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      Vol. 29 ， Issue 5 ， 2023

        Original Article

      • Afsane Bahrami,Amir Masoud Jafari-Nozad,Samira Karbasi,Malaksima Ayadilord,Gordon A. Ferns
        Vol. 29, Issue 5, Pages: 387-393(2023) DOI: 10.1007/s11655-023-3732-3
        Abstract：Objective:To assess the efficacy of a curcumin supplementation on cognitive abilities in women suffering from premenstrual syndrome (PMS) and dysmenorrhea.Methods:A randomized, triple-blind, placebo-controlled trial was conducted from December 2019 to March 2020. A total of 124 women who had both PMS and dysmenorrhea were enrolled, and were equally and randomly assigned to the curcumin group or placebo group, 62 cases in each. Each subject received either a capsule containing 500 mg of curcuminoid, or a placebo daily, for 10 days (7 days before and until 3 days after the onset of menstrual bleeding) over 3 menstrual cycles. The cognitive abilities questionnaire was used to measures cognitive functions in 7 specific areas. Adverse reactions were monitored during and after the trial in both groups.Results:Administration of curcumin was associated with a significant increase in memory score (P=0.002), inhibitory control and selective attention (P=0.020), and total cognitive ability task (P=0.024). In addition, significant increments were found in scores of memory (3.5±3.1 vs. 0.4±3.8 in the curcumin and placebo groups, respectively; P=0.035), inhibitory control and selective attention (3.0±3.7 vs. 0.4±3.7; P=0.027) and total cognitive abilities (8.3±12.3 vs. 2.2±12.4; P=0.025) in the curcumin group versus placebo groups. Curcumin was safe and well-tolerable in current clinical trial.Conclusion:Curcumin has a beneficial efficacy on cognitive function scores in women with PMS and dysmenorrhea, with improvements in memory, inhibitory control and selective attention. (Registration No. IRCT20191112045424N1, available at: https://www.irct.ir)  
        Keywords：curcumin;memory;cognition;dysmenorrheal;premenstrual syndrome;triple-blind;placebo-controlled clinical trial   
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        Published：2023-04-27
      • WANG Qing,CHEN Yang-yang,YANG Zhi-chao,YUAN Hai-jun,DONG Yi-wei,MIAO Qiang,LI Yan-qing,WANG Jing,YU Jie-zhong,XIAO Bao-guo,MA Cun-gen
        Vol. 29, Issue 5, Pages: 394-404(2023) DOI: 10.1007/s11655-022-3587-7
        Abstract：Objective:To examine the anti-inflammatory effect of grape seed extract (GSE) in animal and cellular models and explore its mechanism of action.Methods:This study determined the inhibitory effect of GSE on macrophage inflammation and Th1 and Th17 polarization in vitro. Based on the in vitro results, the effects and mechanisms of GSE on multiple sclerosis (MS)-experimental autoimmune encephalomyelitis (EAE) mice model were further explored. The C57BL/6 mice were intragastrically administered with 50 mg/kg of GSE once a day from the 3rd day to the 27th day after immunization. The activation of microglia, the polarization of Th1 and Th17 and the inflammatory factors such as tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-6, IL-12, IL-17 and interferon-γ (IFN-γ) secreted by them were detected in vitro and in vivo by flow cytometry, enzyme linked immunosorbent assay (ELISA), immunofluorescence staining and Western blot, respectively.Results:GSE reduced the secretion of TNF-α, IL-1β and IL-6 in bone marrow-derived macrophages stimulated by lipopolysaccharide (P<0.01), inhibited the secretion of TNF-α, IL-1β, IL-6, IL-12, IL-17 and IFN-γ in spleen cells of EAE mice immunized for 9 days (P<0.05 or P<0.01), and reduced the differentiation of Th1 and Th17 mediated by CD3 and CD28 factors (P<0.01). GSE significantly improved the clinical symptoms of EAE mice, and inhibited spinal cord demyelination and inflammatory cell infiltration. Peripherally, GSE downregulated the expression of toll-like-receptor 4 (TLR4) and Rho-associated kinase (ROCKⅡ, P <0.05 or P<0.01), and inhibited the secretion of inflammatory factors (P<0.01 or P<0.05). In the central nervous system, GSE inhibited the infiltration of CD45+ CD11b+ and CD45+ CD4+ cells, and weakened the differentiation of Th1 and Th17 (P<0.05). Moreover, it reduced the secretion of inflammatory factors (P<0.01), and prevented the activation of microglia (P<0.05).Conclusion:GSE hada beneficial effect on the pathogenesis and progression of EAE by inhibiting inflammatory response as a potential drug and strategy for the treatment of MS.  
