The properties and meridian affinities of Chinese herbal medicine are closely associated with their therapeutic efficacy. This review focuses on approved antitumour Chinese medicines listed in the Pharmacopoeia of the People's Republic of China (2020 Edition, Volume I), highlighting their key components. Statistical methods were used to analyse the properties, flavours and channel tropisms of antitumour traditional Chinese medicine (TCM), including both proprietary formulations and commercially available individual herbs. Distinctive patterns were identified by comparing herb profiles with contemporary experimental studies on antitumour TCM. Analysis revealed that bitter-cold herbs represented the highest proportion of antitumour TCM, with most showing tropism towards the liver channel. These findings provide a reference framework for antitumour drug development, indicating that bitter-cold herbs merit priority as candidate ingredients.

The purpose of the present study was to evaluate cimigenol (Cim) treatment effects to cell proliferation by breaking bone marrow stromal cells (BMSCs) through C-X-C chemokine receptor type 4 (CXCR4)/stromal cell-derived factor-1α (SDF-1α) pathway. MV-4-11 and U937 cell lines were used. The present study was divided into two parts. First, the cell lines were divided into normal control (NC), BMSC (cells co-cultured with BMSCs), BMSC + DMSO, BMSC + Low (treated with 5 mg/ml Cim), BMSC + Middle (treated with 10 mg/ml Cim), BMSC + High (treated with 20 mg/ml Cim). In the second step, the cell lines were divided into NC, BMSC, BMSC + BL8040 (treated with BL8040 which inhibits CXCR4), BMSC + Cim and BMSC + Cim + BL8040. EdU positive cell numbers were measured by EdU assay and apoptosis rate by flow cytometry and TUNEL assay. Relative gene and protein expression was measured by reverse transcription-quantitative PCR and western blotting assay. BMSCs were able to protect proliferation of cancer cells and decreased cell apoptosis compared with the NC group (P<0.001, respectively). With Cim supplement, the cell proliferation was decreased with cell apoptosis increasing compared with NC group (P<0.001 respectively). However, the anti-tumor effects of Cim were not significantly different from the BL8040 treated groups (P<0.001, respectively). In conclusion Cim decreased acute myeloid leukemia cells protected by BMSCs through the CXCR4/SDF-1α pathway.

PURPOSE:Cimicifuga dahurica (C. dahurica), which has been used in traditional oriental medicine for a long period, was reported to exert extensive antitumor activity, but the effect and molecular biological mechanism of C. dahurica on multiple myeloma (MM) has not been elaborated. Tumor-associated macrophages (TAMs) exhibit a sustained polarization between tumor killing M1 subtype and tumor supporting M2 subtype. And a lower ratio of M1/M2 is associated with tumor angiogenesis, proliferation and invasion. We explored the inhibitory effect of the aqueous extract of the root of C. dahurica (CRAE) on tumor growth by reprogramming macrophage polarization in the tumor microenvironment.METHODS:Mice bearing SP2/0 multiple myeloma were treated with CRAE. Western blotting (WB), immunohistochemistry (IHC) and immunofluorescence staining were utilized to assess tumor growth and TAM populations. Macrophages were depleted by injection of clodronate liposomes to determine and measure the role of CRAE as an anti-tumor agent by targeting macrophages. To simulate tumor microenvironment, MM cells H929 and TAMs were co-cultured using the transwell co-culture system. By using CRAE as an immunoregulator in M2-like macrophages, we analyzed CRAE-treated macrophage-associated surface markers and cytokines by flow cytometry and WB.RESULTS:The results indicated that CRAE treatment could reduce tumor burden of MM mice and a high degree of M1-like macrophages infiltration was detected in tumor tissues. In vitro co-culture system, CRAE significantly promoted the polarization of M2 to M1 phenotype, which led to the increase in apoptosis of myeloma cells. It was found that the M1 polarization induced by CRAE depended on the TLR4-MyD88-TAK1-NF-κB signal transduction.CONCLUSION:This study elucidated the anticancer mechanism of the aqueous extract of C. dahurica (CRAE) through reprogramming macrophage polarization and highlighted that CRAE could act as a potential novel option for cancer immunotherapy.

