Ginseng-derived panaxadiol ameliorates STZ-induced type 1 diabetes through inhibiting RORγ/IL-17A axis.

Retinoic-acid-receptor-related orphan receptor γ (RORγ) is a major transcription factor for proinflammatory IL-17A production. Here, we revealed that the RORγ deficiency protects mice from STZ-induced Type 1 diabetes (T1D) through inhibiting IL-17A production, leading to improved pancreatic islet β cell function, thereby uncovering a potential novel therapeutic target for treating T1D. We further identified a novel RORγ inverse agonist, ginseng-derived panaxadiol, which selectively inhibits RORγ transcriptional activity with a distinct cofactor recruitment profile from known RORγ ligands.

Efficacy of argon-helium cryosurgical ablation on primary hepatocellular carcinoma: a pilot clinical study.

Background And Objective: Recent years, great progression has been made in treating primary hepatocellular carcinoma (HCC) with argon-helium cryosurgical ablation. This study was to evaluate its efficacy on unresectable primary HCC.

Methods: A total of 124 primary HCC patients were divided into early stage, middle stage and advanced stage groups according to BCLC staging classification.

Synthesis of platelet-activating factor and its receptor expression in Kupffer cells in rat carbon tetrachloride-induced cirrhosis.

Aim: To determine the platelet-activating factor (PAF) synthesis and its receptor expression in Kupffer cells in rat carbon tetrachloride-induced cirrhosis.

Methods: Kupffer cells, isolated from the livers of control and CCl4-induced cirrhotic rats, were placed in serum-free medium overnight. PAF saturation binding, ET-1 saturation and competition binding were assayed.

Hepatic stellate cells may be potential effectors of platelet activating factor induced portal hypertension.

Aim: To determine platelet activating factor (PAF) receptor expression in cirrhotic hepatic stellate cells.

Methods: Hepatic stellate cells, isolated from the livers of control and CCl(4)-induced cirrhotic rats, were placed in serum-free medium after overnight culture. We determined the PAF receptor in hepatic stellate cells by saturation binding technique and semiquantitative reverse transcriptase polymerase chain reaction (RT-PCR), and the effects of PAF and its antagonist BN52021 on prostaglandin E(2) (PGE(2)) release by stellate cells.

Augmenter of liver regeneration promotes hepatocyte proliferation induced by Kupffer cells.

Aim: To observe the effects of augmenter of liver regeneration (ALR) on Kupffer cells and to determine whether ALR promotes hepatocyte proliferation induced by Kupffer cells.

Methods: Kupffer cells and hepatocytes were cultured in vitro and various concentrations of recombinant rat ALR (rrALR) were added. 3H-thymidine, BrdU and 3H-leucine incorporation was determined in cultured Kupffer cells and hepatocytes, in hepatocytes conditioned by Kupffer cells, and in associated medium.

Effect of increased hepatic platelet activating factor and its receptor portal hypertension in CCl4-induced liver cirrhosis.

Aim: To evaluate the changes in hepatic platelet activating factor (PAF) and its receptors and their effect on portal pressure of cirrhotic rats induced by CCl4.

Methods: A model of liver cirrhosis was replicated in rats by intra-peritoneal injection of CCl4 for 8 wk. We determined the effect of hepatic PAF and its receptor level on portal and arterial pressure by EIA, saturation binding and RT-PCR technique.

[Influence of platelet activating factor and its antagonist on portal hypertension associated with liver cirrhosis: an experiment with rats].

Objective: To investigate the influence of platelet activating factor (PAF) and its antagonist BN52021 on portal hypertension associated with liver cirrhosis.

Methods: Ten SD rats were injected intraperitoneally with carbon tetrachloride to establish a liver cirrhosis model and 10 rats were injected with olive oil as controls. The concentrations of PAF in the blood and liver was examined by rapid (3)H-PAF scintillation proximity assay and the hepatic PAF binding capacity was examined by receptor saturation binding technique.

Autologous cytokine-induced killer cell therapy in clinical trial phase I is safe in patients with primary hepatocellular carcinoma.

Aim: To investigate the influence of autologous cytokine-induced killer (CIK) cells on the phenotypes of CIK effector cells, peripheral T lymphocyte subsets and dendritic cell subsets in patients with primary hepatocellular carcinoma (HCC).

Methods: Peripheral blood mononuclear cells (PBMC) were collected by a blood cell separator from 13 patients with HCC, then expanded by priming them with interferon-gamma (IFN-gamma) followed by monoclonal antibody (mAb) against CD3 and interleukin-2 (IL-2) the next day. The phenotypic patterns of CIK cells were characterized by flow cytometry on d 0, 4, 7, 10, 13 and 15 of incubation, respectively.

[Identification of immunological effector cells after autologous cytokine-induced killer cells treatment and its clinical implication in hepatocellular carcinoma patients].

Objective: To investigate the alteration of the cellular profiles of T lymphocyte subsets and dendritic cell subsets in peripheral blood of primary hepatocellular carcinoma (HCC) patients after being transfused with autologous cytokine-induced killer cells (CIK) in patients, then to evaluate the clinical efficacy of the immune therapeutic strategy.

Methods: Peripheral blood mononuclear cells (PBMCs) from 13 patients with primary were collected using blood cell separator, and expanded in the fresh AIM-V medium in the presence of cytokine cocktail including interferon-gamma (IFN-gamma), monoclonal antibody (mAb) against CD3 and interleukin-2 (IL-2). The phenotypic patterns of CIK cells were longitudinally characterized by flow cytometry on day 0, 4, 7, 10,13 and 15 during the incubation period.