        Keywords：grape seed extract;experimental autoimmune encephalomyelitis;demyelination;inflammatory cell;inflammatory factor   
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        Published：2023-04-27
      • WANG Zhe,CHENG Ya-ting,LU Ye,SUN Guo-qiang,PEI Lin
        Vol. 29, Issue 5, Pages: 405-412(2023) DOI: 10.1007/s11655-022-3590-z
        Abstract：Objective:To investigate the role of hippocampal neurodevelopment in the antidepressant effect of baicalin.Methods:Forty male Institute of Cancer Research mice were divided into control, corticosterone (CORT, 40 mg/kg), CORT+baicalin-L (25 mg/kg), CORT+baicalin-H (50 mg/kg), and CORT+fluoxetine (10 mg/kg) groups according to a random number table. An animal model of depression was established by chronic CORT exposure. Behavioral tests were used to assess the reliability of depression model and the antidepressant effect of baicalin. In addition, Nissl staining and immunofluorescence were used to evaluate the effect of baicalin on hippocampal neurodevelopment in mice. The protein and mRNA expression levels of neurodevelopment-related factors were detected by Western blot analysis and real-time polymerase chain reaction, respectively.Results:Baicalin significantly ameliorated the depressive-like behavior of mice resulting from CORT exposure and promoted the development of dentate gyrus in hippocampus, thereby reversing the depressive-like pathological changes in hippocampal neurons caused by CORT neurotoxicity. Moreover, baicalin significantly decreased the protein and mRNA expression levels of glycogen synthase kinase 3β (GSK3β), and upregulated the expression levels of cell cycle protein D1, p-mammalian target of rapamycin (mTOR), doublecortin, and brain-derived neurotrophic factor (allP<0.01). There were no significant differences between baicalin and fluoxetine groups (P>0.05).Conclusion:Baicalin can promote the development of hippocampal neurons via mTOR/GSK3β signaling pathway, thus protect mice against CORT-induced neurotoxicity and play an antidepressant role.  
        Keywords：baicalin;depression;neurodevelopment;hippocampal neuronal;mammalian target of rapamycin/glycogen synthase kinase 3β pathway   
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        Published：2023-04-27
      • WANG Kan,YANG Rong,CHEN Tuan-tuan,QIN Mei-rong,WANG Ping,KONG Ming-wang
        Vol. 29, Issue 5, Pages: 413-423(2023) DOI: 10.1007/s11655-022-3589-5
        Abstract：Objective:To explore the specific pharmacological molecular mechanisms of Kai Xin San (KXS) on treating Alzheimer's disease (AD) based on network pharmacology and experimental validation.Methods:The chemical compounds of KXS and their corresponding targets were screened using the Encyclopedia of Traditional Chinese Medicine (ETCM) database. AD-related target proteins were obtained from MalaCards database and DisGeNET databases. Key compounds and targets were identified from the compound-target-disease network and protein-protein interaction (PPI) network analysis. Functional enrichment analysis predicted the potential key signaling pathways involved in the treatment of AD with KXS. The binding affinities between key ingredients and targets were further verified using molecular docking. Finally, the predicted key signaling pathway was validated experimentally. Positioning navigation and space search experiments were conducted to evaluate the cognitive improvement effect of KXS on AD rats. Western blot was used to further examine and investigate the expression of the key target proteins related to the predicted pathway.Results:In total, 38 active compounds and 469 corresponding targets of KXS were screened, and 264 target proteins associated with AD were identified. The compound-target-disease and PPI networks identified key active ingredients and protein targets. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis suggested a potential effect of KXS in the treatment of AD via the amyloid beta (Aβ)-glycogen synthase kinase-3 beta (GSK3β)-Tau pathway. Molecular docking revealed a high binding affinity between the key ingredients and targets. In vivo, KXS treatment significantly improved cognitive deficits in AD rats induced by Aβ1-42, decreased the levels of Aβ, p-GSK3β, p-Tau and cyclin-dependent kinase 5, and increased the expressions of protein phosphatase 1 alpha (PP1A) and PP2A (P<0.05 or P<0.01).Conclusion:KXS exerted neuroprotective effects by regulating the Aβ-GSK3β-Tau signaling pathway, which provides novel insights into the therapeutic mechanism of KXS and a feasible pharmacological strategy for the treatment of AD.  