主动脉夹层是一种病势急、漏诊率及死亡率高的心血管系统危重症.临床接诊过程中,剧烈的胸痛、腹痛是主动脉夹层的普遍症状,但不典型症状如神经系统症状为首发症状时,常被临床医师忽视,造成误诊、漏诊.

多发性骨髓瘤(multiple myeloma,MM)是一种以骨髓中单克隆浆细胞恶性增殖为特征的浆细胞疾病,是目前全球第二高发的血液系统肿瘤.骨痛是MM常见的临床症状之一,大约2/3的MM患者因骨痛就诊,80％的MM患者确诊时即出现骨质疏松及病理性骨折等骨骼病变,即多发性骨髓瘤骨病(multiple myeloma bone disease,MBD)[1].

Solasonine, the main active ingredient of Solanum nigrum L ., has been reported to exert extensive antitumor activity. However, the antitumor effects in acute monocytic leukemia and the exact mechanisms involved are unknown. In this study, we investigated the role of solasonine on inhibiting the progression of acute monocytic leukemia. Our findings showed that solasonine inhibited the proliferation of acute monocytic leukemic cell lines (THP-1 and MV4-11) in vitro . Solasonine promoted apoptosis and induced cell cycle arrest in the G2/M phase. Analysis of RNA-seq data suggested that solasonine correlated with increased expression of genes in the AMPK/FOXO3A pathway. Inhibition of AMPK with compound C followed by treatment with solasonine showed that solasonine reduced apoptosis, caused less cell cycle arrest, and inactivated the AMPK/FOXO3A axis in THP-1 and MV4-11 cells. Solasonine also inhibited tumor growth by the activation of the AMPK/FOXO3A axis. In conclusion, solasonine inhibited the progress of acute monocytic leukemia in vitro and in vivo and triggered the apoptosis and cell cycle arrest in the G2/M phase by upregulating the AMPK/FOXO3A pathway.

Purpose: Proteinuria is an independent risk factor of chronic kidney disease (CKD). Albumin-induced tubulointerstitial inflammation and epithelial-mesenchymal transition (EMT) via the activation of NLRP3 inflammasome is a potential therapeutic target for CKD. Suyin Detoxification Granule (SDG) improves proteinuria and postpones renal failure. However, the underlying mechanism is still unknown. Methods: Firstly, the rat model of renal failure was established using intragastric administration of adenine. Renal function, proteinuria, inflammatory indicators in serum, and renal pathology were assessed, and renal immunohistochemical staining of NLRP3 inflammasomes was performed after intervention with low and high concentrations of SDG. Secondly, the model of renal tubular epithelial HK-2 cells was established using albumin in vitro, and the cell viability, EMT phenotype, and the expression of proteins in the NLRP3 inflammasome signaling pathway were measured after the freezedried powder of Suyin Detoxification Prescription (SDP) and CY-09, which is a selective and direct NLRP3 inhibitor, were co-incubated with albumin. ATP, SOD, mitochondrial membrane potential, and ROS were further measured in vitro, and changes in the mitochondrial function after SDP intervention were observed. The mitochondrial antiviral signaling protein (MAVS) was knocked down using siRNA, and the interaction between MAVS and NLRP3 was verified using Western blotting, polymerase chain reaction (PCR), and immunofluorescence. Results: SDG improved renal function and proteinuria, alleviated renal fibrosis, and reduced serum inflammation and the expression of the components of the NLRP3 inflammasome in the kidney. In vitro, SDP and CY-09 enhanced cell viability after injury with albumin and inhibited pyroptosis induced by the NLRP3 inflammatory signaling pathway and expression of proteins involved in EMT. It was further found that SDP alleviated the mitochondrial dysfunction caused by albumin. The knockdown of MAVS reduced the expression of NLRP3 pathway proteins and their mRNA levels and also weakened the co-localization of NLRP3, thus, reducing cell pyroptosis. Conclusion: SDP protected renal tubular epithelial cells from cell pyroptosis and EMT by regulating the albumin-induced mitochondrial dysfunction/ MAVS/ NLRP3-ASC-caspase-1 inflammasome signaling pathway.

