1.Expression of epidermal growth factor receptor of cervical carcinoma and its correlation with prognosis
Linghong DENG ; Shuyu FENG ; Jiali KANG ; Yanna ZHANG ; Qiaoer LIN ; Miaoling NIE ; Haiyan CHENG ; Jinrui SUN
Clinical Medicine of China 2009;25(6):590-592
Objective To study the expression of epidermal growth factor receptor (EGFR) in cervical car-cinoma and cervical intraepithelial neoplasia(CIN),and to elucidate its relation with the genesis, infiltration, metas-tasis and prognosis of cervical carcinoma. Methods EGFR was determined by means of S-P immunohistochemistry in tissue of 100 cases of cervical carcinoma,60 cases of CIN and 40 cases of controls. Results The overexpression rates of EGFR were 0% (0/40), 51.67% (31/60),78.00% (78/100), respectively in normal cervical epithelium, CIN and cervical tumor tissues. The overexpression rate of EGFR was significantly higher in cervical tumor tissue than in control group(P<0.01). The overexpression of EGFR didn't demonstrate significant association with clinical staging, tumor size, pathological type, differentiation, cervical invasion depth, cervical canal invasion, lymphnode me-tastasis or the prognosis of cervical neoplasm (P>0.05). Conclusion Overexpression of EGFR is worsened with the severity of cervical lesion, suggesting that overexpression of EGFR is correlated with the genesis of cervical neo-plasms,which may be a valuable biological indicator of cervical carcinoma,but is not correlated with clinical patho-logical features and prognosis of cervical carcinoma.
2.Preventive effects of curcumin on status epilepticus induced by lithium chloride-pilocarpine
Zhiling HUANG ; Bo XIAO ; Liming TAN ; Shuyu LI ; Kang WANG ; Niangui XU ; Weiping LIU ; Xiaoyan LONG
Journal of Chinese Physician 2001;0(08):-
Objective To investigate the preventive effects of curcumin for status epilepticus(SE) induced by lithium chloride-pilocarpine.Methods Totally 45 Sprague-Dawley(SD) rats were randomly divided into three groups: preventive group(n=15),non-preventive group(n=15),and control group(n=15).The latency peroid and incidence of SE were recorded.The surviving neurons were stained by using nissl staining,and the programme death cells were detected by using terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling(TUNEL) in hippocampal CA3.Results The SE incidence of preventive group was 66.7%,which was significantly lower than that of non-preventive group(P0.05).Conclusion Pretreatment of curcumin can prevent the SE induced by lithium chloride-pilocarpine and the pretreatment can not protect the neuron.
3.Ref-1 protects against FeCl3 -induced thrombosis and tissue factor expression via the GSK3β–NF-κB pathway
Ikjun LEE ; Harsha NAGAR ; Seonhee KIM ; Su-jeong CHOI ; Shuyu PIAO ; Moonsang AHN ; Byeong Hwa JEON ; Sang-Ha OH ; Shin Kwang KANG ; Cuk-Seong KIM
The Korean Journal of Physiology and Pharmacology 2021;25(1):59-68
Arterial thrombosis and its associated diseases are considered to constitute a major healthcare problem. Arterial thrombosis, defined as blood clot formation in an artery that interrupts blood circulation, is associated with many cardiovascular diseases. Oxidative stress is one of many important factors that aggravates the pathophysiological process of arterial thrombosis. Apurinic/apyrimidinic endonuclease 1/redox factor-1 (Ref-1) has a multifunctional role in cells that includes the regulation of oxidative stress and anti-inflammatory function. The aim of this study was to investigate the therapeutic effect of adenovirus-mediated Ref-1 overexpression on arterial thrombosis induced by 60% FeCl3 solution in rats. Blood flow was measured to detect the time to occlusion, thrombus formation was detected by hematoxylin and eosin staining, reactive oxygen species (ROS) levels were detected by high-performance liquid chromatography, and the expression of tissue factor and other proteins was detected by Western blot. FeCl3 aggravated thrombus formation in carotid arteries and reduced the time to artery occlusion. Ref-1 significantly delayed arterial obstruction via the inhibition of thrombus formation, especially by downregulating tissue factor expression through the Akt-GSK3β-NF-κB signaling pathway. Ref-1 also reduced the expression of vascular inflammation markers ICAM-1 and VCAM-1, and reduced the level of ROS that contributed to thrombus formation. The results showed that adenovirus-mediated Ref-1 overexpression reduced thrombus formation in the rat carotid artery. In summary, Ref-1 overexpression had anti-thrombotic effects in a carotid artery thrombosis model and could be a target for the treatment of arterial thrombosis.