        Keywords：Kai Xin San;Alzheimer's disease;Tau protein;network pharmacology;molecular docking;experimental validation;Chinese medicine   
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        Published：2023-04-27
      • CHEN Ming-jun,FENG Yang,GAO Lu,LIN Ming-xiong,WANG Shi-da,TONG Zhan-qi
        Vol. 29, Issue 5, Pages: 424-433(2023) DOI: 10.1007/s11655-022-3317-1
        Abstract：Objective:To investigate the effects of composite Sophora colon-soluble Capsule (CSCC) on gut microbiota-mediated short-chain fatty acids (SCFAs) production and downstream group 3 innate lymphoid cells (ILC3s) of dextran sulfate sodium (DSS)-induced ulcerative colitis (UC) mice model.Methods:The main components of CSCC were analyzed by hybrid ultra-high-performance liquid chromatography ion mobility spectromety quadrupole time-of-flight mass spectrometry (UHPLC-IM-QTOF/MS). Twenty-four male BALB/c mice were randomly divided into 4 groups (n=6) by using a computer algorithm-generated random digital, including control, DSS model, mesalazine, and CSCC groups. A DSS-induced colitis mice model was established to determine the effects of CSCC by recording colonic weight, colonic length, index of colonic weight, and histological colonic score. The variations in ILC3s were assessed by immunofluorescence and flow cytometry. The results of gut microbiota and SCFAs were acquired by 16s rDNA and gas chromatography-mass spectrometry (GC-MS) analysis. The expression levels of NCR+ ILC3-, CCR6+ Nkp46- (Lti) ILC3-, and ILCreg-specific markers were detected by enzyme-linked immunosorbent assay, and real-time quantitative polymerase chain reaction and Western blot, respectively.Results:The main components of CSCC were matrine, ammothamnine, Sophora flavescens neoalcohol J, and Sophora oxytol U. After 7 days of treatment, CSCC significantly alleviated colitis by promoting the reproduction of intestinal probiotics manifested as upregulation of the abundance of Bacteroidetes species and specifically the Bacteroidales_S24-7 genus (P<0.05). Among the SCFAs, the content of butyric acid increased the most after CSCC treatment. Meanwhile, compared with the model group, Lti ILC3s and its biomarkers were significantly downregulated and NCR+ ILC3s were significantly elevated in the CSCC group (P<0.01). Further experiments revealed that ILC3s were differentiated from Lti ILC3s to NCR+ ILC3s, resulting in interleukin-22 production which regulates gut epithelial barrier function.Conclusion:CSCC may exert a therapeutic effect on UC by improving the gut microbiota, promoting metabolite butyric acid production, and managing the ratio between NCR+ ILC3s and Lti ILC3s.  