Shengma Biejia decoction (SMBJD), a traditional Chinese formula recorded in the Golden Chamber , has been widely used for the treatment of malignant tumors. However, its underlying molecular targets and mechanisms are still unclear. This study showed that SMBJD inhibited tumor growth and stimulated hemogram recovery significantly in a multiple myeloma xenograft model. Western blot and immunohistochemistry assays of tumor tissues showed that SMBJD reduced the ratio of autophagy-related proteins LC3-II/LC3-I, while P62 and apoptosis-related proteins cleaved caspase-3/caspase-3 and Bax/Bcl-2 were upregulated. In vitro experiments demonstrated the time-dependent and dose-dependent cytotoxicity of SMBJD on multiple myeloma cell lines H929 and U266 through MTT assays. The LC3-II/LC3-I ratio and number of GFP-LC3 puncta showed that SMBJD inhibited the autophagy process of H929 and U266 cells. Moreover, both SMBJD and 3-methyladenine (3-MA) caused a decrease in LC3-II/LC3-I, and SMBJD could not reverse the upregulation of LC3-II/LC3-I caused by bafilomycin A1 (Baf-A1). Furthermore, the results of annexin V-FITC and propidium iodide double staining demonstrated that SMBJD treatment induced the apoptosis of H929 and U266 cells. These data prove that SMBJD inhibits autophagy and promotes apoptosis in H929 and U266 cells. The results also show that rapamycin could reduce the rate of SMBJD-induced apoptosis in H929 and U266 cells, at a concentration which had no effect on apoptosis but activated autophagy. In addition, analysis of the mechanism indicated that levels of phosphorylated ERK and phosphorylated mTOR were increased by treatment with SMBJD in vivo and in vitro . These results indicate that SMBJD, an old and effective herbal compound, could inhibit the viability of H929 and U266 cells and induce autophagy-mediated apoptosis through the ERK/mTOR pathway. Thus, it represents a potential therapy strategy for multiple myeloma.

Background Tumor associated macrophages (TAMs), a kind of inflammatory cells in the tumor microenvironment, are crucial for the occurrence and development of various tumors which increased the expression of CD163. Nevertheless, not much has been established regarding soluble CD163 and its connection to tumor diagnosis. In this case, a meta-analysis was conducted to determine the tumor diagnostic importance of serum sCD163. Methods In order to assess the correlation between sCD163 and the overall survival (OS) or progression-free survival (PFS) among tumor patients, a systematic perusal of literature published until June 2020 was conducted. Relevant data were primarily obtained from papers that have the following qualifications: 1) a confidence interval (CI) of 95%; 2) a report of the hazard ratios; and, 3) pooled by means of the Mantel-Haenszel random-effect representation. Results For the final meta-analysis, eight papers comprised of 1,236 cases were involved. Through pooled investigation, it was determined that a correlation exists between elevated serum sCD163 and worse OS (HR = 2.24, 95% CI: 1.50-3.35, P < 0.001) and PFS (HR = 3.90, 95% CI: 2.33-6.52, P < 0.001) among tumor cases. Subgroup analysis stratified by medium age at diagnosis demonstrated that patients over 60 years old with high sCD163 had worse OS (HR 2.28, 95% CI: 1.58-3.29, P < 0.001) than under 60 (HR 1.43, 95% CI: 1.15-1.77, P = 0.001). Subgroup analysis revealed that analysis method and medium age at diagnosis were the potential source of heterogeneity. Conclusions Overall, diagnosis of tumor cases can be adversely determined through substantial sCD163 levels. Consequently, it is encouraged that extensive researches regarding the rates of cancer survival be accomplished.

骨髓增生异常综合征(MDS)是一类起源于造血干/祖细胞的恶性克隆性疾病,其主要特征为外周血常规呈一系、两系或全血细胞减少,是急性白血病的高危因素.中医药在治疗MDS方面疗效颇佳. MDS可分为急性期和缓解期,急性期患者以邪气亢盛为主要矛盾,治疗应以祛邪为主;缓解期患者以正气虚弱为主要矛盾,治疗以扶助正气为主兼以祛邪.在分期论治的基础上,结合脏腑辨证,以补益脾肾、益气活血、疏肝理气、调畅情志和疏导郁结为治疗原则,能为MDS的中西医结合治疗提供新思路.

