scholarly journals Immune Modulatory Activities of Arginyl-Fructose (AF) and AF-Enriched Natural Products in In-Vitro and In-Vivo Animal Models

Molecules ◽  
2021 ◽  
Vol 26 (8) ◽  
pp. 2251
Author(s):  
Jin-A Yu ◽  
Jung-Yun Lee ◽  
Tae Yang Kim ◽  
Hanna Kang ◽  
Su-Young Lee ◽  
...  
Keyword(s):  
Natural Products ◽  
Treated Group ◽  
Dependent Manner ◽  
Red Ginseng ◽  
Mice Model ◽  
Mouse Splenocytes ◽  
Higher Weights ◽  
In Vivo Animal Models

The immune system plays an important role in maintaining body homeostasis. Recent studies on the immune-enhancing effects of ginseng saponins have revealed more diverse mechanisms of action. Maillard reaction that occurs during the manufacturing processes of red ginseng produces a large amount of Amadori rearrangement compounds (ARCs), such as arginyl-fructose (AF). The antioxidant and anti-hyperglycemic effects of AF have been reported. However, the possible immune enhancing effects of non-saponin ginseng compounds, such as AF, have not been investigated. In this study the effects of AF and AF-enriched natural product (Ginofos, GF) on proliferation of normal mouse splenocytes were evaluated in vitro and male BALB/c mice models. The proliferation of splenocytes treated with mitogens (concanavalin A, lipopolysaccharide) were further increased by addition of AF (p < 0.01) or GF (p < 0.01), in a dose dependent manner. After the 10 days of oral administration of compounds, changes in weights of spleen and thymus, serum immunoglobulin, and expression of cytokines were measured as biomarkers of immune-enhancing potential in male BALB/c mice model. The AF or GF treated groups had higher weights of the thymus (0.94 ± 0.25 and 0.86 ± 0.18, p < 0.05, respectively) than that of cyclophosphamide treated group (0.59 ± 0.18). This result indicates that AF or AF-enriched extract (GF) increased humoral immunity against CY-induced immunosuppression. In addition, immunoglobulin contents and expression of cytokines including IgM (p < 0.01), IgG (p < 0.05), IL-2 (p < 0.01), IL-4 (p < 0.01), IL-6 (p < 0.01), and IFN-γ (p < 0.05) were also significantly increased by supplementation of AF or GF. These results indicate that AF has immune enhancing effects by activation of adaptive immunity via increase of expression of immunoglobulins and cytokines such as IgM, IgG, IL-2, IL-4, IL-6 and thereby proliferating the weight of thymus. Our findings provide a pharmacological rationale for AF-enriched natural products such as ginseng and red ginseng that can possibly have immune-enhancement potential and should be further evaluated.

scholarly journals Tolerogenic Splenic IDO+Dendritic Cells from the Mice Treated with Induced-Treg Cells Suppress Collagen-Induced Arthritis

2014 ◽  
Vol 2014 ◽  
pp. 1-12 ◽  
Author(s):  
Jie Yang ◽  
Yiming Yang ◽  
Huahua Fan ◽  
Hejian Zou
Keyword(s):  
Dendritic Cells ◽  
Immune Responses ◽  
Foxp3 Expression ◽  
Treated Group ◽  
Treg Cells ◽  
Therapeutic Effects ◽  
Dependent Manner ◽  
Collagen Induced Arthritis

TGF-β-induced regulatory T cells (iTregs) retain Foxp3 expression and immune-suppressive activity in collagen-induced arthritis (CIA). However, the mechanisms whereby transferred iTregs suppress immune responses, particularly the interplay between iTregs and dendritic cells (DCs)in vivo, remain incompletely understood. In this study, we found that after treatment with iTregs, splenic CD11c+DCs, termed “DCiTreg,” expressed tolerogenic phenotypes, secreted high levels of IL-10, TGF-β, and IDO, and showed potent immunosuppressive activityin vitro. After reinfusion with DCiTreg, marked antiarthritic activity improved clinical scores and histological end-points were observed. The serological levels of inflammatory cytokines and anti-CII antibodies were low and TGF-βproduction was high in the DCiTreg-treated group. DCiTregalso induced new iTregsin vivo. Moreover, the inhibitory activity of DCiTregon CIA was lost following pretreatment with the inhibitor of indoleamine 2,3-dioxygenase (IDO). Collectively, these findings suggest that transferred iTregs could induce tolerogenic characteristics in splenic DCs and these cells could effectively dampen CIA in an IDO-dependent manner. Thus, the potential therapeutic effects of iTregs in CIA are likely maintained through the generation of tolerogenic DCsin vivo.

