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| 1 | Qingyi decoction protects against myocardial injuries induced by severe acute pancreatitis显示文摘BACKGROUND We studied the protective effects of Qingyi decoction(QYD)(a Traditional Chinese Medicine)against severe acute pancreatitis(SAP)-induced myocardial infarction(MI).AIM To study the function and mechanism of QYD in the treatment of myocardial injuries induced by SAP.METHODS Ultrasonic cardiography,hematoxylin and eosin staining,immunohistochemistry,qRT-PCR,western blot,enzyme-linked immunosorbent assays,and apoptosis staining techniques were used to determine the effects of QYD following SAP-induced MI in Sprague-Dawley rats.RESULTS Our SAP model showed severe myocardial histological abnormalities and marked differences in the symptoms,mortality rate,and ultrasonic cardiography outputs among the different groups compared to the control.The expression of serum cytokines[interleukin(IL)-1?,IL-6,IL-8,IL-12,amyloidβ,and tumor necrosis factor-α]were significantly higher in the SAP versus QYD treated group(P<0.05 for all).STIM1 and Orai1 expression in myocardial tissue extracts were significantly decreased post QYD gavage(P<0.001).There was no significant histological difference between the 2-aminoethyl diphenylborinate inhibitor and QYD groups.The SAP group had a significantly higher apoptosis index score compared to the QYD group(P<0.001).CONCLUSION QYD conferred cardio-protection against SAP-induced MI by regulating myocardial-associated protein expression(STIM1 and Orai1). | Lei Li Yong-Qi Li Zhong-Wei Sun Cai-Ming Xu Jun Wu Ge-Liang Liu Ahmed MH Bakheet Hai-Long Chen | 2020 | World Journal of Gastroenterology2020，26，12： | 17 |
| 2 | Progression of diethylnitrosamine-induced hepatic carcinogenesis in carnitine-depleted rats显示文摘AIM:To investigate whether carnitine deficiency is a risk factor during the development of diethylnitrosamine (DENA)-induced hepatic carcinogenesis. METHODS:A total of 60 male Wistar albino rats were divided into six groups with 10 animals in each group.Rats in group 1(control group)received a single intraperitoneal(i.p.)injection of normal saline. Animals in group 2(carnitine-supplemented group) were given L-carnitine(200 mg/kg per day)in drinking water for 8 wk.Animals in group 3(carnitine-depleted group)were given D-carnitine(200 mg/kg per day)and mildronate(200 mg/kg per day)in drinking water for 8 wk.Rats in group 4(DENA group)were injected with a single dose of DENA(200 mg/kg,i.p.)and 2 wk later received a single dose of carbon tetrachloride(2 mL/kg) by gavage as 1:1 dilution in corn oil.Animals in group 5(DENA-carnitine depleted group)received the same treatment as group 3 and group 4.Rats in group 6 (DENA-carnitine supplemented group)received the same treatment as group 2 and group 4.RESULTS:Administration of DENA resulted in a significant increase in alanine transaminase(ALT), gamma-glutamyl transferase(G-GT),alkaline phosphatase(ALP),total bilirubin,thiobarbituric acid reactive substances(TBARS)and total nitrate/ nitrite(NOx)and a significant decrease in reduced glutathione(GSH),glutathione peroxidase(GSHPx), catalase(CAT)and total carnitine content in liver tissues.In the carnitine-depleted rat model,DENA induced a dramatic increase in serum ALT,G-GT,ALP and total bilirubin,as well as a progressive reduction in total carnitine content in liver tissues.Interestingly, L-carnitine supplementation resulted in a complete reversal of the increase in liver enzymes,TBARS and NOx,and a decrease in total carnitine,GSH,GSHPx, and CAT induced by DENA,compared with the control values.Histopathological examination of liver tissues confirmed the biochemical data,where L-carnitine prevented DENA-induced hepatic carcinogenesis while D-carnitine-mildronate aggravated DENA-induced hepatic damage. CONCLUSION:Data from this study suggest for the first time that:(1)carnitine deficiency is a risk factor and should be viewed as a mechanism in DENA- induced hepatic carcinogenesis;(2)oxidative stress plays an important role but is not the only cause of DENA-induced hepatic carcinogenesis;and(3) long-term L-carnitine supplementation prevents the development of DENA-induced liver cancer. | Salim S Al-Rejaie Abdulaziz M Aleisa Abdulaziz A Al-Yahya Saleh A Bakheet Abdulmalik Alsheikh Amal G Fatani Othman A Al-Shabanah Mohamed M Sayed-Ahmed | 2009 | World Journal of Gastroenterology2009，15，11： | 4 |