To evaluate the effectiveness and safety of Huachansu in the treatment of cancer-related pain,four Chinese databases( CNKI,VIP,Wan Fang,Sino Med) and three English databases( Cochrane Library,Medline,PubMed) were systematically and comprehensively retrieved since the establishment of each database to October 2018. Randomized controlled trials( RCTs) for the treatment of cancer-related pain with Huachansu were screened out according to pre-established inclusion criteria and exclusion criteria. Rev Man5. 3 software was used for Meta-analysis. A total of 241 articles were retrieved,and finally 10 studies were included. The total sample size was 1 293,including 648 in the experimental group and 645 in the control group. The overall quality of the included studies was generally low. The results of Meta-analysis showed that Huachansu combined with Western medicine acesodynes was superior to the single use of Western medicine acesodynes in the treatment of short-term pain relief,improvement of quality of life and reduction of constipation,nausea and vomiting,dizziness,drowsiness,anorexia and other adverse reactions. And it also has the advantage of a shorter onset time and longer duration time of analgesia,but cannot reduce the incidence of dysuria. Based on the findings,Huachansu had a certain effect in the treatment of cancer-related pain,and a significant positive effect on the improvement of quality of life and the reduction of adverse reactions. No serious adverse reactions occurred. However,due to the small number of studies included,the low quality of the included studies,published biases and other restrictions,the evidence in this study has a low quality,and the conclusion shall be adopted with caution. The effectiveness and safety of Huachansu in the treatment of cancer-related pain remained to be further confirmed in the future with a well-designed,rigorous,and standardized report,with a large sample size,multiple centers,and sufficient follow-up time for randomized controlled trials.

缓和医疗是一种综合性治疗方式,是一种中西医结合的治疗手段.国内外学者采用针灸疗法在恶性肿瘤的治疗上取得了一些进展,其在缓解癌性疼痛、改善放化疗不良反应、改善术后并发症、缓解心理精神痛苦、提高患者免疫力等方面发挥积极作用.针灸治疗契合缓和医疗理念,作为抗肿瘤治疗辅助手段,具有作用广泛、安全有效、实用易操作的特点,是缓和医疗的重要组成部分.未来,深入探究针灸在恶性肿瘤缓和医疗中的作用,可为恶性肿瘤临床治疗提供更多选择,同时也为国内缓和医疗研究提供新思路.

乳腺恶性肿瘤发病位于乳腺上皮、导管等部位, 发病率逐渐升高, 特别是在城市女性中.其治疗从手术根治性切除, 逐渐过度到综合、全程治疗.以往临床对生存率、生存期重视程度高, 随着缓和医疗快速发展, 对病患"全人照顾"的认识得到广泛认可, 目前逐渐对患者生活质量更为重视[1].乳腺癌手术治疗后最为常见并发症是上肢淋巴水肿, 疾病进程中也会导致其发生.乳腺癌相关上肢淋巴水肿 (breast cancer related lymphedema, BCRL) 会限制患者肩关节活动, 导致上肢功能障碍, 影响整体美观度并降低生活质量.现代临床医学将其划分为致残疾类型, 具有进展性、难治性特点.西医对BCRL治疗方法有限, 无法解决根本问题, 手术治疗也无对应适应症, 术后并发症多, 适用性差.中医药治疗成为提高临床疗效的重要途径.

骨髓增殖性肿瘤(MPN)是来源于克隆性造血干细胞的恶性肿瘤，包括真性红细胞增多症(PV)、原发性血小板增多症(ET)和骨髓纤维化(MF)。MPN患者存在疲劳、头痛、恶心、盗汗、瘙痒等不适症状，严重降低患者生活质量。近年来，研究重点转向对患者自我感知不适症状了解及控制上，本文介绍了MPN症状负荷及相关症状管理工具，突出中医药治疗MPN优势。 Myeloproliferative neoplasms (MPN) are clonal hematopoietic stem cell-derived malignancies that include polycythemia vera (PV), essential thrombocythemia (ET) and myelofibrosis (MF). Symptoms experienced by MPN patients are fatigue, headache, nausea, night sweats, itching and so on, and these symptoms seriously reduce the quality of life, which in the group of this disease. In recent years, researchers pay attention to the self perceived symptom of MPN patients, and focus on the understanding and management towards these symptoms. This paper introduces the symptom burden of MPN and Symptom Assessment Tools, and emphasises on the advantage of Chinese medicine in the treatment of MPN.