Reticulon 3-mediated Chk2/p53 activation suppresses hepatocellular carcinogenesis and is blocked by hepatitis B virus

Gut ◽  
2020 ◽  
pp. gutjnl-2020-321386
Author(s):  
Shushu Song ◽  
Yinghong Shi ◽  
Weicheng Wu ◽  
Hao Wu ◽  
Lei Chang ◽  
...  
Keyword(s):  
Cellular Proliferation ◽  
Dependent Manner ◽  
Mice Model ◽  
Calcium Dependent ◽  
B Virus ◽  
P53 Activation ◽  
Underlying Mechanisms ◽  
Induced Apoptosis

ObjectiveDysfunction of endoplasmic reticulum (ER) proteins is closely related to homeostasis disturbance and malignant transformation of hepatocellular carcinoma (HCC). Reticulons (RTN) are a family of ER-resident proteins critical for maintaining ER function. Nevertheless, the precise roles of RTN in HCC remain largely unclear. The aim of the study is to examine the effect of reticulon family member RTN3 on HCC development and explore the underlying mechanisms.DesignClinical HCC samples were collected to assess the relationship between RTN3 expression and patients’ outcome. HCC cell lines were employed to examine the effects of RTN3 on cellular proliferation, apoptosis and signal transduction in vitro. Nude mice model was used to detect the role of RTN3 in modulating tumour growth in vivo.ResultsWe found that RTN3 was highly expressed in normal hepatocytes but frequently downregulated in HCC. Low RTN3 expression predicted poor outcome in patients with HCC in TP53 gene mutation and HBV infection status-dependent manner. RTN3 restrained HCC growth and induced apoptosis by activating p53. Mechanism studies indicated that RTN3 facilitated p53 Ser392 phosphorylation via Chk2 and enhanced subsequent p53 nuclear localisation. RTN3 interacted with Chk2, recruited it to ER and promoted its activation in an ER calcium-dependent manner. Nevertheless, the tumour suppressive effects of RTN3 were abrogated in HBV-positive cells. HBV surface antigen competed with Chk2 for RTN3 binding and blocked RTN3-mediated Chk2/p53 activation.ConclusionThe findings suggest that RTN3 functions as a novel suppressor of HCC by activating Chk2/p53 pathway and provide more clues to better understand the oncogenic effects of HBV.

scholarly journals Anti-osteosarcoma effect of antiserum against cross antigen TPD52 between osteosarcoma and Trichinella spiralis

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Tao-Tao Yue ◽  
Nan Zhang ◽  
Jian-Hua Li ◽  
Xiang-Yun Lu ◽  
Xiao-Cen Wang ◽  
...  
Keyword(s):  
Trichinella Spiralis ◽  
Serum Levels ◽  
Enzyme Linked Immunosorbent Assay ◽  
Cdna Expression Library ◽  
Dependent Manner ◽  
Expression Library ◽  
Muscle Larvae ◽  
In Vivo Animal Models

Abstract Background Trichinella spiralis (T. spiralis) is a parasite occurring worldwide that has been proven to have antitumour ability. However, studies on the antitumour effects of cross antigens between the tumour and T. spiralis or antibodies against cross antigens between tumours and T. spiralis are rare. Methods To study the role of cross antigens between osteosarcoma and T. spiralis, we first screened the cDNA expression library of T. spiralis muscle larvae to obtain the cross antigen gene tumour protein D52 (TPD52), and prepared fusion protein TPD52 and its antiserum. The anti-osteosarcoma effect of the anti-TPD52 antiserum was studied using cell proliferation and cytotoxicity assays as well as in vivo animal models; preliminary data on the mechanism were obtained using western blot and immunohistochemistry analyses. Results Our results indicated that TPD52 was mainly localized in the cytoplasm of MG-63 cells. Anti-TPD52 antiserum inhibited the proliferation of MG-63 cells and the growth of osteosarcoma in a dose-dependent manner. The tumour inhibition rate in the 100 μg treatment group was 61.95%. Enzyme-linked immunosorbent assay showed that injection of anti-TPD52 antiserum increased the serum levels of IFN-γ, TNF-α, and IL-12 in nude mice. Haematoxylin and eosin staining showed that anti-TPD52 antiserum did not cause significant pathological damage. Apoptosis of osteosarcoma cells was induced by anti-TPD52 antiserum in vivo and in vitro. Conclusions Anti-TPD52 antiserum exerts an anti-osteosarcoma effect by inducing apoptosis without causing histopathological damage. Graphical abstract

scholarly journals CircSETD3 (Hsa_circ_0000567) Suppresses Hepatoblastoma Pathogenesis via Targeting the miR-423-3p/Bcl-2-Interacting Mediator of Cell Death Axis