        Keywords：composite Sophora colon-soluble capsule;ulcerative colitis;group 3 innate lymphoid cells;gut microbiota;butyric acid   
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        Published：2023-04-27
      • ZHANG Zhi-ying,LIU Chao,WANG Peng-xiang,HAN Yi-wei,ZHANG Yi-wen,HAO Mei-li,SONG Zi-xu,ZHANG Xiao-ying
        Vol. 29, Issue 5, Pages: 434-440(2023) DOI: 10.1007/s11655-022-3687-4
        Abstract：Objective:To investigate the effect and potential mechanism of dihydromyricetin (Dmy) on H9C2 cell proliferation, apoptosis, and autophagy.Methods:H9C2 cells were randomly divided into 7 groups, namely control, model, EV (empty pCDH-CMV-MCS-EF1-CopGFP-T2A-Puro vector), IV (circHIPK3 interference), Dmy (50 μmol/L), Dmy+IV, and Dmy+EV groups. Cell proliferation and apoptosis were detected by cell counting kit-8 assay and flow cytometry, respectivley. Western blot was used to evaluate the levels of light chain 3 Ⅱ/Ⅰ (LC3Ⅱ/Ⅰ), phospho-phosphoinositide 3-kinase (p-PI3K), protein kinase B (p-AKT), and phospho-mammalian target of rapamycin (p-mTOR). The level of circHIPK3 was determined using reverse transcriptase polymerase chain reaction. Electron microscopy was used to observe autophagosomes in H9C2 cells.Results:Compared to H9C2 cells, the expression of circHIPK in H9C2 hypoxia model cells increased significantly (P<0.05). Compared to the control group, the cell apoptosis and autophagosomes increased, cell proliferation rate decreased significantly, and the expression of LC3Ⅱ/Ⅰ significantly increased (all P<0.05). Compared to the model group, the rate of apoptosis and autophagosomes in IV, Dmy, and Dmy+IV group decreased, the cell proliferation rate increased, and the expression of LC3Ⅱ/Ⅰ decreased significantly (all P<0.05). Compared to the control group, the expressions of p-PI3K, p-AKT, and p-mTOR in the model group significantly reduced (P<0.05), whereas after treatment with Dmy and sh-circHIPK3, the above situation was reversed (P<0.05).Conclusion:Dmy plays a protective role in H9C2 cells by inhibiting circHIPK expression and cell apoptosis and autophagy, and the mechanism may be related to PI3K/AKT/mTOR pathway.  
        Keywords：dihydromyricetin;circHIPK;autophagy;cell apoptosis;PI3K/AKT/mTOR   
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        Published：2023-04-27

        Clinical Experience

      • LIU Xiao-qing,ZHANG Run-shun,ZHOU Xue-zhong,ZHOU Hong,HE Yu-yao,HAN Shu,ZHANG Jing,SHU Zi-xin,ZHANG Xue-bin,JI Jing-hui,ZHONG Quan,ZHANG Li-li,MOU Zi-jun,HE Li-yun,ZHANG Lun-zhong,YANG Jie,HU Yan-jie,CHEN Zheng-guang,LI Xiao-zhen,TAN Yan,YAN Zhan-feng,CAO Ke-gang,MENG Wei,ZHAO He,ZHANG Wei,ZHONG Li-qun
        Vol. 29, Issue 5, Pages: 441-447(2023) DOI: 10.1007/s11655-022-3571-2
        Abstract：Objective:To derive the Chinese medicine (CM) syndrome classification and subgroup syndrome characteristics of ischemic stroke patients.Methods:By extracting the CM clinical electronic medical records (EMRs) of 7, 170 hospitalized patients with ischemic stroke from 2016 to 2018 at Weifang Hospital of Traditional Chinese Medicine, Shandong Province, China, a patient similarity network (PSN) was constructed based on the symptomatic phenotype of the patients. Thereafter the efficient community detection method BGLL was used to identify subgroups of patients. Finally, subgroups with a large number of cases were selected to analyze the specific manifestations of clinical symptoms and CM syndromes in each subgroup.Results:Seven main subgroups of patients with specific symptom characteristics were identified, including M3, M2, M1, M5, M0, M29 and M4. M3 and M0 subgroups had prominent posterior circulatory symptoms, while M3 was associated with autonomic disorders, and M4 manifested as anxiety; M2 and M4 had motor and motor coordination disorders; M1 had sensory disorders; M5 had more obvious lung infections; M29 had a disorder of consciousness. The specificity of CM syndromes of each subgroup was as follows. M3, M2, M1, M0, M29 and M4 all had the same syndrome as wind phlegm pattern; M3 and M0 both showed hyperactivity of Gan (Liver) yang pattern; M2 and M29 had similar syndromes, which corresponded to intertwined phlegm and blood stasis pattern and phlegm-stasis obstructing meridians pattern, respectively. The manifestations of CM syndromes often appeared in a combination of 2 or more syndrome elements. The most common combination of these 7 subgroups was wind-phlegm. The 7 subgroups of CM syndrome elements were specifically manifested as pathogenic wind, pathogenic phlegm, and deficiency pathogens.Conclusions:There were 7 main symptom similarity-based subgroups in ischemic stroke patients, and their specific characteristics were obvious. The main syndromes were wind phlegm pattern and hyperactivity of Gan yang pattern.  
