Electroacupuncture-reduced sedative and analgesic requirements for diagnostic EUS: a prospective, randomized, double-blinded, sham-controlled study.

BACKGROUND AND AIMS: The role of electroacupuncture (EA) in reducing sedative and analgesic requirements during EUS is uncertain. The aim of this study was to investigate the efficacy of EA in reducing procedure-related pain and discomfort during EUS. METHODS: This was a double-blinded randomized controlled study conducted between March 2014 and July 2016. Consecutive patients who were scheduled for diagnostic EUS were recruited and randomized to receive EA or sham-electroacupuncture (SA). The primary outcome was the dosage of propofol used. Other outcome measurements included pain scores, anxiety scores, satisfaction scores, patients' willingness to repeat the procedure, total procedure time, and adverse events. RESULTS: A total of 128 patients were recruited to the study. The patients who received EA had significantly fewer requirements for patient-controlled sedation and analgesia (PCA). The median (interquartile range) number of demands for PCA (2 [1-5] vs 16.5 [8.5-33.8]; P < .001), the number of successful demands (2 [1-4] vs 9 [5.3-13]; P < .001), and the total dose of propofol (0.15 [0.08-0.34] vs 0.77 [0.38-1.09]; P < .001) and alfentanil (0.38 [0.20-0.86] vs 1.92 [0.94-2.72]; P < .001) were all significantly less. Patients who received EA also had significantly lower procedural pain scores and anxiety scores (P < .001), and higher satisfaction scores (P < .001), and they were more willing to repeat the procedure (P < .001). Being in the SA group and the procedure time were significant predictors of increased PCA demands (P < .001 and P = .009, respectively). CONCLUSIONS: In conclusion, the use of EA reduced sedative and analgesia demands, improved patient experience, and was associated with a low risk of adverse events during diagnostic EUS. (Clinical trial registration number: NCT02066194.).

Preparation of Galipea officinalis Hancock type tetrahydroquinoline alkaloid analogues as anti-tumour agents.

The preparation of chiral tetrahydroquinolines using Ir-catalysed asymmetric hydrogenation and their possible cytotoxic potential anti-cancer activity were reported. Both of the in vitro cytotoxicity assay on a series of human cancer cell lines including A549 small cell lung cancer, MDA-MB-231 breast cancer, SaoS2 sacroma, SKHep-1 hepatoma and Hep3B hepatocellular carcinoma as well as in vivo animal model using Hep3B hepatocellular tumour xenograft on athymic nude mice suggest that 1,2,3,4-tetrahydroquin-8-ol is a potential anti-tumour alkaloid which may be further developed as a novel cancer chemotherapeutic agent.

In vivo anti-tumour activity of corilagin on Hep3B hepatocellular carcinoma.

We have investigated the potential in vivo anti-tumour activity of corilagin using the Hep3B hepatocellular carcinoma cell line and an athymic nude mice xenograft model. The purity of corilagin was confirmed by high performance liquid chromatographic analysis. Corilagin was administrated intraperitoneally for a continuous period of 7 days at a concentration of 15 mg/kg of body weight per day. A significant inhibition of tumour growth was observed when treated mice are compared with control groups. Furthermore, analysis of enzymes markers of liver function, including alanine aminotransferase and asparate aminotransferase, suggested that current therapeutic dosage of corilagin did not exert adverse effect on liver. Our observations support the view that corilagin is considerably effective to retard the in vivo growth of xenografted Hep3B hepatocellular carcinoma.

Novel use of silymarin as delayed therapy for acetaminophen-induced acute hepatic injury.

AIM: Recently, we have demonstrated that silymarin has a comparable pharmaceutical activity as Phyllanthus urinaria extract when used to rescue mice from acetaminophen-induced acute liver injury. In the present study, we further compared the therapeutic action of silymarin with N-acetyl cysteine (commonly used in clinical practice for emergency treatments) as a rescuer in mice after administering a lethal dose of acetaminophen for 24 h. METHODS: Acute liver injury was induced in the treatment groups by intraperitoneally administered acetaminophen at a dose of 550 mg/kg body weight on day 1. The control group received an equal volume of physiological saline intraperitoneally. From day 2 to 4, the treatment groups received various doses of silymarin or N-acetyl cysteine orally once daily, while the control group and the acetaminophen group received an equal volume of water orally. The mortality rate was recorded in all groups. On day 5, all mice were sacrificed for examination. RESULTS: Silymarin greatly improved the counteracting effects on mortality rate as compared to N-acetyl cysteine. CONCLUSION: Silymarin should be further considered as an antidote for patients with acetaminopheninduced acute hepatic injury and delayed treatment.