2021 ◽  
Vol 12 ◽  
Author(s):  
Xin Li ◽  
Haojie Wang ◽  
Zhijie Liu ◽  
Alimujiang Abudureyimu
Keyword(s):  
Regulatory Mechanism ◽  
Epithelial Mesenchymal Transition ◽  
Circular Rna ◽  
Cell Counting ◽  
Dependent Manner ◽  
Mice Model ◽  
Gain Of Function ◽  
Mesenchymal Transition

Background: Up until now, the role of circSETD3 (Has_circ_0000567) in regulating cancer development has been reported in several tumors, but the role and regulatory mechanism of circSETD3 in hepatoblastoma (HB) remain unclear.Methods: The qPCR and western blotting were used to determine the mRNA and protein levels in the present study. Stability of circular RNA was detected by RNA digested experiments. The gain-of-function and rescue experiments were used to explore the function and mechanism of circSETD3 in HB. Cell counting kit-8, colony formation, transwell assay, and xenograft mice model were used to detect effects and regulatory mechanism of circSETD3/miR-423-3p/Bim axis on cell aggressive phenotype in vitro and in vivo.Results: Here, we identified that circSETD3 downregulated in both HB clinical tissues and cell lines, compared to that of normal tissues and cells. Further gain-of-function experiments validated that circSETD3 overexpression inhibited cell proliferation, viability, migration, epithelial-mesenchymal transition (EMT) and tumorigenesis, and induced cell apoptosis in HB cells. Next, we validated that miR-423-3p targeted both circSETD3 and 3′ untranslated region (3′UTR) of Bim, and circSETD3 positively regulated Bim in HB cells through sponging miR-423-3p in a competing endogenous RNA (ceRNA)-dependent manner. Furthermore, through conducting reversal experiments, we evidenced that the inhibiting effects of circSETD3 overexpression on HB development were abrogated by upregulating miR-423-3p and downregulating Bim.Conclusion: Taken together, we evidenced that circSETD3 sponged miR-423-3p to upregulate Bim, resulting in the inhibition of HB development.

scholarly journals Red Ginseng Extract Attenuates Kainate-Induced Excitotoxicity by Antioxidative Effects

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Jin-Yi Han ◽  
Sun-Young Ahn ◽  
Eun-Hye Oh ◽  
Sang-Yoon Nam ◽  
Jin Tae Hong ◽  
...  
Keyword(s):  
Hippocampal Neurons ◽  
Mossy Fiber ◽  
Neuroprotective Effect ◽  
Order Rate Constant ◽  
Neuroprotective Activity ◽  
Dependent Manner ◽  
Red Ginseng ◽  
Ginseng Extract

This study investigated the neuroprotective activity of red ginseng extract (RGE,Panax ginseng, C. A. Meyer) against kainic acid- (KA-) induced excitotoxicityin vitroandin vivo. In hippocampal cells, RGE inhibited KA-induced excitotoxicity in a dose-dependent manner as measured by the MTT assay. To study the possible mechanisms of the RGE-mediated neuroprotective effect against KA-induced cytotoxicity, we examined the levels of intracellular reactive oxygen species (ROS) and [Ca2+]iin cultured hippocampal neurons and found that RGE treatment dose-dependently inhibited intracellular ROS and [Ca2+]ielevation. Oral administration of RGE (30 and 200 mg/kg) in mice decreased the malondialdehyde (MDA) level induced by KA injection (30 mg/kg, i.p.). In addition, similar results were obtained after pretreatment with the radical scavengers Trolox andN,N′-dimethylthiourea (DMTU). Finally, after confirming the protective effect of RGE on hippocampal brain-derived neurotropic factor (BDNF) protein levels, we found that RGE is active compounds mixture in KA-induced hippocampal mossy-fiber function improvement. Furthermore, RGE eliminated 1,1-diphenyl-2-picrylhydrazyl (DPPH) radicals, and the IC50was approximately 10 mg/ml. The reductive activity of RGE, as measured by reaction with hydroxyl radical (•OH), was similar to trolox. The second-order rate constant of RGE for•OH was 3.5–4.5×109 M−1·S−1. Therefore, these results indicate that RGE possesses radical reduction activity and alleviates KA-induced excitotoxicity by quenching ROS in hippocampal neurons.

