OBJECTIVES: To explore the clinical effect of electroacupuncture (EA) on promoting gastrointestinal function recovery in patients undergoing laparoscopic gastrectomy. METHODS: One hundred and twenty patients undergoing laparoscopic gastrectomy were randomly divided into an EA group (40 cases, 1 case was eliminated), a placebo EA (PEA) group (40 cases, 1 case dropped out) and a conventional treatment group (40 cases, 1 case dropped out). The patients in the conventional treatment group received perioperative routine treatment. On the basis of routine treatment, patients in the EA group and the PEA group were given electroacupuncture or placebo electroacupuncture stimulation at 24,48 and 72 h after anesthesia recovery. Bilateral Neiguan (PC 6), Zusanli (ST 36) and Shangjuxu (ST 37) were selected, and the electrodes of SDV-Z electroacupuncture instrument were connected to Zusanli (ST 36) and Shangjuxu (ST 37) on the same side respectively. Continuous wave was selected, the frequency was 5 Hz, and the needles were retained for 30 min each time. The postoperative gastrointestinal-2 ( GI-2 ) time, the incidence of grade A/B delayed gastric emptying were compared among the three groups, and the safety of acupuncture was evaluated. RESULTS: The GI-2 time of the EA group was significantly shorter than that of the PEA group and the conventional treatment group (P<0.05). The incidence of grade A and grade B of delayed gastric emptying in the EA group was lower than that in the PEA group and the conventional treatment group (P<0.05). No acupuncture-related adverse reactions occurred. CONCLUSIONS: EA can promote the recovery of gastrointestinal function in patients undergoing laparoscopic gastrectomy, and the treatment plan is safe, which is worthy of promotion and application into the enhanced recovery surgery program.
Electroacupuncture , Gastrectomy , Humans , Acupuncture Points , Electroacupuncture/adverse effects , Gastroparesis/etiology , Laparoscopy , Recovery of Function
Severe acute pancreatitis (SAP) onset and development are closely associated with intestinal barrier injury. Evidence from clinical practice and research has shown that electroacupuncture (EA) at the Zusanli (ST36) acupoint can improve intestinal barrier function and abdominal symptoms in patients with SAP; however, the specific mechanisms of action remain unclear. This study aimed to observe the changes in the intestinal microbiota and metabolites in SAP rats and to explore the effect of EA at ST36 on intestinal barrier injury in SAP rats. 16S rRNA gene sequencing combined with microbial diversity analysis, short-chain fatty acids (SCFAs)-targeted metabolomics, immunohistochemistry, immunofluorescence, western blotting, and other techniques were used to explore the mechanism of EA at bilateral ST36 acupoints on SAP-related intestinal barrier injury. Our results showed that EA at ST36 could repair intestinal barrier injury by modulating intestinal microecology, thereby reducing intestinal inflammation, restoring intestinal function, and ultimately alleviating the prognosis of SAP. Our study provides new insights into the mechanisms and treatment of intestinal barrier injury in patients with SAP from the perspectives of microbiota and SCFAs regulation.
Electroacupuncture , Pancreatitis , Humans , Animals , Rats , Acute Disease , RNA, Ribosomal, 16S/genetics , Pancreatitis/therapy , Intestines
Increasing evidence has shown that THZ1, a covalent cyclin-dependent kinase 7 (CDK7) inhibitor, exhibits therapeutic effects in various tumors. However, the possible effect of THZ1 on hepatocellular carcinoma (HCC) remains unknown. Our study was to investigate the roles of THZ1 in HCC cells and in subcutaneous HCC model and illustrate the molecular mechanisms. The phosphorylation levels of Ser2, Ser5, and Ser7 within RNA polymerase II (RNAPII) C-terminal domain (CTD) and the expression levels of Ki67, Mcl-1, survivin, XIAP, and p53 in HCC cells under different conditions were examined by Western blot analysis. Cell growth and apoptosis were assessed via 3-(4,5-dimethylthiazolyl-2)-2, 5-diphenyltetrazolium bromide (MTT) assay and flow cytometry analysis, respectively. Tumor volume was assessed in HCC mice with THZ1 or vehicle treatment and immunohistochemical (IHC) analysis was conducted on excised tumors. THZ1 significantly inhibited the phosphorylation of Ser2, Ser5, and Ser7 within RNAPII-CTD in the dose-dependent and irreversible manner. MTT assay and flow cytometry analysis showed that THZ1 inhibited HCC cell proliferation and induced apoptosis, respectively. Western blot analysis indicated THZ1 significantly upregulated p53 expression and downregulated the expressions of Mcl-1, survivin, XIAP, and Ki67. THZ1 suppressed tumor growth in Hep3B xenografted mice in a time-dependent manner. IHC analysis indicated that tumors in THZ1 group had less Ki67+ cells and more cleaved caspase-3+ cells than those in vehicle group. THZ1 exhibited anti-HCC effects through irreversibly inhibiting CDK7 activity, decreasing RNAPII-CTD phosphorylation, inducing p53 expression and inhibiting antiapoptotic gene expressions, which subsequently induced apoptosis and inhibited proliferation of HCC cells.
Carcinoma, Hepatocellular/drug therapy , Cyclin-Dependent Kinases/antagonists & inhibitors , Liver Neoplasms/drug therapy , Phenylenediamines/pharmacology , Protein Kinase Inhibitors/pharmacology , Pyrimidines/pharmacology , Animals , Antineoplastic Agents/pharmacology , Apoptosis/drug effects , Carcinoma, Hepatocellular/metabolism , Carcinoma, Hepatocellular/pathology , Cell Line, Tumor , Cell Proliferation/drug effects , Humans , Liver Neoplasms/metabolism , Liver Neoplasms/pathology , Male , Mice, Nude , Myeloid Cell Leukemia Sequence 1 Protein/metabolism , Survivin/metabolism , Tumor Suppressor Protein p53/metabolism , X-Linked Inhibitor of Apoptosis Protein/metabolism , Xenograft Model Antitumor Assays , Cyclin-Dependent Kinase-Activating Kinase
The case we presented here was a 73-year-old gentleman, who was admitted to endocrinology department due to recurrent fatigue for 1 year. He had medical histories of type 2 diabetes for 18 years and developed CKD 4 years ago. He also suffered from dilated cardiomyopathy, and coronary heart disease, moderate sleep apnea syndrome, primary hypothyroidism, and gout. His treatment regimen was complicated which included Caltrate D and compound α-keto acid (1200 mg calcium/d). Laboratory examination revealed that his serum calcium level elevated, 24-hour urine calcium output decreased, PTH level was suppressed, and 25-hydroxyvitamin D was in normal low range. No other specific abnormalities were found in serum bone turnover markers, ultrasonography, computed tomography, and bone scintigraphy. The diagnosis was suggested to be hypocalciuric hypercalcemia but was different from familial or acquired hypocalciuric hypercalcemia which were featured by elevated PTH level. The patient was asked to restrict calcium intake and to take diuretics; then his serum calcium level gradually lowered. In brief, patients with CKD could present with hypocalciuric hypercalcemia due to impaired renal calcium excretion. In this case, calcium restriction should be applied for treatment.