        Keywords：ischemic stroke;patient similarity network;subgroup;syndrome;Chinese medicine   
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        Published：2023-04-27

        Acupuncture Research

      • WANG Yuan,WANG Qiang,LUO Di,ZHAO Pu,ZHONG Sha-sha,DAI Biao,WANG Jia-ju,WAN Yi-tong,LIU Zhi-bin,YANG Huan
        Vol. 29, Issue 5, Pages: 448-458(2023) DOI: 10.1007/s11655-023-3592-5
        Abstract：Objective:To investigate the molecular mechanisms underlying the beneficial effect of electroacupuncture (EA) in experimental models of Alzheimer's disease (AD) in vivo.Methods:Senescence-accelerated mouse prone 8 (SAMP8) mice were used as AD models and received EA at Yingxiang (LI 20, bilateral) and Yintang (GV 29) points for 20 days. For certain experiments, SAMP8 mice were injected intravenously with human fibrin (2 mg). The Morris water maze test was used to assess cognitive and memory abilities. The changes of tight junctions of blood-brain barrier (BBB) in mice were observed by transmission electron microscope. The expressions of fibrin, amyloid-β (Aβ), and ionized calcium-binding adapter molecule 1 (IBa-1) in mouse hippocampus (CA1/CA3) were detected by reverse transcription-quantitative polymerase chain reaction (qRT-PCR), Western blot or immunohistochemical staining. The expression of fibrin in mouse plasma was detected by enzyme-linked immunosorbent assay. The expressions of tight junction proteins zonula occludens-1 and claudin-5 in hippocampus were detected by qRT-PCR and immunofluorescence staining. Apoptosis of hippocampal neurons was detected by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining.Results:Fibrin was time-dependently deposited in the hippocampus of SAMP8 mice and this was inhibited by EA treatment (P<0.05 or P<0.01). Furthermore, EA treatment suppressed the accumulation of Aβ in the hippocampus of SAMP8 mice (P<0.01), which was reversed by fibrin injection (P<0.05 or P<0.01). EA improved SAMP8 mice cognitive impairment and BBB permeability (P <0.05 or P<0.01). Moreover, EA decreased reactive oxygen species levels and neuroinflammation in the hippocampus of SAMP8 mice, which was reversed by fibrin injection (P <0.05 or P<0.01). Mechanistically, EA inhibited the promoting effect of fibrin on the high mobility group box protein 1 (HMGB1)/toll-like receptor 4 (TLR4) and receptor for advanced glycation end products (RAGE)/nicotinamide adenine dinucleotide phosphate (NADPH) signaling pathways (P<0.01).Conclusion:EA may potentially improve cognitive impairment in AD via inhibition of fibrin/Aβ deposition and deactivation of the HMGB1/TLR4 and RAGE/NADPH signaling pathways.  