scholarly journals Cnicin as an Anti-SARS-CoV-2: An Integrated In Silico and In Vitro Approach for the Rapid Identification of Potential COVID-19 Therapeutics

Antibiotics ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 542
Author(s):  
Hani A. Alhadrami ◽  
Ahmed M. Sayed ◽  
Hossam M. Hassan ◽  
Khayrya A. Youssif ◽  
Yasser Gaber ◽  
...  
Keyword(s):  
Natural Products ◽  
In Silico ◽  
Structural Information ◽  
Chemical Constituents ◽  
Rapid Identification ◽  
Dependent Manner ◽  
Modeling Tools ◽  
Clinical Experiments

Since the emergence of the SARS-CoV-2 pandemic in 2019, it has remained a significant global threat, especially with the newly evolved variants. Despite the presence of different COVID-19 vaccines, the discovery of proper antiviral therapeutics is an urgent necessity. Nature is considered as a historical trove for drug discovery, especially in global crises. During our efforts to discover potential anti-SARS CoV-2 natural therapeutics, screening our in-house natural products and plant crude extracts library led to the identification of C. benedictus extract as a promising candidate. To find out the main chemical constituents responsible for the extract’s antiviral activity, we utilized recently reported SARS CoV-2 structural information in comprehensive in silico investigations (e.g., ensemble docking and physics-based molecular modeling). As a result, we constructed protein–protein and protein–compound interaction networks that suggest cnicin as the most promising anti-SARS CoV-2 hit that might inhibit viral multi-targets. The subsequent in vitro validation confirmed that cnicin could impede the viral replication of SARS CoV-2 in a dose-dependent manner, with an IC50 value of 1.18 µg/mL. Furthermore, drug-like property calculations strongly recommended cnicin for further in vivo and clinical experiments. The present investigation highlighted natural products as crucial and readily available sources for developing antiviral therapeutics. Additionally, it revealed the key contributions of bioinformatics and computer-aided modeling tools in accelerating the discovery rate of potential therapeutics, particularly in emergency times like the current COVID-19 pandemic.

scholarly journals HDM-induced Atg5 Mediates TSLP Expressing to Disrupt Epithelial Barrier

2021 ◽  
Author(s):  
Changhui Yu ◽  
Zicong Zhou ◽  
Shixiu Liang ◽  
Zili Zhou ◽  
Jieyi Liu ◽  
...  
Keyword(s):  
Epithelial Barrier ◽  
Dependent Manner ◽  
Airway Epithelial ◽  
Mice Model ◽  
Rt Pcr ◽  
Intracellular Process ◽  
Self Protection ◽  
One Way Anova

Abstract Background: Asthma is a complex and heterogeneous disease. Autophagy, process of self-protection in cells, is an intracellular process when cells are being attacked by certain stress. Our team focused upon the disruption of airways epithelial barrier in asthma, and we interested in whether autophagy played a key role in asthma. Methods: 400U HDM was used to treat HBECs and established asthmatic mice model. Western blotting, RT-PCR and immunofluorescence were mainly used to detect autophagy process in vivo and in vitro. One way ANOVA and Mann Whitney test were used for statistic. Results: After treated with HDM, expression of LC3ab increased in vivo and in vitro. Using Rapamycin, 3-MA and Chloroquine to treat HBECs, then we surprisingly found that HDM disrupts epithelial barrier through incomplete autophagy. To find out the connection between asthma and autophagy, we chose known autophagy related genes to determine the association between autophagy and disruption of airway epithelial barrier. Atg5 and atg12 were chosen because these two genes varied upon the time dependent manner. Knocked down the expression of atg5 or atg12 by siRNA, the expression of TSLP, which can induce the disruption of airway epithelial barrier, remarkably reduced. Conclusions: These results demonstrated that HDM induced inflammatory in airway epithelium through autophagy, and then knocked down autophagy related genes alleviated the inflammatory in HBECs.