Phyllanthus urinaria extract attenuates acetaminophen induced hepatotoxicity: involvement of cytochrome P450 CYP2E1.

Acetaminophen is a commonly used drug for the treatment of patients with common cold and influenza. However, an overdose of acetaminophen may be fatal. In this study we investigated whether mice, administered intraperitoneally with a lethal dose of acetaminophen, when followed by oral administration of Phyllanthus urinaria extract, may be prevented from death. Histopathological analysis of mouse liver sections showed that Phyllanthus urinaria extract may protect the hepatocytes from acetaminophen-induced necrosis. Therapeutic dose of Phyllanthus urinaria extract did not show any toxicological phenomenon on mice. Immunohistochemical staining with the cytochrome P450 CYP2E1 antibody revealed that Phyllanthus urinaria extract reduced the cytochrome P450 CYP2E1 protein level in mice pre-treated with a lethal dose of acetaminophen. Phyllanthus urinaria extract also inhibited the cytochrome P450 CYP2E1 enzymatic activity in vitro. Heavy metals, including arsenic, cadmium, mercury and lead, as well as herbicide residues were not found above their detection limits. High performance liquid chromatography identified corilagin and gallic acid as the major components of the Phyllanthus urinaria extract. We conclude that Phyllanthus urinaria extract is effective in attenuating the acetaminophen induced hepatotoxicity, and inhibition of cytochrome P450 CYP2E1 enzyme may be an important factor for its therapeutic mechanism.

Activities of fresh juice of Scutellaria barbata and warmed water extract of Radix Sophorae Tonkinensis on anti-proliferation and apoptosis of human cancer cell lines.

The possible antiproliferative and apoptotic inducing potentials of fresh juice prepared from Scutellaria barbata (SBJ) and warmed water extract of Radix Sophorae Tonkinensis (RSTE) have been tested on a series of cancer cell lines, including HepG2 hepatoblastoma, Hep3B hepatocellular carcinoma, MDA-MB231 breast carcinoma, A549 lung cancer and KG-1 acute myelogenous leukaemia in vitro. Both SBJ and RSTE were able to inhibit the growth of cancer cell lines and induce apoptosis. Further analysis of the action of RSTE on HepG2 cells suggested that the activity of the central machinery of apoptosis, caspase 3, was significantly elevated. Oligo-nucleosomal length DNA fragments formation was readily detected by TdT-mediated dUTP nick end labelling assay after RSTE treatment. Taken together, we believe that, although Radix Sophorae Tonkinensis was demonstrated to have toxic components including matrine and oxymatrine, it is still worthwhile to further investigate its anti-cancer potential under a safety toxicological precaution.

Anti-angiogenic potential of Gleditsia sinensis fruit extract.

Blood supply plays a crucial role in solid tumour development and leukaemogenesis. It has been suggested that blocking of angiogenesis could be possible in cancer therapy. We have demonstrated the antiproliferative activity of Gleditsia sinensis fruit extract (GSE) on various human solid tumour cancer cell lines as well as leukaemia cell lines and primary cultured leukaemia cells obtained from leukaemia patients. However, the antiangiogenic potential of GSE has not been demonstrated. Here we demonstrated that GSE could reduce vascular endothelial growth factor (VEGF) mRNA expression in dose- and time course-dependently in MDA-MB231 breast cancer and HepG2 hepatoblastoma cell lines as measured by reverse transcriptase polymerase chain reaction. Enzyme-linked immunosorbent assay further showed that GSE could reduce the VEGF secretion from various cancer cell lines including MDA-MB231, HepG2, HL-60 (acute promyelocytic leukaemia) and eleven primary cultured leukaemia cells obtained from acute myelogenous leukaemia patients. In vivo chick chorioallantoic membrane assay illustrated that GSE could reduce the angiogenic activity of basic fibroblast growth factor. Taken together, the information suggested that GSE could be potentially used as an angiogenic inhibitor in both solid tumour and leukaemia therapy.