Guanylate-Binding Protein 1 (GBP1) Enhances IFN-α Mediated Antiviral Activity against Hepatitis B Virus Infection.

Interferon-alpha (IFN-α) is a first-line drug for treating chronic hepatitis B (CHB). Guanylate-binding protein 1 (GBP1) is one of the interferon-stimulating factors, which participates in the innate immunity of the host and plays an antiviral and antibacterial role. In this study, we explored how GBP1 is involved in IFN-α antiviral activity against HBV. Before being gathered, HepG2-NTCP and HepG2 2.15 cells were transfected with the wild-type hGBP1 plasmid or si-GBP1, respectively, and followed by stimulation with Peg-IFNα-2b. We systematically explored the role of GBP1 in regulating HBV infection in cell models. Additionally, we also examined GBP1 levels in CHB patients. GBP1 activity increased, and its half-life was prolonged after HBV infection. Overexpression of GBP1 inhibited the production of HBsAg and HBeAg, as well as HBs protein and HBV total RNA levels, whereas silencing of GBP1 inhibited its ability to block viral infections. Interestingly, overexpressing GBP1 co-treatment with Peg-IFNα-2b further increased the antiviral effect of IFN-α, while GBP1 silencing co-treatment with Peg-IFNα-2b partly restored its inhibitory effect on HBV. Mechanistically, GBP1 mediates the anti-HBV response of Peg-IFNα-2b by targeting HBs. Analysis of clinical samples revealed that GBP1 was elevated in CHB patients and increased with Peg-IFNα-2b treatment, while GBP1 showed good stability in the interferon response group. Our study demonstrates that GBP1 inhibits HBV replication and promotes HBsAg clearance. It is possible to achieve antiviral effects through the regulation of IFN-α induced immune responses in response to HBV.

Reactive Carbonyl Species Scavenger: Epigallocatechin-3-Gallate.

Epigallocatechin-3-gallate (EGCG), a prominent polyphenol found abundantly in tea, has garnered significant attention for its potential in preventing and ameliorating a wide range of diseases. Its remarkable antioxidant properties and ability to capture reactive carbonyl species make it a key player among tea's polyphenolic components. This paper delves into the synthesis and origins of both EGCG and reactive carbonyl species (RCS), emphasizing the toxicity of RCS in various food sources and their formation during food processing. Understanding EGCG's capability to capture and metabolize RCS is crucial for harnessing its health benefits. Thus, this paper explores the underlying mechanisms of EGCG for RCS inhibition and its role in capturing these compounds to generate EGCG-RCS adducts. And the absorption and metabolism of EGCG-RCS adducts is also discussed.

Development and Validation of a Novel Prognosis Model Based on a Panel of Three Immunogenic Cell Death-Related Genes for Non-Cirrhotic Hepatocellular Carcinoma.

Purpose: The accurate prediction of non-cirrhotic hepatocellular carcinoma (NCHCC) risk facilitates improved surveillance strategy and decreases cancer-related mortality. This study aimed to explore the correlation between immunogenic cell death (ICD) and NCHCC prognosis using The Cancer Genome Atlas (TCGA) datasets, and the potential prognostic value of ICD-related genes in NCHCC. Methods: Clinical and transcriptomic data of patients with NCHCC patients were retrieved from TCGA database. Weighted gene co-expression network analysis was performed to obtain the NCHCC phenotype-related module genes. Consensus clustering analysis was performed to classify the patients into two clusters based on intersection genes among differentially expressed genes (DEGs) between cancer and adjacent tissues, NCHCC phenotype-related genes, and ICD-related genes. NCHCC-derived tissue microarray was used to evaluate the correlation of the expression levels of key genes with NCHCC prognosis using immunohistochemical staining. Results: Cox regression analyses were performed to construct a prognostic risk score model comprising three genes (TMC7, GRAMD1C, and GNPDA1) based on DEGs between two clusters. The model stratified patients with NCHCC into two risk groups. The overall survival (OS) of the high-risk group was significantly lower than that of the low-risk group. Univariable and multivariable Cox regression analyses revealed that these signature genes are independent predictors of OS. Functional analysis revealed differential immune status between the two risk groups. Next, a nomogram was constructed, which demonstrated the potent distinguishing ability of the developed model based on receiver operating characteristic curves. In vitro functional validation revealed that the migration and invasion abilities of HepG2 and Huh7 cells were upregulated upon GRAMD1C knockdown but downregulated upon TMC7 knockdown. Conclusion: This study developed a prognostic model comprising three genes, which can aid in predicting the survival of patients with NCHCC and guide the selection of drugs and molecular markers for NCHCC.

