[Adjuvant function of guilu erxian glue cataplasm in treating carcinoma of the large intestine patients with myelosuppression after chemotherapy: a clinical observation].

OBJECTIVE: To observe the clinical effect of Guilu Erxian Glue Cataplasm (GEGC) on carcinoma of the large intestine patients with myelosuppression after chemotherapy, and further to confirm its efficiency and safety. METHODS: Totally 60 patients with carcinoma of the large intestine were randomly assigned to two groups. Meanwhile, they all accepted FOLFIRI chemotherapy. Patients in the treatment group were additionally applied at Shenque (RN8), exchanging once per every other day, for 14 successive days. Patients in the control group took placebos with the same dose and dosage as the treatment group. The blood cell counts (WBC, NE, and PLT) were detected before chemotherapy, at day 7, 10, and 14. The TCM symptoms integrals, Karnofsky performance score (KPS), liver and kidney functions were observed before chemotherapy, at day 7 and day 14. Adverse skin reactions were observed each day. And the usage of hematopoietic growth factors was recorded. RESULTS: (1) The KPS score at day 7 was more stable in the treatment group than in the control group; the WBC and NE counts in the peripheral blood at day 14 were higher in the treatment group than in the control group; and TCM symptoms integrals at day 14 was lower in the treatment group than in the control group, all with statistical difference (P < 0.05). (2) Compared with the control group, the PLT count was higher in the treatment group than in the control group, the usage of rhG-CSF and antibiotics was less in the treatment group than in the control group, all with no statistical difference (P > 0.05). (3) No obvious adverse reactions such as liver injury, renal injury, or skin allergy were observed. CONCLUSIONS: Adjuvant treatment of GEGC could improve carcinoma of the large intestine patients with myelosuppression to some extent. No relevant adverse reactions were found.

Ginsenoside compound K increases glucagon-like peptide-1 release and L-cell abundance in db/db mice through TGR5/YAP signaling.

BACKGROUND: Incretin impairment refers to L-cell-derived glucagon-like peptide-1 (GLP-1) deficiency, commonly observed in patients with type 2 diabetes mellitus (T2DM). Promoting the enteroendocrine L-cell population to elevate GLP-1 secretory capacity represents a potential therapeutic strategy for T2DM. It has been established that ginsenoside compound K (CK) could stimulate GLP-1 secretion; however, the underlying mechanisms remain elusive. METHODS: CK was intragastrically administered to male db/db mice for 4 weeks that subsequently underwent oral glucose tolerance testing. Serum samples were collected to measure the GLP-1 secretion, insulin level, inflammatory factors, and bile acid (BA) profiles. Ileum epithelial injury was detected by Hematoxylin and Eosin (H&E) and Masson staining. Gene markers associated with L-cell differentiation were evaluated by RT-PCR, and L-cells were labeled by Gcg via immunofluorescence assays. TGR5 and YAP expression was analyzed by immunoblotting and immunofluorescence assays. RESULTS: Compound K attenuated hyperglycemia and inflammation in db/db mice and upregulated TGR5 expression by increasing lithocholic acid (LCA) and deoxycholic acid (DCA) levels in response to ileum epithelium injury. Meanwhile, fibrosis was alleviated, and the crypt architecture was restored, with increased L-cell abundance and serum GLP-1 levels. The upregulation in genes associated with L-cell differentiation promoted transformation into L-cells. Further mechanistic analyses showed that the effects of CK on the L-cell population required YAP activation, which triggered actin cytoskeleton dynamics. CONCLUSIONS: Our results indicate that TGR5 could modulate the abundance of L-cells to enhance GLP-1 release through YAP-driven intestinal regeneration in db/db mice. Accordingly, CK has huge prospects for application to alleviate incretin impairment in T2DM.