Antiproliferative Effect of 2-Hydroxypropyl-β-Cyclodextrin (HP-β-CyD) Against Chronic Myeloid Leukemia In Vitro and In Vivo.

Blood ◽  
2012 ◽  
Vol 120 (21) ◽  
pp. 2442-2442
Author(s):  
Masako Yokoo ◽  
Yasushi Kubota ◽  
Sakiko Mochinaga ◽  
Aya Maeda ◽  
Tatsuo Ichinohe ◽  
...  
Keyword(s):  
Nude Mice ◽  
Myeloid Leukemia ◽  
Leukemic Cell ◽  
Dependent Manner ◽  
Mice Model ◽  
Leukemic Cell Line ◽  
Ic50 Value ◽  
Dose Dependent

Abstract Abstract 2442 Cyclodextrins (CyDs) are cyclic oligosaccharides that can remove cholesterol from cell membranes and thereby affect receptor function, and are widely used in the pharmaceutical field because of those abilities to improve solubility, dissolution rate and bioavailability of the drugs. A number of studies have demonstrated that methyl-β- cyclodextrin (MβCD) can damage tumor cells and induce cell death. Very recently, Yan et al reported, on the basis of in vitro experiments, that MβCD induces apoptosis of chronic myeloid leukemia (CML) cells and have synergistic anti-leukemic effect combined with imatinib. 2-Hydroxypropyl-β-cyclodextrin (HP-β-CyD) is clinically used as a pharmaceutical excipient, which has been successfully applied to poorly water-soluble drugs. Recently HP-β-CyD has been approved for the treatment of Niemann-Pick type C disease, a rare lysosomal lipid storage disorder. In the present study, we examined the antiproliferative effect of HP-β-CyD on the in vitro growth of leukemic cell lines and in vivo model using mice transplanted with leukemic cell line. First in vitro proliferation was assessed using the modified MTT assay. The human Ph+ leukemic cell line BV173 and BaF3 cells expressing p190 wild type BCR-ABL (hereafter BaF3/BCR-ABL) were used for evaluation. The growth of BV173 and BaF3/BCR-ABL cells were similarly inhibited by HP-β-CyD in a time- and dose-dependent manner with IC50 value of 4.68 ± 0.98 and 6.01 ± 1.04 mM, respectively. In contrast, IC50 value for hepatocytes was 18.65 ± 4.84 mM, suggesting some therapeutic window between normal cells and CML cells. We next determined if the inhibition of leukemic cell growth by HP-β-CyD was associated with the induction of apoptosis. BaF3/BCR-ABL and BV173 cells were exposed to HP-β-CyD for 12, 24, 48 hours at concentrations of 5, 10, 15 and 25mM. Assessment of apoptosis by 7-AAD/Annexin V double staining revealed that HP-β-CyD induced apoptosis in both cell lines in a time- and dose-dependent manner. The toxicity of HP-β-CyD on normal hematopoietic progenitors was also examined. The susceptibility of normal hematopoieic progenitors was investigated by colony-forming units (CFU-C) assay. When normal progenitors were treated with 5, 15 or 25 mM HP-β-CyD, the percentage of colonies was 92.7 ± 8.6 %, 83.8 ± 23.5 % and 52.4 ± 9.7 % of control, respectively. These results also indicate that HP-β-CyD may not induce bone marrow suppression up to 15mM. Because in vitro assay showed significant effects against leukemia cell growth, we also investigated the in vivo efficacy of HP-β-CyD. Six-week-old nude mice were injected with 1×106 BaF3/BCR-ABL cells, and were intraperioneally treated with 200 μl of either vehicle, 50mM HP-β-CyD or 150mM HP-β-CyD twice a day (BID) for 20 days from 3days after transplantation. The vehicle-treated mice died of a condition resembling acute leukemia by 29 days after transplantation; HP-β-CyD- treated mice survived more than 40 days, significantly improved the survival (50mM: P=0.003, 150mM: P=0.001, respectively) compared with control mice (Figure 1). These results clearly demonstrate that HP-β-CyD itself has a certain level of anti-leukemic potential. Though further investigations are required to elucidate the mechanisms underlying the antiproliferative function of HP-β-CyD, we should take notice of additional effect when the evaluation of drug efficacy is performed for anti-cancer agents complexed with HP-β-CyD. Figure 1. Administration of HP-β-CyD prolonged the survival in mice model of BCR-ABL-induced leukemia. Nude mice were injected with 1×106 BaF3 cells expressing p190 BCR-ABL. These mice were treated with vehicle or HP-β-CyD (50 or 150mM) for 20days from 3 days after transplantation. Figure 1. Administration of HP-β-CyD prolonged the survival in mice model of BCR-ABL-induced leukemia. Nude mice were injected with 1×106 BaF3 cells expressing p190 BCR-ABL. These mice were treated with vehicle or HP-β-CyD (50 or 150mM) for 20days from 3 days after transplantation. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Endocannabinoid system acts as a regulator of immune homeostasis in the gut