The expression of interleukin-1ß in patients with chronic hepatitis B treated with pegylated-interferon-alpha combined with tenofovir disoproxil fumarate and monotherapy.

BACKGROUND: Anti-hepatitis B virus (HBV) treatment uses tenofovir disoproxil fumarate (TDF) along with Pegylated-interferon-alpha (Peg-IFN-α), which is more effective than TDF/Peg-IFN-α monotherapy. We have previously shown that interleukin-1beta (IL-1ß) is related to the effectiveness of IFN-α treatment in chronic hepatitis B (CHB) patients. The aim was to investigate the expression of IL-1ß in CHB patients treated with Peg-IFN-α combination with TDF and TDF/Peg-IFN-α monotherapy. METHODS: Huh7 cells infected with HBV were stimulated by Peg-IFN-α and/or Tenofovir (TFV) for 24h. A single-center cohort study of prospective recruitment of CHB patients: untreated CHB (Group A), TDF combined with Peg-IFN-α therapy (Group B), Peg-IFN-α monotherapy (Group C), TDF monotherapy (Group D). Normal donors served as controls. The clinical datas and blood of patients were collected at 0, 12, and 24 weeks. According to the early response criteria, Group B and C were divided into two subgroups: the early response group (ERG) and the non-early response group (NERG). Stimulation of HBV-infected hepatoma cells with IL-1ß to validate the antiviral activity of IL-1ß. To test the blood sample, cell culture supernatant, and cell lysates and to assess the expression of IL-1ß and HBV replication levels in various treatment protocols, Enzyme-Linked Immunosorbent Assay (ELISA) and quantitative reverse transcription polymerase chain reaction (qRT-PCR) were used. SPSS 26.0 and GraphPad Prism 8.0.2 software were used for statistical analysis. P values < 0.05 was considered to be statistically significant. RESULTS: In vitro experiments, Peg-IFN-α plus TFV treatment group expressed higher IL-1ß and inhibited HBV more effectively than monotherapy. Finally, 162 cases were enrolled for observation (Group A (n = 45), Group B (n = 46), Group C (n = 39), and Group D (n = 32)), and normal donors (n = 20) were enrolled for control. The early virological response rates of Group B, C, and D were 58.7%, 51.3%, and 31.2%. At 24 weeks, IL-1ß in Group B(P = 0.007) and C(P = 0.034) showed higher than at 0 week. In Group B, the IL-1ß showed an upward trend at 12w and 24w in the ERG. IL-1ß significantly reduced HBV replication levels in hepatoma cells. CONCLUSION: The increased expression of IL-1ß may enhance the efficacy of TDF combined with Peg-IFN-α therapy in achieving an early response for CHB patients.

18F-FDG PET/CT and contrast-enhanced CT in the diagnosis of Castleman disease.

OBJECTIVE: Castleman disease (CD) is a rare group of lymphoproliferative disorders, which is easily confused with lymphoma or other solid tumors. Hence, this study aimed to investigate the diagnostic role of 18F-FDG PET/CT and contrast-enhanced CT (CECT) in patients with CD. METHODS: Clinicopathological characteristics, and 18F-FDG PET/CT and CECT findings and parameters were retrospectively reviewed in 32 patients with CD. RESULTS: These 32 patients (12 males, 20 females; median age, 41 years) consisted of 17 unicentric CD (UCD) patients and 15 multicentric CD (MCD) patients. Compared with MCD, UCD had a higher prevalence in female (82.4% vs. 40.0%) and hyaline vascular subtype (94.1% vs. 40.0%) (P < 0.05). FDG uptake was avid in all cases, including moderate uptake in 7 cases and intense uptake in 25 cases. The median SUVmax, SUVmean, MLV, and TLG of all cases were 4.4 (range, 1.4-23.6), 2.7 (range, 1.1-15.2), 26.6 (range, 4.8-393.0), and 78.8 (range, 9.4-1545.6), respectively. The lesions of 29 cases showed homogeneous enhancement, and marked enhancement was observed in 27 cases. 18F-FDG PET/CT corrected 6.3% CECT diagnoses, while CECT corrected 37.5% PET/CT diagnosis. The accuracy of combined PET/CT and CECT was superior to PET/CT or CECT alone (78.1%, 31.3%, and 62.5%). Besides, higher SUVmax and SUVmean were found in male subjects, MCD, and plasma cell subtype (P < 0.05), while higher MLV and TLG were observed in larger lesion size and volume (P < 0.05). CONCLUSION: Castleman disease most commonly appears as marked and homogeneous enhancement meanwhile with moderate or intense FDG uptake. 18F-FDG PET/CT combined with CECT was the effectively diagnostic modality for CD. The glucose metabolism of CD was associated with gender, clinical classification, histopathological classification, and lesion size and volume.