| 3 | Sinapic acid ameliorates D-galactosamine/lipopolysaccharideinduced fulminant hepatitis in rats:Role of nuclear factor erythroidrelated factor 2/heme oxygenase-1 pathways显示文摘BACKGROUND Sinapic acid(SA)has been shown to have various pharmacological properties such as antioxidant,antifibrotic,anti-inflammatory,and anticancer activities.Its mechanism of action is dependent upon its ability to curb free radical production and protect against oxidative stress-induced tissue injuries.AIM To study the hepatoprotective effects of SA against lipopolysaccharide(LPS)/Dgalactosamine(D-GalN)-induced acute liver failure(ALF)in rats.METHODS Experimental ALF was induced with an intraperitoneal(i.p.)administration of 8μg LPS and 800 mg/kg D-GalN in normal saline.SA was administered orally once daily starting 7 d before LPS/D-GalN treatment.RESULTS Data showed that SA ameliorates acute liver dysfunction,decreases serum levels of alanine transaminase(ALT),and aspartate aminotransferase(AST),as well as malondialdehyde(MDA)and NO levels in ALF model rats.However,pretreatment with SA(20 mg/kg and 40 mg/kg)reduced nuclear factor kappalight-chain-enhancer of activated B cells(NF-κB)activation and levels of inflammatory cytokines(tumor necrosis factor-αand interleukin 6).Also,SA increased the activity of the nuclear factor erythroid-related factor 2/heme oxygenase-1(Nrf2/HO-1)signaling pathway.CONCLUSION In conclusion,SA offers significant protection against LPS/D-GalN-induced ALF in rats by upregulating Nrf2/HO-1 and downregulating NF-κB. | Mushtaq Ahmad Ansari Mohammad Raish Yousef A Bin Jardan Ajaz Ahmad Mudassar Shahid SheikhFayaz Ahmad Nazrul Haq Mohammad Rashid Khan Saleh A Bakheet | 2021 | World Journal of Gastroenterology2021，27，7： | 2 |
| 4 | The fetal basis of amyloidogenesis:exposure to lead and latent overexpression of amyloid precursor protein and beta-amyloid in the aging brain显示文摘 | Basha MR Wei W Bakheet SA | 2005 | J Neurosci2005，25，4： | 1 |
| 5 | ARED:human AU-rich element-containing mRNA database reveals an unexpectedly di-verse functional repertoire of encoded proteins显示文摘 | Bakheet T Frevel M Williams BR | 2001 | Nucleic Acids Res2001，29，1： | 1 |
| 6 | Casuses of ^18F - FDG uptake on whole body maging 显示文摘 | Bakheet SM Powel Benign | 1998 | Semin Nuclmed1998，28，4： | 1 |
| 7 | Poly(ADP-ribose) lymemse-1 inhibitor modulates T regulatory and IL-17 cells in the prevention of adjuvant induced arthritis in mice model 显示文摘 | Ahmad SF Zoheir KM Bakheet SA | 2014 | Cytokine2014，68，2： | 1 |
| 8 | Giutaric aciduria type Ih observations in seven patients with neonatal- and late-onset disease显示文摘 | al-Essa MA Hashed MS Bakheet SM Patay ZJ Ozand PT | 2000 | Perinatol2000，20，2： | 1 |
| 9 | Properties and identification of humanprotein drug targets显示文摘 | BAKHEET T M DOIG A J | 2009 | Bioinformatics2009，25，4： | 1 |
| 10 | Properties and identification of human protein drug targets显示文摘 | Bakheet T M Doig A J | 2009 | Bioinformatics2009，25，4： | 1 |
| 11 | Electro-Peroxone Treatment of Orange II Dye Wastewater显示文摘 | Bakheet B Yuan Shi Li Zhaoxin | 2013 | Water Res2013，47，16： | 1 |
| 12 | Predictors of stroke recur- rence in patients with recent lacunar stroke and response to inter- ventions according to risk status: secondary prevention of small subcortical strokes trial显示文摘 | Hart RG Pearce LA Bakheet MF | 2014 | J Stroke Cerebrovasc Dis2014，23，4： | 1 |
| 13 | Predictors of Stroke Recur- rence in Patients with Recent Lacunar Stroke and Response to Inter- ventions according to Risk Status : Secondary Prevention of Small Sub- cortical Strokes Trial显示文摘 | Hart RG Pearce LA Bakheet MF | 2014 | Journal of Stroke and Cerebrovascular Dis- eases2014，23，4： | 1 |
| 14 | Molecular cytogenet- ic evaluation of the mechanism of micronuelei formation in- duced by camptothecin, topoteean, and irinoteean显示文摘 | Attia SM Aleisa AM Bakheet SA etal | 2009 | Environ Mol Mutagen2009，50，2： | 1 |
| 15 | Properties and identification of human protein drug targets显示文摘 | BAKHEET T M DOIG A J | 2009 | Bioinformatics2009，25，4： | 1 |
| 16 | Benign causes of 18-FDG uptake on wholebody imaging显示文摘 | Bakheet SM Powe J | 1998 | Semin Nucl Mexi1998，28，： | 1 |
| 17 | F-18 fluorodeoxyglucose chest uptake in lung inflammation and infection显示文摘 | Saleem M Povue J | 2000 | Clini Nucl Med2000，25，4： | 1 |
| 18 | F-18 FDG positron emission tomography in primary breast non-Hodgkin's lymphoma 显示文摘 | Bakheet SM Bakheet R Ezzat A | 2001 | Clin Nucl Med2001，26，： | 1 |
| 19 | Predictors of Stroke Recurrence in Patients with Recent Lacunar Stroke and Response to Interventions According to Risk Status: Secondary Prevention of Small Subcortical Strokes Trial显示文摘 | Robert G. Hart Lesly A. Pearce Majid F. Bakheet Oscar R. Benavente Robin A. Conwit Leslie A. McClure Robert L. Talbert David C. Anderson | 2014 | Journal of Stroke and Cerebrovascular Diseases2014，，4： | 1 |
| 20 | Patterns of radioiodine uptake by the lactaring breast显示文摘 | Bakheet SM Hammami MM | 1994 | Eur J Nucl Med1994，21，： | 1 |
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