists suggested discontinuing empagliflozin and metformin， and giving intravenous infusion of 10% Glucose injection instead of 5% Glucose injection for fluid resuscitation. Clinical pharmacists monitored the patient’s laboratory indicators such as arterial blood gas analysis， blood/urine ketones and electrolytes. They assisted physicians to decide when to stop intravenous supplements of liquid and insulin. Clinical pharmacists also assisted physicians to adjust the antidiabetic drugs and educated the patient to avoid empagliflozin or other sodium- glucose linked transporter 2 inhibitors （SGLT2i）. RESULTS Physicians adopted the suggestions of clinical pharmacists. After treatment， the patient’s condition improved， and he was allowed to be discharged with medication. CONCLUSIONS euDKA is a relatively rare and serious adverse reaction associated with SGLT2i， and the patients with LGMD are susceptible to euDKA. Clinical pharmacists assist physicians in developing personalized medication plans by evaluating the association between euDKA and empagliflozin， adjusting medication regimens，conducting pharmaceutical monitoring，and other pharmaceutical services. Meanwhile， they provide medication education to patients to ensure their medication safety.

OBJECTIVE To provide a reference for the pharmaceutical care of a patient with type 2 diabetes mellitus （T2DM） and limb-girdle muscular dystrophy （LGMD） who developed euglycemic diabetic ketoacidosis （euDKA） after taking empagliflozin. METHODS Clinical pharmacists provided pharmaceutical care for a patient with T2DM and LGMD who developed euDKA after taking empagliflozin. According to the patient’s recent use of medications and his conditions， clinical pharmacists assessed the correlation between euDKA and empagliflozin as “very likely”. As to euDKA， clinical pharmacists suggested discontinuing empagliflozin and metformin， and giving intravenous infusion of 10% Glucose injection instead of 5% Glucose injection for fluid resuscitation. Clinical pharmacists monitored the patient’s laboratory indicators such as arterial blood gas analysis， blood/urine ketones and electrolytes. They assisted physicians to decide when to stop intravenous supplements of liquid and insulin. Clinical pharmacists also assisted physicians to adjust the antidiabetic drugs and educated the patient to avoid empagliflozin or other sodium- glucose linked transporter 2 inhibitors （SGLT2i）. RESULTS Physicians adopted the suggestions of clinical pharmacists. After treatment， the patient’s condition improved， and he was allowed to be discharged with medication. CONCLUSIONS euDKA is a relatively rare and serious adverse reaction associated with SGLT2i， and the patients with LGMD are susceptible to euDKA. Clinical pharmacists assist physicians in developing personalized medication plans by evaluating the association between euDKA and empagliflozin， adjusting medication regimens，conducting pharmaceutical monitoring，and other pharmaceutical services. Meanwhile， they provide medication education to patients to ensure their medication safety.

Objective: To investigate the epidemiological characteristics of pertussis in Jiaxing City from 2004 to 2023 and spatio-temporal clustering characteristics from 2022 to 2023, so as to provide insights into formulation of pertussis control measures. Methods: Data of pertussis cases in Jiaxing City from 2004 to 2023 were collected through the Infectious Disease Report Information System of Chinese Disease Prevention and Control Information System. The epidemiological characteristics of pertussis cases in Jiaxing City from 2004 to 2023 were descriptively analyzed, and the spatio-temporal clustering characteristics from 2022 to 2023 were analyzed using spatio-temporal scanning. Results: A total of 478 pertussis cases were reported in Jiaxing City from 2004 to 2023, with an average annual reported incidence of 0.53/105. The reported incidence showed an upward trend from 2004 to 2023 (P<0.05), with the highest in 2022 (3.17/105). Higher incidence of pertussis was reported in June to August (149 cases, 31.17%) and November to December (112 cases, 23.43%). There was no statistically significant difference in the reported incidence between males and females (0.56/105 vs. 0.50/105, P>0.05). The cases aged under one year accounted for the highest proportion, with 199 cases (41.63%). Haining City (0.68/105), Jiashan County (0.64/105) and Tongxiang City (0.60/105) ranked the top three in the reported incidence of pertussis. Spatio-temporal scanning analysis showed that from 2022 to 2023, the primary clustering area of pertussis was centered in Daqiao Town of Nanhu District, covering 27 towns (streets) in Nanhu District, Jiashan County, Xiuzhou District and Pinghu City, and the clustering time was from November to December, 2023. Conclusions The reported incidence of pertussis was at a low level in Jiaxing City, but showed an upward trend from 2004 to 2023. The incidence of pertussis was higher among infants under one year of age, peaked in June to August and November to December, and was concentrated in Nanhu District and its surrounding areas.