2017 ◽  
Vol 114 (19) ◽  
pp. 5005-5010 ◽  
Author(s):  
Nandini Acharya ◽  
Sasi Penukonda ◽  
Tatiana Shcheglova ◽  
Adam T. Hagymasi ◽  
Sreyashi Basu ◽  
...  
Keyword(s):  
Cannabinoid Receptors ◽  
Cannabinoid Receptor ◽  
Endocannabinoid System ◽  
Nod Mice ◽  
Immune Homeostasis ◽  
Dependent Manner ◽  
Mice Model ◽  
Nonobese Diabetic

Endogenous cannabinoids (endocannabinoids) are small molecules biosynthesized from membrane glycerophospholipid. Anandamide (AEA) is an endogenous intestinal cannabinoid that controls appetite and energy balance by engagement of the enteric nervous system through cannabinoid receptors. Here, we uncover a role for AEA and its receptor, cannabinoid receptor 2 (CB2), in the regulation of immune tolerance in the gut and the pancreas. This work demonstrates a major immunological role for an endocannabinoid. The pungent molecule capsaicin (CP) has a similar effect as AEA; however, CP acts by engagement of the vanilloid receptor TRPV1, causing local production of AEA, which acts through CB2. We show that the engagement of the cannabinoid/vanilloid receptors augments the number and immune suppressive function of the regulatory CX3CR1hi macrophages (Mϕ), which express the highest levels of such receptors among the gut immune cells. Additionally, TRPV1−/− or CB2−/− mice have fewer CX3CR1hi Mϕ in the gut. Treatment of mice with CP also leads to differentiation of a regulatory subset of CD4+ cells, the Tr1 cells, in an IL-27–dependent manner in vitro and in vivo. In a functional demonstration, tolerance elicited by engagement of TRPV1 can be transferred to naïve nonobese diabetic (NOD) mice [model of type 1 diabetes (T1D)] by transfer of CD4+ T cells. Further, oral administration of AEA to NOD mice provides protection from T1D. Our study unveils a role for the endocannabinoid system in maintaining immune homeostasis in the gut/pancreas and reveals a conversation between the nervous and immune systems using distinct receptors.

scholarly journals Overcome Cancer Cell Drug Resistance Using Natural Products

2015 ◽  
Vol 2015 ◽  
pp. 1-14 ◽  
Author(s):  
Pu Wang ◽  
Hua Li Yang ◽  
Ying Juan Yang ◽  
Lan Wang ◽  
Shao Chin Lee
Keyword(s):  
Drug Resistance ◽  
Natural Products ◽  
Cancer Cell ◽  
Chinese Literature ◽  
Resistance Management ◽  
Herbal Extract ◽  
Cancer Drug ◽  
Dependent Manner

Chemotherapy is one of the major treatment methods for cancer. However, failure in chemotherapy is not uncommon, mainly due to dose-limiting toxicity associated with drug resistance. Management of drug resistance is important towards successful chemotherapy. There are many reports in the Chinese literature that natural products can overcome cancer cell drug resistance, which deserve sharing with scientific and industrial communities. We summarized the reports into four categories: (1)in vitrostudies using cell line models; (2) serum pharmacology; (3)in vivostudies using animal models; and (4) clinical studies. Fourteen single compounds were reported to have antidrug resistance activity for the first time.In vitro, compounds were able to overcome drug resistance at nontoxic or subtoxic concentrations, in a dose-dependent manner, by inhibiting drug transporters, cell detoxification capacity, or cell apoptosis sensitivity. Studiesin vivoshowed that single compounds, herbal extract, and formulas had potent antidrug resistance activities. Importantly, many single compounds, herbal extracts, and formulas have been used clinically to treat various diseases including cancer. The review provides comprehensive data on use of natural compounds to overcome cancer cell drug resistance in China, which may facilitate the therapeutic development of natural products for clinical management of cancer drug resistance.

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