Compound and heterozygous mutations of DSG2 identified by Whole Exome Sequencing in arrhythmogenic right ventricular cardiomyopathy/dysplasia with ventricular tachycardia.

BACKGROUNDS: This study was designed to identify the pathogenic mutations in two Chinese families of arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/D) using the Whole Exome Sequencing (WES). METHODS AND RESULTS: The proband 1 (Family 1, II:1) and proband 2 (Family 2, II:1) underwent the WES of DNA from peripheral blood. The genes susceptible to arrhythmias and cardiomyopathies were analyzed and both the probands carried the same exonic mutation of DSG2 p.F531C (NM_001943, exon 11: c.T1592G). The proband 1 also carried the splicing mutation of DSG2 (NM_001943: exon 4:c.217-1G>T), and proband 2 carried the intronic mutation of DSG2 (NM_001943: exon 6: c.524-3C>G) that potentially influenced the splicing function predicted by Human Splicing Finder. The compound heterozygous mutations of the two probands inherited from their paternal and maternal side, respectively. The carriers with DSG2 p.F531C showed early abnormal electrocardiograms, characterized as the subclinical phenotype of ARVC/D. CONCLUSIONS: The DSG2 p.F531C was the main reason for ARVC/D. More severe phenotypes of ARVC/D occurred when coexisting with 217-1G>T or 524-3C>G mutation that potentially affecting the splicing function, as a compound heterozygous recessive inheritance.

A salting out-acetonitrile homogeneous extraction coupled with gas chromatography-mass spectrometry method for the simultaneous determination of thirteen N-nitrosamines in skin care cosmetics.

A sensitive gas chromatography-mass spectrometry method was established for the simultaneous determination of thirteen N-nitrosamines (NAs) in skin care cosmetics. The cosmetics samples were firstly dispersed by water and subsequently extracted and purified using salting out-acetonitrile homogeneous extraction method. Finally, the extracting solution was concentrated by slow nitrogen gas blowing. All of the samples were separated by INNOWAX capillary chromatographic column, and detected by selected ion monitoring (SIM) mode of gas chromatography-mass spectrometry (GC-MS) and quantified by isotope internal standard method. The method was validated for linearity and range, accuracy, precision and sensitivity. Under the optimized condition, the calibration curves were linear over the selected concentration ranges of 2-500µg/L for all the thirteen analytes, with calculated coefficients of determination (R(2)) of greater than 0.996. The limits of detection (LODs) and the limits of quantitation (LOQs) of the method were 3-15µg/kg and 10-50µg/kg, respectively. Recoveries were calculated at three levels of concentration spiked in two kinds of cosmetics (skin care cream and water). The values were found between 93.8% and 121.0% with relative standard deviation (RSD) values of 2.5-7.2% for intra-day precision (n=6) and 3.3-6.7% for inter-day precision (n=5). The method was successfully applied to analyze twenty-two cosmetics samples and N-nitrosodimethylamine (NDMA) was detected in one sample with the concentration of 207µg/kg.

FSP1(+) fibroblast subpopulation is essential for the maintenance and regeneration of medullary thymic epithelial cells.

Thymic epithelial cells (TECs) form a 3-dimentional network supporting thymocyte development and maturation. Besides epithelium and thymocytes, heterogeneous fibroblasts are essential components in maintaining thymic microenvironments. However, thymic fibroblast characteristics, development and function remain to be determined. We herein found that thymic non-hematopoietic CD45(-)FSP1(+) cells represent a unique Fibroblast specific protein 1 (FSP1)(-)fibroblast-derived cell subset. Deletion of these cells in FSP1-TK transgenic mice caused thymus atrophy due to the loss of TECs, especially mature medullary TECs (MHCII(high), CD80(+) and Aire(+)). In a cyclophosphamide-induced thymus injury and regeneration model, lack of non-hematopoietic CD45(-)FSP1(+) fibroblast subpopulation significantly delayed thymus regeneration. In fact, thymic FSP1(+) fibroblasts released more IL-6, FGF7 and FSP1 in the culture medium than their FSP1(-) counterparts. Further experiments showed that the FSP1 protein could directly enhance the proliferation and maturation of TECs in the in vitro culture systems. FSP1 knockout mice had significantly smaller thymus size and less TECs than their control. Collectively, our studies reveal that thymic CD45(-)FSP1(+) cells are a subpopulation of fibroblasts, which is crucial for the maintenance and regeneration of TECs especially medullary TECs through providing IL-6, FGF7 and FSP1.

