Thymosinβ4 alleviates cholestatic liver fibrosis in mice through downregulating PDGF/PDGFR and TGFβ/Smad pathways.

Liver fibrosis is an important health problem without adequate and effective therapeutics. In this study, effects of thymosinβ4 (Tβ4) on hepatic fibrogenesis and the underlying molecular mechanisms were explored in bile duct ligation (BDL)-induced mice cholestatic liver fibrosis model. Results showed exogenous Tβ4 significantly reduced the mortality and liver/body weight ratio in BDL mice.

Inhibition of acetaminophen-induced hepatotoxicity in mice by exogenous thymosinβ4 treatment.

Objective: To study the effects of exogenous thymosinβ4 (Tβ4) treatment in acetaminophen (APAP)-induced hepatotoxicity.

Methods: Liver injury was induced in mice by a single intraperitoneal injection of APAP (500 mg/kg). Exogenous Tβ4 was intraperitoneally administrated at 0 h, 2 h and 4 h after APAP injection.

3-methyadenine attenuates chloroform-induced hepatotoxicity via autophagy activation.

Chloroform is a common contaminant in the drinking water. Exposure of human to chloroform leads to severe hepatotoxicity. In the present study, chloroform-induced acute liver injury was investigated in mice using 3-methyadenine (3-MA), a common autophagy inhibitor.

Effects of exogenous thymosin β4 on carbon tetrachloride-induced liver injury and fibrosis.

The present study investigated the effects of exogenous thymosin β4 (TB4) on carbon tetrachloride (CCl)-induced acute liver injury and fibrosis in rodent animals. Results showed that both in mice and rats CCl rendered significant increases in serum alanine aminotransferase and aspartate aminotransferase, hepatic malondialdehyde formation, decreases in antioxidants including superoxide dismutase and glutathione, and up-regulated expressions of transforming growth factor-β1, α-smooth muscle actin, tumor necrosis factor-α and interleukin-1β in the liver tissues. Hydroxyproline contents in the rat livers were increased by CCl.

Role of thioredoxin nitration in bleomycin-induced pulmonary fibrosis in rats.

Oxidant stimulation has been suggested to play an important role in the pathogenesis of idiopathic pulmonary fibrosis (IPF). Our study aimed to investigate the role and mechanisms of thioredoxin (Trx) nitration during the development of IPF. A rat model of IPF was established by intratracheal instillation of bleomycin (BLM).

Ginsenoside Rg3 sensitizes human non-small cell lung cancer cells to γ-radiation by targeting the nuclear factor-κB pathway.

At present, it is elusive how non-small cell lung cancer (NSCLC) develops resistance to γ-radiation; however, the transcription factor nuclear factor-κB (NF-κB) and NF-κB-regulated gene products have been proposed as mediators. Ginsenoside Rg3 is a steroidal saponin, which was isolated from Panax ginseng. Ginsenoside Rg3 possesses high pharmacological activity and has previously been shown to suppress NF-κB activation in various types of tumor cell.

Chlamydia pneumoniae infection induces vascular smooth muscle cell migration via Rac1 activation.

Chlamydia pneumoniae infection has been shown to be associated with the development of atherosclerosis by promoting the migration of vascular smooth muscle cells (VSMCs). However, how C. pneumoniae infection induces VSMC migration is not fully understood.

Chlamydophila (Chlamydia) pneumoniae infection promotes vascular smooth muscle cell adhesion and migration through IQ domain GTPase-activating protein 1.

The mechanisms for Chlamydophila (Chlamydia) pneumoniae (C. pneumoniae) infection-induced atherosclerosis are still unclear. Cell adhesion has important roles in vascular smooth muscle cell (VSMC) migration required in the development of atherosclerosis.

Choline autoradiography of human prostate cancer xenograft: effect of castration.

The purpose of this study was to investigate the effects of castration and tracer uptake time interval on the level of radiolabeled choline accumulation in murine-implanted human prostate tumor xenografts using quantitative autoradiography. We implanted androgen-dependent (CWR22) and androgen-independent (PC3) human prostate cancer cells in castrated (n = 9) and noncastrated (n = 9) athymic male mice and allowed tumors to grow to 1 cm3. The mice were euthanized at 5, 10, and 20 minutes after injection of 5 microCi [14C]-choline.

Recombinant thymosin beta 4 can promote full-thickness cutaneous wound healing.

Human thymosin beta 4 (TB4) is a small acidic peptide involved in angiogenesis, wound healing, cancer metastasis and cardiac repair. Currently human TB4 is synthesized chemically for research and this is costly. In order to obtain sufficient biologically active human TB4 economically, we cloned and overexpressed this protein in an Escherichia coli system.

Glucose metabolism of human prostate cancer mouse xenografts.

We hypothesized that the glucose metabolism of prostate cancer is modulated by androgen. We performed in vivo biodistribution and imaging studies of [F-18] fluorodeoxyglucose (FDG) accumulation in androgen-sensitive (CWR-22) and androgen-independent (PC-3) human prostate cancer xenografts implanted in castrated and noncastrated male athymic mice. The growth pattern of the CWR-22 tumor was best approximated by an exponential function (tumor size in mm3 = 14.

Progressive hearing loss in mice lacking the cyclin-dependent kinase inhibitor Ink4d.

Maintenance of the post-mitotic state in the post-natal mammalian brain is an active process that requires the cyclin-dependent kinase inhibitors (CKIs) p19Ink4d (Ink4d) and p27Kip1 (Kip1). In animals with targeted deletions of both Ink4d and Kip1, terminally differentiated, post-mitotic neurons are observed to re-enter the cell cycle, divide and undergo apoptosis. However, when either Ink4d or Kip1 alone are deleted, the post-mitotic state is maintained, suggesting a redundant role for these genes in mature neurons.

Establishment and characterization of a schwannoma cell line from a patient with neurofibromatosis 2.

By using retroviral mediated gene transfer technique, a primary schwannoma culture from a 56-year-old Neurofibromatosis type 2 (NF2) patient was immortalized with HPV E6-E7 genes. This cell line, HEI193, has a unique splice site mutation of the NF2 gene. Both immunocytochemistry and molecular biology techniques were used to demonstrate that this cell line is of Schwann cell origin.