Objective:To explore the efficacy honey-fried Radix asteris decoction (HFRAD)of different concentration on cell cy-cle and proliferation of colorectal cancer LOVO cells.Methods:The changes of cellular morphology of LOVO cells treated with dif-ferent concentration HFRAD were observed by optical microscopy.MTT colorimetric assay was applied to observe proliferation of LOVO cells;flow cytometry was used to analyze cell cycle of LOVO cells.Results:MTT results indicated that proliferation of LO-VO cells treated with low concentration HFRAD(≤20mg·mL -1 )has been obviously promoted,and the cell proliferation rate could be up to 99.7%.Moreover,normal cellular morphology and membrane structure were observed by optical microscopy.Com-pared with the low concentration groups,it was found that cell proliferation of LOVO cells treated with high concentration HFRAD (>20mg·mL -1 )was obviously inhibited,the cell inhibitor rate can be up to above 80.34%.Optical microscopy results indica-ted that LOVO cells treated with high concentration HFRAD had lowest cell viability and the number of normal morphology cells can be significantly reduced.Flow cytometry results showed that the proportions of G1,S and G2 phase cells vary from different concentration HFARD and were significantly different from the control group.The proportion of S phase LOVO cells increased when treated with 10 and 20mg·mL -1 HFRAD.However,it was also found that the proportion of S phase LOVO cells decreased and the proportion of G2 phase increased with 30mg·mL -1 HFRAD.Conclusion:Different concentrate HFRAD has distinct effi-cacy on cell proliferation and cell cycle of LOVO cells.Cell proliferation of LOVO cells can be significantly promoted in concentra-tion of HFRAD(≤20mg·mL -1 ).However,high concentration HFRAD(>20mg·mL -1 )can inhibit cell proliferation.Moreo-ver,inhibition of G2 phase might be due to high concentration HFRAD.Our findings can provide experimental evidences for HFRAD in clinical therapy of Colorectal cancer.

目的:探讨蜜炙紫菀水煎剂对大肠癌LOVO细胞凋亡及迁移的影响方法:应用荧光显微镜观察DAPI染色后蜜炙紫菀水煎剂作用前后对LOVO细胞凋亡情况的影响;流式细胞仪检测蜜炙紫菀水煎剂对LOVO细胞凋亡率的影响;划痕实验和Transwell小室法检测不同质量浓度的蜜炙紫菀水煎剂处理LOVO细胞后对大肠癌LOVO细胞的迁移情况的影响.结果:荧光显微镜下观察发现蜜炙紫菀水煎剂实验组和空白对照组均未见细胞核凝集、染色体碎裂等细胞凋亡改变;流式细胞术结果也发现,不同浓度蜜炙紫菀水煎剂处理LOVO细胞48 h后,在细胞周期图G0期均未出现二倍峰,且凋亡率未见明显改变;浓度为5 ～30 mg·mL-1的蜜炙紫菀水煎剂处理LOVO细胞24、48 h后,与对照组相比,划痕实验结果显示大肠癌LOVO细胞的划痕距离较大,划痕未见明显愈合,均可以抑制大肠癌LOVO细胞的迁移,在蜜炙紫菀水煎剂浓度为40 mg· mL-1和80 mg·mL-1时,会导致大肠癌LOVO细胞非凋亡性死亡,Transwell小室结果显示,药物实验组穿透Transwell小室上层膜到达下室的LOVO细胞数明显少于空白对照组,蜜炙紫菀水煎剂浓度为30 mg·mL-1的实验组迁移率最低,为50.7％.结论:不同浓度的蜜炙紫菀水煎剂对大肠癌LOVO细胞的凋亡没有影响,但在高浓度时可以导致非凋亡性细胞死亡.同时,确定一定浓度的蜜炙紫菀水煎剂可以有效抑制大肠癌LOVO细胞的迁移,为有效预防大肠癌复发提供实验基础.