Microgravity activates p38 MAPK-C/EBPß pathway to regulate the expression of arginase and inflammatory cytokines in macrophages.

OBJECTIVE AND DESIGN: Molecular mechanisms of microgravity-caused immunosuppression are not fully elucidated. In the present study, we investigated the effects of simulated microgravity on macrophage functions and tried to identify the related intracellular signal pathways. MATERIAL OR SUBJECTS: Primary mouse macrophages were used in the present study. The gene expression and function of IL-4-treated mouse macrophages were detected after simulated microgravity or 1 g control. METHODS: Freshly isolated primary mouse macrophages were cultured in a standard simulated microgravity situation using a rotary cell culture system (RCCS-1) and 1 g control conditions. Real-time PCR, western blots and flow cytometry were used to investigate the related intracellular signals and molecule expression. RESULTS: The arginase mRNA and protein levels in freshly isolated primary mouse macrophages under simulated microgravity using RCCS-1 were significantly higher than those under normal gravity. Meanwhile, simulated microgravity induced over-expression of C/EBPß, a transcription factor of arginase promoter, and activation of p38 MAPK, which could increase C/EBPß expression. Furthermore, up-regulation of Interleukin-6 (IL-6) and down-regulation of IL-12 p40 (IL-12B) in LPS-stimulated macrophages were also detected after simulated microgravity, which is regulated by C/EBPß. CONCLUSIONS: Simulated microgravity activates a p38 MAPK-C/EBPß pathway in macrophages to up-regulate arginase and IL-6 expression and down-regulate IL-12B expression. Both increased arginase expression and decreased IL-12B expression in macrophages during inflammation could result in immunosuppression under microgravity.

[Study on effect of total flavanones of Sedum sarmentosum on apoptosis of hepatic stellate cells and its mechanism].

OBJECTIVE: To study the effect of total flavanones of Sedum sarmentosum (SSTF) on the apoptosis of rat hepatic stellate cells (HSC-T6) and its mechanism. METHOD: Different concentrations of SSTF and HSC-T6 cells were co-cultured for different period of time. The MTT assay was used to detect the inhibitory effect of SSTF on the proliferation of HSC-T6 cells. The flow cytometry Annexin-V/PI double staining method was adopted to detect SSTF's effect on HSC-T6 cell apoptosis. Western blotting and Real-time PCR methods were applied to observe the effect on the protein and mRNA expressions of apoptosis-related cytokines Bcl-2, Bax and Caspase-3. RESULT: SSTF significantly inhibited HSC-T6 cell proliferation and induced cell apoptosis in a dose and time dependent manner. According to Western blotting result, SSTF promoted apoptosis by inhibiting Bcl-2, Bax and promoting the protein expression of Caspase-3; according to a further Real-time PCR study, Bcl-2 mRNA levels can inhibit Bcl-2 and promote Bax and Caspase-3 expressions. CONCLUSION: SSTF has the effect of promoting the apoptosis of HSC-T6 mainly by inhibiting Bcl-2 and promoting protein and mRNA expressions of Bax and caspase-3.

Thymic epithelial cell development and its dysfunction in human diseases.

Thymic epithelial cells (TECs) are the key components in thymic microenvironment for T cells development. TECs, composed of cortical and medullary TECs, are derived from a common bipotent progenitor and undergo a stepwise development controlled by multiple levels of signals to be functionally mature for supporting thymocyte development. Tumor necrosis factor receptor (TNFR) family members including the receptor activator for NF κ B (RANK), CD40, and lymphotoxin ß receptor (LT ß R) cooperatively control the thymic medullary microenvironment and self-tolerance establishment. In addition, fibroblast growth factors (FGFs), Wnt, and Notch signals are essential for establishment of functional thymic microenvironment. Transcription factors Foxn1 and autoimmune regulator (Aire) are powerful modulators of TEC development, differentiation, and self-tolerance. Dysfunction in thymic microenvironment including defects of TEC and thymocyte development would cause physiological disorders such as tumor, infectious diseases, and autoimmune diseases. In the present review, we will summarize our current understanding on TEC development and the underlying molecular signals pathways and the involvement of thymus dysfunction in human diseases.

