Use of Chinese herbal medicine therapies in comprehensive hospitals in central China: A parallel survey in cancer patients and clinicians.

Chinese herbal medicine (CHM), as the largest application category of traditional Chinese medicine (TCM), is widely accepted among cancer patients in China. Herbal slice (HS) and Chinese patent drug (CPD) are commonly used CHM in China. This study aimed to investigate the utilization of CHM among clinicians and cancer patients in central China. Five hundred and twenty-five patients and 165 clinicians in 35 comprehensive hospitals in central China were asked to complete an anonymous questionnaire that was designed to evaluate the use of CHM. The results showed that 90.74% clinicians and 72.24% cancer patients used CHM during cancer treatment. The educational backgrounds of the clinicians and the age, education level, annual income, and cancer stage of the cancer patients were related to use of CHM. More than 90% clinicians and cancer patients had used CPD. Comparatively, the percentage of HS use was 10% lower than that of CPD use among clinicians and cancer patients. More clinicians preferred to use CHM after surgery than cancer patients did (20.41% vs. 5.37%). Enhancing physical fitness and improving performance status were regarded as the most potential effect of CHM on cancer treatment (85.71% among clinicians and 94.07% among cancer patients), in comparison with directly killing tumor cells (24.49% among clinicians and 31.36% among patients). As for refusal reasons, imprecise efficacy was the unanimous (100%) reason for clinicians' rejection of CHM, and 95.58% patients objected to using CHM also for this reason. Furthermore, the side effects of CHM were more concerned by clinicians than by patients (33.33% vs. 15.81%). In conclusion, our survey revealed that CHM was popularly accepted by clinicians and cancer patients in central China. The reasons of use and rejection of CHM were different between clinicians and cancer patients.

Emodin regulating excision repair cross-complementation group 1 through fibroblast growth factor receptor 2 signaling.

AIM: To investigate the molecular mechanisms underlying the reversal effect of emodin on platinum resistance in hepatocellular carcinoma. METHODS: After the addition of 10 µmol/L emodin to HepG2/oxaliplatin (OXA) cells, the inhibition rate (IR), 50% inhibitory concentration (IC50) and reversal index (IC50 in experimental group/IC50 in control group) were calculated. For HepG2, HepG2/OXA, HepG2/OXA/T, each cell line was divided into a control group, OXA group, OXA + fibroblast growth factor 7 (FGF7) group and OXA + emodin group, and the final concentrations of FGF7, emodin and OXA in each group were 5 ng/mL, 10 µg/mL and 10 µmol/L, respectively. Single-cell gel electrophoresis was conducted to detect DNA damage, and the fibroblast growth factor receptor 2 (FGFR2), phosphorylated extracellular signal-regulated kinase 1/2 (p-ERK1/2) and excision repair cross-complementing gene 1 (ERCC1) protein expression levels in each group were examined by Western blotting. RESULTS: Compared with the IC50 of 120.78 µmol/L in HepG2/OXA cells, the IC50 decreased to 39.65 µmol/L after treatment with 10 µmol/L emodin; thus, the reversal index was 3.05. Compared with the control group, the tail length and Olive tail length in the OXA group, OXA + FGF7 group and OXA + emodin group were significantly increased, and the differences were statistically significant (P < 0.01). The tail length and Olive tail length were lower in the OXA + FGF7 group than in the OXA group, and this difference was also statistically significant. Compared with the OXA + FGF7 group, the tail extent, the Olive tail moment and the percentage of tail DNA were significantly increased in the OXA + emodin group, and these differences were statistically significant (P < 0.01). In comparison with its parental cell line HepG2, the HepG2/OXA cells demonstrated significantly increased FGFR2, p-ERK1/2 and ERCC1 expression levels, whereas the expression of all three molecules was significantly inhibited in HepG2/OXA/T cells, in which FGFR2 was silenced by FGFR2 shRNA. In the examined HepG2 cells, the FGFR2, p-ERK1/2 and ERCC1 expression levels demonstrated increasing trends in the OXA group and OXA + FGF7 group. Compared with the OXA group and OXA + FGF7 group, the FGFR2, p-ERK1/2, and ERCC1 expression levels were significantly lower in the OXA + emodin group, and these differences were statistically significant. In the HepG2/OXA/T cell line that was transfected with FGFR2 shRNA, the FGFR2, p-ERK1/2 and ERCC1 expression levels were significantly inhibited, but there were no significant differences in these expression levels among the OXA, OXA + FGF7 and OXA + emodin groups. CONCLUSION: Emodin markedly reversed OXA resistance by enhancing OXA DNA damage in HepG2/OXA cells, and the molecular mechanism was related to the inhibitory effect on ERCC1 expression being mediated by the FGFR2/ERK1/2 signaling pathway.