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Xie W.,Guangxi Medical University | Fang L.,Central Hospital of Hengyang | Liang A.,Guangxi Medical University | Lu Y.,Guangxi Medical University | And 9 more authors.
Chinese Journal of Clinical Oncology | Year: 2012

Objective: This study aims to investigate the expression of excision repair cross complementing 1 ( ERCCl ) of hepatocellular carcinoma ( HCC ) and its clinical significance. Methods: The ERCCl expression status of 226 patients with HCC, 65 with paraneoplastic tissue, and 17 with normal liver tissues was detected using immunohistochemistry. The correlation between ERCCl expression and major clinico-pathological characteristics and prognosis factors of HCC was analyzed. Results: The positive expression rate of ERCCl in HCC was 44.2% ( 100 / 226 ), which was significantly higher compared with the paraneoplastic and non-cancer liver tissues ( 16.9% and 5.9%, respectively, all P < 0.05 ). The positive rate of ERCCl in HCC cases with portal vein invasion was significantly higher compared with those without portal vein invasion ( 66.7% vs. 42.3%, P < 0.05 ). Meanwhile, the expression of ERCCl was not significantly associated with age and other clinical characteristics ( P > 0.05, respectively ). In the HCC group treated with radical resection ( 184 patients), the positive rate of ERCCl noticeably decreased when the median time to recurrence or metastasis ( TTR/M ) became longer. The group with positive expression of ERCCl exhibited a shorter TTR/M compared with the group with negative expression ( 10.3 m vs. 20.3 m, P < 0.05 ). The Cox regression model analysis showed that the preoperative serum levels of aspartate amionotransferase ≥ 2.5 N, tumor size ≥ 5 cm, and the positive expression of ERCCl were the independent risk factors of recurrence or metastasis of HCC. Conclusion: ERCCl expression was obviously higher in HCC than in the paraneoplastic and normal liver tissues, respectively. The overexpression of ERCCl was significantly correlated with the portal vein invasion and the risk of recurrence or metastasis of HCC after radical resection. Source

Cui L.-B.,University of South China | Yu X.-H.,University of South China | Jiang C.-H.,Central Hospital of Hengyang | Tang Y.-L.,University of South China | And 6 more authors.
Progress in Biochemistry and Biophysics | Year: 2015

Probucol is a potent hypolipidemic drug that decreases plasma high-density lipoprotein cholesterol (HDL-C) levels but attenuates atherosclerosis. However, the detailed mechanisms are not fully understood. The aim of this study was to explore the molecular mechanisms of the HDL-C-lowering and antiatherogenic effects of probucol. New Zealand white rabbits were randomly divided into normal diet group, normal diet+probucol group, high fat diet (HFD) group and HFD+probucol (HFD+P) group. After 7 weeks of treatments, the extent of the atherosclerotic lesions, hepatic lipid accumulation and plasma levels of triglycerides, total cholesterol, low-density lipoprotein cholesterol and HDL-C were significantly reduced in HFD+P group as compared to HFD group. Probucol effectively inhibited down-regulation of hepatic scavenger receptor class B type I (SR-B I) expression, and ATP-binding cassette (ABC) transporters G5 (ABCG5) and G8 (ABCG8) expression in the liver and small intestine induced by HFD but further promoted HFD-induced reduction in hepatic ABC transporter A1 (ABCA1) expression. In addition, probucol also significantly prevented HFD-induced increases of tumor necrosis factor-α, interleukin-1, interleukin-6 and monocyte chemotactic protein-1 levels in the aortic arch and plasma. Thus, our data provide strong evidence that probucol alleviates atherosclerosis through regulating ABCA1, SR-B I, ABCG5 and ABCG8 expression and inhibiting the secretion of proinflammatory cytokines in hypercholesterolemic rabbits. Source

Zhao G.-J.,Guilin Medical University | Yu S.-Y.,University of South China | Liu Y.,University of South China | Tang Y.-H.,Central Hospital of Hengyang | And 5 more authors.
Progress in Biochemistry and Biophysics | Year: 2015