Microgravity inhibition of lipopolysaccharide-induced tumor necrosis factor-α expression in macrophage cells.

OBJECTIVE AND DESIGN: Microgravity environments in space can cause major abnormalities in human physiology, including decreased immunity. The underlying mechanisms of microgravity-induced inflammatory defects in macrophages are unclear. MATERIAL OR SUBJECTS: RAW264.7 cells and primary mouse macrophages were used in the present study. Lipopolysaccharide (LPS)-induced cytokine expression in mouse macrophages was detected under either simulated microgravity or 1g control. METHODS: Freshly isolated primary mouse macrophages and RAW264.7 cells were cultured in a standard simulated microgravity situation using a rotary cell culture system (RCCS-1) and 1g control conditions. The cytokine expression was determined by real-time PCR and ELISA assays. Western blots were used to investigate the related intracellular signals. RESULTS: LPS-induced tumor necrosis factor-α (TNF-α) expression, but not interleukin-1ß expression, in mouse macrophages was significantly suppressed under simulated microgravity. The molecular mechanism studies showed that LPS-induced intracellular signal transduction including phosphorylation of IKK and JNK and nuclear translocation of NF-κB in macrophages was identical under normal gravity and simulated microgravity. Furthermore, TNF-α mRNA stability did not decrease under simulated microgravity. Finally, we found that heat shock factor-1 (HSF1), a known repressor of TNF-α promoter, was markedly activated under simulated microgravity. CONCLUSIONS: Short-term treatment with microgravity caused significantly decreased TNF-α production. Microgravity-activated HSF1 may contribute to the decreased TNF-α expression in macrophages directly caused by microgravity, while the LPS-induced NF-κB pathway is resistant to microgravity.

Phosphatase Wip1 is essential for the maturation and homeostasis of medullary thymic epithelial cells in mice.

Thymic epithelial cells (TECs) are a key cell type in the thymic microenvironment essential for T cell development. However, intrinsic molecular mechanisms controlling TEC differentiation and activities are poorly defined. In this study, we found that deficiency of p53-induced phosphatase 1 (Wip1) in mice selectively caused severe medullary TEC (mTEC) maturation defects in an intrinsic manner. Wip1 knockout (KO) mice had decreased mature epithelial cell adhesion molecule⁺Ulex europaeus agglutinin-1 (UEA-1)⁺mTECs, including UEA-1⁺MHC class II(high), UEA-1⁺CD80⁺, UEA-1⁺CD40⁺, and UEA-1⁺Aire⁺ cells, but not decreased numbers of cortical epithelial cell adhesion molecule⁺BP-1⁺ TECs, in the postnatal stage but not in the fetal stage. Wip1-deficient mTECs express fewer tissue-restricted Ags and UEA-1⁺involucrin⁺ terminal-differentiated cells. Animal models, including grafting fetal Wip1-deficient thymic tissue into T cell-deficient nude mice and reconstitution of lethally irradiated Wip1KO mouse recipients with wild-type bone marrow cells, also showed the impaired mTEC components in Wip1KO thymi, indicating the intrinsic regulatory role of Wip1 in mTEC maturation. Furthermore, thymus regeneration was significantly less efficient in adult Wip1KO mice than in wild-type mice after cyclophosphamide treatment. Wip1 deficiency resulted in elevated p38 MAPK activity in mTECs. Activated p38 MAPK has the ability to suppress CD40 expression on mTECs. Wip1-deficient thymi displayed poor response to CD40L in the fetal thymus organ culture system. Thus, Wip1 positively controls mTEC maturation, homeostasis, and regeneration through limiting the p38 MAPK pathway.

Thymic epithelial cell development and differentiation: cellular and molecular regulation.

Thymic epithelial cells (TECs) are one of the most important components in thymic microenvironment supporting thymocyte development and maturation. TECs, composed of cortical and medullary TECs, are derived from a common bipotent progenitor, mediating thymocyte positive and negative selections. Multiple levels of signals including intracellular signaling networks and cell-cell interaction are required for TEC development and differentiation. Transcription factors Foxn1 and autoimmune regulator (Aire) are powerful regulators promoting TEC development and differentiation. Crosstalks with thymocytes and other stromal cells for extrinsic signals like RANKL, CD40L, lymphotoxin, fibroblast growth factor (FGF) and Wnt are also definitely required to establish a functional thymic microenvironment. In this review, we will summarize our current understanding about TEC development and differentiation, and its underlying multiple signal pathways.

