Hepatocellular carcinoma (HCC) is the second leading cause of disease-related death in China and greatly threatens the health of residents. Recent studies have shown that traditional Chinese medicine plays an important role in the comprehensive treatment of HCC. Huaier granules have been recommended for the treatment of HCC, and its mechanism of action includes inhibiting angiogenesis, inhibiting the proliferation of HCC cells, inhibiting invasion and metastasis, inducing cell apoptosis, and regulating immune function. This article summarizes the research advances in the anti-HCC mechanism of Huaier granules and its application in clinical practice, in order to provide a reference for subsequent research and clinical treatment.

ObjectiveTo investigate the protective effect of microRNA-155 (miR-155) antisense oligonucleotid (ASO) on acute lung injury (ALI) mice by establishing a lentiviral expression vector of ASO of miRNA.Methods miR-155 antisense oligonucleotides amplified by polymerase chain reaction (PCR) from genomic, using BamH Ⅰ and Nhe Ⅰ double digestion, ligated into lentiviral expression vector. Sequence and virus titer were measured. According to the random number table method, 54 male BALB/c mice of 4-6 weeks old were divided into three groups. ALI animal models were prepared by intraperitoneal injection of 10 mg/kg lipopolysaccharide (LPS). The three groups were injected with 200μL phosphate buffered saline (PBS) containing 1×108/mL pmiR-155-ASO virus (pmiR-155-ASO group) or 200μL PBS containing 1×108/mL pSMPUW-miR-GFP empty virus (pmiR-cont group) or the same amount of PBS (PBS group) at 24 hours before the molding. Ten mice in each group were used to observe the 7-day survival rate. Blood samples and lung tissues of the remaining 8 mice were harvested after the model was established, and the levels of serum inflammatory cytokines were determined by enzyme linked immunosorbent assay (ELISA); the expression of miR-155 in lung tissue was detected by real-time reverse transcription-polymerase chain reaction (RT-PCR); histopathological changes of lung and distribution of macrophages were observed under microscope.Results There was no significant difference in each index between pmiR-cont group and PBS group. The mature miR-155 expression in lung tissue in pmiR-155-ASO group was significantly lower than that in pmiR-cont group (2-ΔΔCt: 4.92±0.72 vs. 15.38±0.60,P < 0.05). Compared with pmiR-cont group, the injury degree of ALI mice after pretreatment with miR-155ASO was significantly improved, and the 7-day survival rate was significantly increased (72.1％ vs. 61.9％,P < 0.05 ); gross lung observation showed that congestion in lung tissue was significantly reduced, and the ratio of wet/dry weight (W/D) of lung was significantly decreased (4.50±0.13 vs. 5.64±0.61,P < 0.05);hematoxylin-eosin (HE) staining showed that inflammatory cell infiltration in lung tissue was decreased, while immunofluorescence assay showed that macrophage infiltration in lung tissue was significant decreased; the levels of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL- 6) in serum were significantly decreased [TNF-α (ng/L):379.8±48.9 vs. 495.9±33.3, IL-6 (ng/L): 262.3±61.8 vs. 355.4±22.6, bothP < 0.05], but the level of IL-10 did not change significantly (ng/L: 143.6±32.5 vs. 140.4±22.3,P > 0.05).Conclusion miR-155 ASO has the effect of inhibiting LPS-induced inflammatory response and improving prognosis in ALI mice.

AIM: To explore the effect of ethanol extract of costusroot (EEC) on gastric mucosa in gastric ulcer rats and related mechanism. METHODS: The rats were randomly divided into 5 groups: normal group, model group, sucralfate group, low-EEC group and high-EEC group, and anhydrous alcohol was administrated intragastrically to replicate gastric ulcer model in groups other than the normal. Changes in the area of gastric ulcer were observed and the inhibition rate of ulcer was calculated. The pathological changes of gastric tissue were measured by HE staining, and the protein expression levels of Bax and Bcl-2 were tested by immunohistochemistry and Western blot. RESULTS: EEC inhibited the formation of ulcer area in model rats and alleviated the histopathological damage to the stomach caused by ethanol. While enhancing the expression of Bcl-2 protein (P<0.01), it effectively inhibited the overexpression of Bax (P<0.01). CONCLUSION: EEC has a strong function of anti-gastric ulcers, and its mechanism of action might be related to the regulation of the protein expression level of Bax and Bcl-2 to inhibit the apoptosis of gastri mucosal cells.