4.Ref-1 protects against FeCl3 -induced thrombosis and tissue factor expression via the GSK3β–NF-κB pathway
Ikjun LEE ; Harsha NAGAR ; Seonhee KIM ; Su-jeong CHOI ; Shuyu PIAO ; Moonsang AHN ; Byeong Hwa JEON ; Sang-Ha OH ; Shin Kwang KANG ; Cuk-Seong KIM
The Korean Journal of Physiology and Pharmacology 2021;25(1):59-68
Arterial thrombosis and its associated diseases are considered to constitute a major healthcare problem. Arterial thrombosis, defined as blood clot formation in an artery that interrupts blood circulation, is associated with many cardiovascular diseases. Oxidative stress is one of many important factors that aggravates the pathophysiological process of arterial thrombosis. Apurinic/apyrimidinic endonuclease 1/redox factor-1 (Ref-1) has a multifunctional role in cells that includes the regulation of oxidative stress and anti-inflammatory function. The aim of this study was to investigate the therapeutic effect of adenovirus-mediated Ref-1 overexpression on arterial thrombosis induced by 60% FeCl3 solution in rats. Blood flow was measured to detect the time to occlusion, thrombus formation was detected by hematoxylin and eosin staining, reactive oxygen species (ROS) levels were detected by high-performance liquid chromatography, and the expression of tissue factor and other proteins was detected by Western blot. FeCl3 aggravated thrombus formation in carotid arteries and reduced the time to artery occlusion. Ref-1 significantly delayed arterial obstruction via the inhibition of thrombus formation, especially by downregulating tissue factor expression through the Akt-GSK3β-NF-κB signaling pathway. Ref-1 also reduced the expression of vascular inflammation markers ICAM-1 and VCAM-1, and reduced the level of ROS that contributed to thrombus formation. The results showed that adenovirus-mediated Ref-1 overexpression reduced thrombus formation in the rat carotid artery. In summary, Ref-1 overexpression had anti-thrombotic effects in a carotid artery thrombosis model and could be a target for the treatment of arterial thrombosis.
5.Study on the mechanism of berberine in improving diabetes mellitus type 2 combined with metabolic-associated fatty liver disease
Yi LI ; Shuyu KANG ; Qiwen WANG ; Manting HUANG ; Congyan ZENG ; Jun TONG ; Gengting DONG
China Pharmacy 2025;36(16):1975-1980
OBJECTIVE To investigate the potential mechanism of berberine improving diabetes mellitus type 2 (T2DM) combined with metabolic-associated fatty liver disease (MAFLD) by regulating ceramide. METHODS Thirty-two db/db mice with blood glucose levels>11.1 mmol/L (T2DM model) were divided into four groups: model group, berberine low- and high-dose groups [100, 200 mg/(kg·d)] and metformin group [300 mg/(kg·d)], with 8 mice in each group. Additionally, 8 wt/wt mice were selected as the normal control group. Mice in each group were administered the corresponding drug solution or water by gavage once daily for a continuous period of 6 weeks. During the experiment, the body weight of the mice was monitored, and the differences in final body weight were analyzed. After the last administration, the body shape of the mice in each group was observed, and their fasting blood glucose (FBG) and the lipid indicators [total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C)] were measured. Fasting serum insulin (FINS) levels were also measured, and the insulin resistance index HOMA-IR) and insulin sensitivity index (ISI) were calculated. Liver weight, liver index and serum liver function indicators [alanine transaminase (ALT), aspartate transaminase(AST)] were assessed, and hepatic histopathological changes were observed. Additionally, the expression of fatty acid synthesis-related proteins [sterol regulatory element-binding protein 1 (SREBP1), fatty acid synthase (FASN), acetyl-CoA carboxylase 1 (ACC1)] in liver tissue was examined. Serum samples from the normal control group, model group, and berberine high-dose group were collected for non-targeted lipidomics analysis and validation. RESULTS Compared with the model group, the pathological changes, including disordered liver tissue cell arrangement and lipid vacuoles, were significantly improved in the berberine low- and high-dose groups. The significant decreases or down-regulations were observed in body weight in the last week, as well as FBG, TC, TG, and LDL-C levels, HOMA-IR (except for the berberine low-dose group), liver weight, liver index, AST and ALT levels, and protein expressions of SREBP1, FASN and ACC1. Additionally, HDL-C levels, FINS (except for the berberine high-dose group), and ISI (except for the berberine low-dose group) were significantly increased (P<0.05). A total of 21 potential differential metabolites, including multiple types of ceramides, were identified; these metabolites were primarily enriched in sphingolipid metabolism and glycerophospholipid metabolism pathways. Verification experiments confirmed that high-dose berberine significantly reduced the serum content of ceramide in model mice (P<0.05). CONCLUSIONS Berberine reduces insulin resistance, improves liver damage and lipid accumulation in the T2DM combined with MAFLD mice, and these effects may be related to the reduction of ceramide content.