Selenium nanoparticles inhibit the growth of HeLa and MDA-MB-231 cells through induction of S phase arrest.

In vitro antiproliferative effects of selenium nanoparticles (nanoSe(0), 10-40 µmol/L) on HeLa (human cervical carcinoma) cells and MDA-MB-231 (human breast carcinoma) cells were examined by optical microscopic inspection and MTT assay in the present study. The nanoSe(0) effectively inhibited the growth of MDA-MB-231 cells and HeLa cells in a dose-dependent manner. The morphology analysis with atomic force microscope showed that the HeLa cells treated with 10 µmol/L nanoSe(0) were rough and shrunken with truncated lamellipodia at terminal part of the cells. Flow cytometric analysis demonstrated that HeLa cells were arrested at S phase of the cell cycle after exposed to nanoSe(0) (10 µmol/L). Taken together, our results suggested that nanoSe(0) may be more helpful in cancer chemoprevention as a potential anticancer drug.

Improvement of quality of life with Shenfu injection in non small cell lung cancer patients treated with gemcitabine plus cisplatin regimen.

OBJECTIVE: To observe the effect of Shenfu injection (SFI) in treating non small cell lung cancer (NSCLC) patients on quality of life with gemcitabine (GEM) plus cisplatin (GP) regimen. METHODS: Thirty-four patients were ready to receive GP regimen chemotherapy for treating NSCLC disease, according to lot-drawing, they were divided into SFI pre-treatment group (18 cases) and SFI post-treatment group (16 cases). SFI pre-treatment group: During the first treatment course, chemotherapy was begun with SFI 60 ml, intravenous dripping on the 3rd day, once daily, consecutively for 10 days; on the 1st day, GP regimen (GEM 1250 mg/m(2), intravenous dripping, on the 1st and 8th day; cisplatin 70 mg/m(2) on the 2nd day; 21 days as one cycle) was carried out; in the second treatment course GP regimen was merely given to serve as the self-control. SFI post-treatment group: the medicament sequence order was reversed from that of pre-treatment group. Using dual international quality of life (QOL) scores, the effect of SFI on the patients' QOL was observed through randomized self pre- and post-crossover control. RESULTS: The QOL in the 34 patients after being treated by SFI in combination with GP chemotherapy regimen in one group, and GP chemotherapy regimen alone in the other, was improved in different degrees, with significant difference (P < 0.01); comparison of SFI combined with GP chemotherapy regimen with GP chemotherapy alone showed that QOL in patients was significantly different (P < 0.01). CONCLUSION: SFI could improve QOL in patients with NSCLC who were treated with GP regimen.

[Clinical study on comprehensive treatment of primary liver cancer mainly with chinese medicinal perfusion/embolization].

OBJECTIVE: To study the clinical efficacy and adverse reaction of comprehensive therapy mainly with Chinese anti-cancer medicinal perfusion/embolization and assisted with Chinese drug-therapy based on TCM Syndrome Differentiation in treating primary liver cancer. METHODS: Forty-one patients with liver cancer were divided into the treated group and the control group. To the treated group turmeric oil microballoon, cinobufotalin, Aidi injection and iodized oil were given via hepatic artery perfusion/embolization, and to the control group chemotherapeutic agents and iodized oil were given for instead. Besides, both groups were given Chinese herbs according to TCM Syndrome Differentiation additionally. RESULTS: The tumor inhibitory rate in the treated group and the control group was 77.78% and 69.57% respectively, with insignificant difference between them. The improvement of fatigue and anorexia in the treated group was better than that in the control group (P < 0. 05). The 6-month, 12-month and 24-month survival rate in the treated group and control group was 61.11% vs 56.62%, 27.78% vs 30.43% and 22.22% vs 26.09%, respectively, the difference between the two groups was insignificant. The occurrence of adverse reactions such as decreasing of white blood cells, platelet and hemoglobin, nausea and vomiting were obviously lower in the treated group than those in the control group (P < 0.05). CONCLUSION: Chinese anti-cancer medicinal perfusion/embolization has affirmative short-term clinical effect in treating primary liver cancer with few adverse reactions, which was tolerable to patients, but its long-term clinical efficacy needs further observation.