Anti-inflammation treatment for protection of hepatocytes and amelioration of hepatic fibrosis in rats.

Chronic inflammation is considered as an important pathophysiologic mechanism of hepatic cirrhosis, which induces hepatocyte injury and activates hepatic stellate cells (HSCs), thus resulting in hepatic fibrosis. Previous studies have reported that cyclooxygenase-2 (COX-2) inhibitor can effectively treat liver fibrosis, while somatostatin (SST) analogues inhibit the activation of HSCs. The present study aimed to investigate the effects of a COX-2 inhibitor, celecoxib, combined with a SST analogue, octreotide, for protection of hepatocytes and prevention of fibrosis in a rat model of hepatic fibrosis.

Cyclooxygenase-2 up-regulates hepatic somatostatin receptor 2 expression.

Somatostatin and its analogues, which function by binding to somatostatin receptors (SSTRs) 1-5, play a protective role in liver cirrhosis. Hepatic SSTR-2 expression is up-regulated in subjects with liver cirrhosis. However, little is known about the mechanisms underlying this process.

Morphological and molecular variations induce mitochondrial dysfunction as a possible underlying mechanism of athletic amenorrhea.

Female athletes may experience difficulties in achieving pregnancy due to athletic amenorrhea (AA); however, the underlying mechanisms of AA remain unknown. The present study focuses on the mitochondrial alteration and its function in detecting the possible mechanism of AA. An AA rat model was established by excessive swimming.

Correlations between VEGF-A expression and prognosis in patients with gastric adenocarcinoma.

Angiogenesis induced by vascular endothelial growth factor A (VEGF-A) plays a critical role in tumor growth and metastasis. The study aimed to evaluate the expression of VEGF-A in gastric adenocarcinoma and investigate its correlations with tumor clinicopathological features and prognostic significance. VEGF-A expression was detected by immunohistochemistry on a tissue microarray containing 90 pairs of human gastric adenocarcinoma and paracancerous tissues.

Expression of cyclooxygenase-2 is correlated with lncRNA-COX-2 in cirrhotic mice induced by carbon tetrachloride.

Multiple long non-coding RNAs (lncRNAs) have been demonstrated to be involved in liver disease. Increased cyclooxygenase-2 (COX‑2) levels have also been reported to be involved in the progression of liver cirrhosis. In the present study, the correlations between lncRNA‑COX‑2 RNA expression levels, COX‑2 mRNA expression levels and liver fibrosis were examined.

Collapsed Reticular Network and its Possible Mechanism during the Initiation and/or Progression of Hepatic Fibrosis.

Among the researches on hepatic fibrosis, great attention was paid to both hepatocytes and extracellular matrix (ECM). However, little focus was drawn on reticular fibrous network, which is important for demarcation and support of hepatocytes. The aim of this study was to investigate the change pattern of reticular fibers in hepatic fibrosis/cirrhosis and its underlying mechanism.

Celecoxib and octreotide synergistically ameliorate portal hypertension via inhibition of angiogenesis in cirrhotic rats.

Abnormal angiogenesis is critical for portal hypertension in cirrhosis. Except for etiological treatment, no efficient medication or regime has been explored to treat the early stage of cirrhosis when angiogenesis is initiated or overwhelming. In this study, we explored an anti-angiogenesis effort through non-cytotoxic drugs octreotide and celecoxib to treat early stage of cirrhotic portal hypertension in an animal model.

Inhibition of cyclooxygenase-2 alleviates liver cirrhosis via improvement of the dysfunctional gut-liver axis in rats.

Inflammatory transport through the gut-liver axis may facilitate liver cirrhosis. Cyclooxygenase-2 (COX-2) has been considered as one of the important molecules that regulates intestinal epithelial barrier function. This study was aimed to test the hypothesis that inhibition of COX-2 by celecoxib might alleviate liver cirrhosis via reduction of intestinal inflammatory transport in thiacetamide (TAA) rat model.

Targeting inhibition of extracellular signal-regulated kinase kinase pathway with AZD6244 (ARRY-142886) suppresses growth and angiogenesis of gastric cancer.

AZD6244 (ARRY-142886), a highly selective MAPK-ERK kinase inhibitor, has shown excellent clinical efficacy in many tumors. However, the anti-tumor and anti-angiogenesis efficacy of AZD6244 on gastric cancer has not been well characterized. In this study, high p-ERK expression was associated with advanced TNM stage, increased lymphovascular invasion and poor survival.

Celecoxib attenuates hepatic cirrhosis through inhibition of epithelial-to-mesenchymal transition of hepatocytes.

Background And Aim: The epithelial-mesenchymal transition (EMT) of hepatocytes is a key step for hepatic fibrosis and cirrhosis. Long-term administration of celecoxib, a selective cyclooxygenase-2 (COX-2) inhibitor, can ameliorate hepatic fibrosis. This research aimed to examine the effect of celecoxib on the EMT of hepatocytes during the development of liver cirrhosis.

Decreased copy number of mitochondrial DNA: A potential diagnostic criterion for gastric cancer.

An alteration in the mitochondrial DNA (mtDNA) copy number has been detected in numerous human cancers. However, certain changes in the mtDNA copy number that occur during the initiation and progression of gastric cancer remain undetected. In the present study, using quantitative PCR analysis, the quantitative changes in mtDNA were observed during the initiation and progression of gastric cancer.

Celecoxib ameliorates portal hypertension of the cirrhotic rats through the dual inhibitory effects on the intrahepatic fibrosis and angiogenesis.

Background: Increased intra-hepatic resistance to portal blood flow is the primary factor leading to portal hypertension in cirrhosis. Up-regulated expression of cyclooxygenase-2 (COX-2) in the cirrhotic liver might be a potential target to ameliorate portal hypertension.

Objective: To verify the effect of celecoxib, a selective inhibitor of COX-2, on portal hypertension and the mechanisms behind it.

Octreotide and celecoxib synergistically encapsulate VX2 hepatic allografts following transcatheter arterial embolisation.

To evaluate the encapsulation of VX2 hepatic allografts in rabbits induced by octreotide and celecoxib administration following transcatheter arterial embolisation (TAE), rabbits with hepatic VX2 allografts were divided into four groups: control, TAE, octreotide + celecoxib (O+C) and the multimodality therapy (TAE+O+C). Allograft metastasis, capsule thickness and percentage of clear cells were measured and vascular endothelial growth factor (VEGF) and CD31 were detected by immunohistochemistry and reverse transcription-polymerase chain reaction (RT-PCR) analysis. The extrahepatic metastases of each intervention group were significantly fewer than those of the control group, with the TAE+O+C group exhibiting the fewest extrahepatic metastases.

Transcatheter arterial embolization followed by octreotide and celecoxib synergistically prolongs survival of rabbits with hepatic VX2 allografts.

Objective: To validate the efficacy of an innovative multimodality therapy with transcatheter arterial embolization (TAE) plus octreotide and celecoxib in reducing neoangiogenesis and prolonging the survival of rabbits with hepatocellular carcinoma.

Methods: Rabbits with hepatic VX2 allografts were divided into four groups: control group, TAE group, octreotide + celecoxib (O + C) group and the multimodality therapy (TAE + O + C) group. Survival of the rabbits was analyzed using the Kaplan-Meier method and the expression of CD31 in tumor tissues was detected by immunohistochemistry.