        Keywords：electroacupuncture;fibrin/amyloid-β deposition;high mobility group box protein 1/toll-like receptor 4;receptor for advanced glycation end products/nicotinamide adenine dinucleotide phosphate;Chinese medicine   
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        Published：2023-04-27
      • WANG Lu,CHEN Ying,XU Ming-min,CAO Wei,ZHENG Qian-hua,ZHOU Si-yuan,YAO Jun-peng,XI Meng-han,QIN Hai-yan,LI Ying,ZHANG Wei
        Vol. 29, Issue 5, Pages: 459-469(2023) DOI: 10.1007/s11655-023-3594-3
        Abstract：Objective:To investigate autophagy-related mechanisms of electroacupuncture (EA) action in improving gastrointestinal motility in mice with functional constipation (FC).Methods:According to a random number table, the Kunming mice were divided into the normal control, FC and EA groups in Experiment Ⅰ. The autophagy inhibitor 3-methyladenine (3-MA) was used to observe whether it antagonized the effects of EA in Experiment Ⅱ. An FC model was established by diphenoxylate gavage. Then the mice were treated with EA stimulation at Tianshu (ST 25) and Shangjuxu (ST 37) acupoints. The first black stool defecation time, the number, weight, and water content of 8-h feces, and intestinal transit rate were used to assess intestinal transit. Colonic tissues underwent histopathological assessment, and the expressions of autophagy markers microtubule-associated protein 1 light chain 3 (LC3) and Beclin-1 were detected by immunohistochemical staining. The expressions of phosphoinositide 3-kinases (PI3K)-protein kinase B (AKT)-mammalian target of rapamycin (mTOR) signaling pathway members were investigated by Western blot and quantitative reverse transcription-polymerase chain reaction, respectively. The relationship between enteric glial cells (EGCs) and autophagy was observed by confocal immunofluorescence microscopy, localization analysis, and electron microscopy.Results:EA treatment shortened the first black stool defecation time, increased the number, weight, and water content of 8-h feces, and improved the intestinal transit rate in FC mice (P<0.01). In terms of a putative autophagy mechanism, EA treatment promoted the expressions of LC3 and Beclin-1 proteins in the colonic tissue of FC mice (P<0.05), with glialfibrillary acidic protein (GFAP) and LC3 significantly colocalized. Furthermore, EA promoted colonic autophagy in FC mice by inhibiting PI3K/AKT/mTOR signaling (P<0.05 or P<0.01). The positive effect of EA on intestinal motility in FC mice was blocked by 3-MA.Conclusion:EA treatment can inhibit PI3K/AKT/mTOR signaling in the colonic tissues of FC mice, thereby promoting EGCs autophagy to improve intestinal motility.  
        Keywords：electroacupuncture;gastrointestinal motility;autophagy;enteric glial cells;Chinese medicine   
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        Published：2023-04-27

        Review

      • Rashmi Sahu,Prashant Kumar Gupta,Amit Mishra,Awanish Kumar
        Vol. 29, Issue 5, Pages: 470-480(2023) DOI: 10.1007/s11655-022-3584-x
        Abstract：Coalescence of traditional medicine Ayurveda and in silico technology is a rigor for supplementary development of future-ready effective traditional medicine. Ayurveda is a popular traditional medicine in South Asia, emanating worldwide for the treatment of metabolic disorders and chronic illness. Techniques of in silico biology are not much explored for the investigation of a variety of bioactive phytochemicals of Ayurvedic herbs. Drug repurposing, reverse pharmacology, and polypharmacology in Ayurveda are areas in silico explorations that are needed to understand the rich repertoire of herbs, minerals, herbo-minerals, and assorted Ayurvedic formulations. This review emphasizes exploring the concept of Ayurveda with in silico approaches and the need for Ayurinformatics studies. It also provides an overview of in silico studies done on phytoconstituents of some important Ayurvedic plants, the utility of in silico studies in Ayurvedic phytoconstituents/formulations, limitations/challenges, and prospects of in silico studies in Ayurveda. This article discusses the convergence of in silico work, especially in the least explored field of Ayurveda. The focused coalesce of these two domains could present a predictive combinatorial platform to enhance translational research magnitude. In nutshell, it could provide new insight into an Ayurvedic drug discovery involving an in silico approach that could not only alleviate the process of traditional medicine research but also enhance its effectiveness in addressing health care.  
        Keywords：Ayurveda;in silico approach;confluence;challenge;effective therapeutics   
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        Published：2023-04-27
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