ObjectiveTo explore the possible mechanism of action of Bushen Huoxue Granules （补肾活血颗粒， BHG） in the treatment of Parkinson's disease （PD） through the Nrf2/NLRP3 inflammasome axis. MethodsA total of 84 male C57/BL 6 mice were randomly divided into blank group， model group， Madopar group， dimethyl fumarate group， and low-， medium， and high-dose BHG group， with 12 mice in each group. Except for the blank group， all groups were induced into PD models by intraperitoneal injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine （MPTP） at a concentration of 30 mg/ml for 7 consecutive days. The blank group received an equal volume of saline. After model establishment， the low-， medium， and high-dose BHG groups were treated with 1.5， 3， and 6 g/（kg·d） of the BHG by gavage， respectively. The Madopar group was given 0.113 g/（kg·d） of Madopar tablets by gavage， and the dimethyl fumarate group was given 50 mg/（kg·d） of dimethyl fumarate solution. The blank group and the model group were given 10 ml/（kg·d） of distilled water by gavage. Gavage was administered once daily for 14 days. Behavioral changes were evaluated using the open field test （total distance， central area distance， and average speed）， rotarod test （time on the rod）， and climbing pole test （climbing time）. Serum levels of interleukin-1β （IL-1β）， interleukin-18 （IL-18）， and myeloperoxidase （MPO） were measured by ELISA. Immunohistochemistry was used to detect tyrosine hydroxylase （TH） expression in the brain substantia nigra. Immunofluorescence was used to detect α-synuclein （α-syn） expression. Western Blot was used to detect Nrf2， NLRP3， Caspase-1， and α-syn protein levels in the brain substantia nigra. RT-PCR was used to detect mRNA expression levels of Nrf2， NLRP3， and Caspase-1 in the brain substantia nigra. ResultsCompared with the blank group， the model group showed decreased total distance， central area distance， and average speed， reduced time on the rotarod， prolonged climbing time， reduced TH expression， increased α-syn expression， decreased Nrf2 protein and mRNA expression， increased NLRP3 and Caspase-1 protein and mRNA expression， and elevated serum IL-1β， IL-18， and MPO levels （P＜0.05）. Compared with the model group， all drug interventions significantly improved the above indicators （P＜0.05）. There was no significant differences in all indicators between the high-dose BHG group and the Madopar group （P＞0.05）. Compared with the dimethyl fumarate group， the medium and high-dose BHG groups showed increased Nrf2 mRNA expression in the brain substantia nigra （P＜0.05）. Compared with the high-dose BHG group， the low-dose group showed decreased total distance， central area distance， and average speed， reduced serum IL-18 levels， decreased α-syn， Nrf2， NLRP3， and Caspase-1 protein levels， and lower Nrf2 mRNA expression （P＜0.05）. ConclusionThe mechanism by which BHG treat PD may involve activating the Nrf2/NLRP3 inflammasome axis in the brain substantia nigra， thereby reducing neuroinflammation and α-syn aggregation. The high-dose group showed the best effects.

ObjectiveTo observe the inhibitory effect of the Weiliuan mixture （WLAHJ） on the subcutaneous xenograft tumor of MKN-74 gastric cancer cells， and explore the potential anti-gastric cancer mechanism of WLAHJ by using transcriptomic sequencing technology to reveal related genes and pathways. Methods30 Balb/c nude mice were randomly divided into model， low-， medium-， and high-dose（15，30，45 g·kg^-1） WLAHJ and 5-FU （0.025 g·kg^-1） groups to build a subcutaneous xenograft tumor model with MKN-74 human gastric cancer cells. After modeling，each group was continuously treated with the corresponding drugs for 28 days. During the treatment period， the body weight and tumor size of the mice were observed and recorded every 2 days. At the end of the treatment， the mice were sacrificed， and required samples were collected to calculate the tumor inhibition rate of WLAHJ on the subcutaneous xenograft tumor. High-throughput transcriptomic sequencing （RNA-seq） technology was used to analyze the differentially expressed genes in the subcutaneous tumor tissues of the model group and the medium-dose WLAHJ group， thus exploring the potential mechanism of WLAHJ in gastric cancer intervention. Immunofluorescence experiments were conducted to detect the protein expression levels of glutathione peroxidase 4 （GPX4）， solute carrier family 7 member 11 （SLC7A11）， transferrin receptor protein-1 （TFR-1）， and acyl-CoA synthetase long-chain family member 4 （ACSL4） in subcutaneous xenograft tumors of each group. Cell counting kit-8（CCK-8） and colony formation assays were used to detect the viability and anti-proliferative ability of human gastric cancer AGS and MKN-74 cells at different concentrations of WLAHJ. Kits were used to detect the levels of Fe²⁺， reactive oxygen species （ROS）， malondialdehyde （MDA）， and superoxide dismutase （SOD） activity in cells. Western blot was used to detect the expression levels of GPX4， SLC7A11， TRF-1， ACSL4， spermidine/spermine N1-acetyltransferase 1 （SAT1）， arachidonic acid 15-lipoxygenase （ALOX15）， and key proteins in the phosphatidylinositol 3-kinase （PI3K）/protein kinase B （Akt）/mammalian target of rapamycin （mTOR） signaling pathway. ResultsThe mechanism of WLAHJ in gastric cancer intervention may be related to ferroptosis and the PI3K/Akt /mTOR signaling pathway. The growth of subcutaneous xenograft tumors in nude mice of the WLAHJ and 5-FU groups（P<0.05，P<0.01）， GPX4， and SLC7A11 dropped significantly（P<0.01）， while TFR-1， ACSL4， SAT1， and ALOX15（P<0.05，P<0.01）increased significantly compared with those in the model group. The levels of ROS， Fe²⁺， and MDA increased in the WLAHJ and 5-FU groups and the proliferation of gastric cancer cells， SOD activity， the ratios of phosphorybation （p）-mTOR/mTOR， p-PI3K/PI3K， and p-Akt/Akt protein expressions（P<0.05，P<0.01）decreased compared with those in the blank group. ConclusionThe mechanism of WLAHJ in treating gastric cancer may be related to the regulation of the PI3K/ Akt /mTOR signaling pathway to intervene in ferroptosis.