In order to investigate the roles and mechanisms of liver X receptor alpha (LXRα)-ATP binding cassette transporter A1 (ABCA1) pathway in Chlamydia pneumoniae (C. pneumoniae) infection induced macrophage lipid accumulation. THP-1 macrophage derived foam cells were used as the cell model. Cellular cholesterol was determined by high performance liquid chromatography analysis. Cholesterol efflux was determined by liquid scintillator. ABCA1 and LXRα mRNA expression was detected by RT-PCR and protein expression was detected by Western blot. Furthermore, we pretreated the cells with LXRα specific agonist T0901317, and then observed the changes of indexes mentioned above. The result showed that C. pneumoniae infection could increase the content of total cholesterol, free cholesterol and cholesterol ester, inhibit the efflux of cholesterol from cells, and reduce the expression of ABCA1 and LXRα. The suppression of C. pneumoniae infection on ABCA1 expression was significantly attenuated after the use of ABCA1 agonist 8-Br-cAMP or LXR agonist T0901317, correspondingly, cholesterol efflux was promoted and the content of intracellular cholesterol was elevated. These results suggested that the mechanism of C. pneumoniae infection promoting lipid accumulation in macrophages and suppresses cholesterol efflux may be related to LXRα-ABCA1 pathway. Source

Liang X.,Guangdong Academy of Medical science | Chen Y.,Guangdong Academy of Medical science | Zhang L.,Guangdong Academy of Medical science | Jiang F.,Central Hospital of Hengyang | And 5 more authors.
Molecular Medicine Reports | Year: 2014

Acute kidney injury (AKI) induced by renal ischemia is a common clinical problem associated with a high morbidity and mortality. The present study investigated whether necroptosis was present in an in vitro renal ischemia model and whether the addition of necrostatin-1 (Nec-1) has a protective effect. In addition, whether autophagy was inhibited following the use of Nec-1 was also examined. When apoptosis was inhibited by z-VAD-fmk and energy was depleted with antimycin A for 1 h, the morphological abnormalities of human proximal tubular epithelial (HK-2) cells were markedly attenuated, and the cell viability was significantly improved following incubation with Nec-1. LC3-II/I ratios and LC3-II/GAPDH ratios demonstrated a statistically significant decrease in the Nec-1 + tumor necrosis factor (TNF)-α + z-VAD-fmk + antimycin A (1 h) group compared with the control group. In conclusion, the present study suggested that necroptosis was present in HK-2 cells subjected to TNF-α stimulation and energy depletion. Nec-1 inhibits a caspase-independent necroptotic pathway involving autophagy and may have therapeutic potential to prevent and treat renal ischemic injury. Source

Qiao F.,Central Hospital of Hengyang | Liu Y.-X.,Nanhua University | Liu J.-H.,Guangxi Medical University | Jiang L.-P.,Central Hospital of Hengyang | Cheng Y.-C.,Central Hospital of Hengyang
International Journal of Ophthalmology | Year: 2010

• AIM: To observe the protective effect of EGb761 on retinal ganglion cells (RGC) in rabbits with optic nerve crush injury by myelin basic protein (MBP) in rabbits' retina. • METHODS: Twenty-four rabbits were divided into experimental (right eye) and control (left eye) groups. The rabbits' optic nerves were crushed by mini-vascular nip. EGb761 60mg/kg were injected into the retrobulbar of right eye and the same volume balanced saline solution (BSS) were injected into the retrobulbar of left eye. 4, 7 and 14 days after injury, the number of the RGC was counted by image analysis system, and the immunohisto-chemical staining of the MBP was observed. • RESULTS: Three to fourteen days after injury, the number of RGC in the experimental group and control group were lower than that in normal by microscope. The differences were significant (P < 0.01); the number of RGC in experimental group was higher than that in the control group. The difference was significant (P < 0.01); the results of immunohisto-chemical staining: expression of MBP in both experi-mental group and control group were gradually decreased after injury. The expression of MBP in experimental group was less apparent than that in BSS group and decreased obviously at 14 days, while the expression of MBP in BSS group was still obvious at 14 days. The positive rates of RGC in different durations of experi-mental group were lower than those in the BSS group. The differences were significant (P < 0.01). • CONCLUSION: EGb761 can reduce the content of MBP increase, the survival rate of RGC and may have the protective effect in preventing RGC from degeneration. Source

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