Publications by authors named "Bei-Bei Fu"

12 Publications

  • Page 1 of 1

Xin-Ji-Er-Kang protects myocardial and renal injury in hypertensive heart failure in mice.

Phytomedicine 2021 Oct 18;91:153675. Epub 2021 Jul 18.

Department of Pharmacology, Basic Medical College, Anhui Medical University, Hefei 230032, China. Electronic address:

Background: Xin-Ji-Er-Kang (XJEK) as a herbal formula of traditional Chinese medicine (TCM) has shown the protective effects on myocardial function as well as renal function in mouse models of myocardial infarction.

Hypothesis/purpose: We investigated the effects of XJEK on cardiovascular- and renal-function in a heart failure mouse model induced by high salt (HS) and the associated mechanisms.

Study Design: For the purpose of assessing the effects of XJEK on a hypertensive heart failure model, mice were fed with 8% high salt diet. XJEK was administered by oral gavage for 8 weeks. Cardiovascular function parameters, renal function associated biomarkers and XJEK's impact on renin-angiotensin-aldosterone system (RAAS) activation were assessed. To determine the underlying mechanism, the calpain1/junctophilin-2 (JP2)/sarcoplasmic reticulum Ca ATPase (SERCA2a) pathway was further studied in AC16 cells after angiotensin II-challenge or after calpastatin small interfering RNA (siRNA) transfection.

Results: Mice on HS-diet exhibited hypertensive heart failure along with progressive kidney injury. Similar to fosinopril, XJEK ameliorated hypertension, cardiovascular-and renal- dysfunction in mice of HS-diet group. XJEK inhibited HS-induced activation of RAAS and reversed the abnormal expression pattern of calpain1and JP2 protein in heart tissues. XJEK significantly improved cell viability of angiotensin II-challenged AC16 cells. Moreover, XJEK's impact on calpain1/JP2 pathway was partly diminished in AC16 cells transfected with calpastatin siRNA.

Conclusion: XJEK was found to exert cardiovascular- and renal protection in HS-diet induced heart failure mouse model. XJEK inhibited HS-diet induced RAAS activation by inhibiting the activity and expression of calpain1 and protected the junctional membrane complex (JMC) in cardiomyocytes.
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http://dx.doi.org/10.1016/j.phymed.2021.153675DOI Listing
October 2021

Cholesterol gallstones: Focusing on the role of interstitial Cajal-like cells.

World J Clin Cases 2021 May;9(15):3498-3505

Department of General Surgery, Shengjing Hospital of China Medical University, Shenyang 110004, Liaoning Province, China.

Cholesterol gallstone (CG) is a common, frequent biliary system disease in China, with a complex and multifactorial etiology. Declined gallbladder motility reportedly contributes to CG pathogenesis. Furthermore, interstitial Cajal-like cells (ICLCs) are reportedly present in human and guinea pig gallbladder tissue. ICLCs potentially contribute to the regulation of gallbladder motility, and aberrant conditions involving the loss of ICLCs and/or a reduction in its pacing potential and reactivity to cholecystokinin may promote CG pathogenesis. This review discusses the association between ICLCs and CG pathogenesis and provides a basis for further studies on the functions of ICLCs and the etiologies of CG.
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http://dx.doi.org/10.12998/wjcc.v9.i15.3498DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8130069PMC
May 2021

Effect of cholesterol on cultured interstitial Cajal-like cells isolated from guinea pig gallbladders.

World J Gastrointest Surg 2020 May;12(5):226-235

Department of General Surgery, Shengjing Hospital of China Medical University, Shenyang 110004, Liaoning Province, China.

Background: Loss and/or dysfunction of interstitial Cajal-like cells (ICLCs) in the gallbladder may promote cholesterol gallstone formation by decreasing gallbladder motility.

Aim: To study the effect of cholesterol on the proliferation and apoptosis of ICLCs from guinea pig gallbladders.

Methods: Guinea pig gallbladder ICLCs were isolated and cultured . The cells were exposed to cholesterol solutions at different concentrations (0, 25, 50, and 100 mg/L) for 24 h. Then, cell proliferation was detected by the CCK-8 method and the apoptosis rate was detected by flow cytometry. Further, the expression of the c-Kit protein was detected by Western blot and the expression level of mRNA in the cells was detected by real-time quantitative PCR.

Results: After ICLCs were cultured with cholesterol at concentrations of 25, 50, and 100 mg/L, the proliferation rates decreased significantly ( < 0.05), whereas the apoptosis rates increased significantly ( < 0.05). Moreover, the expression of c-Kit protein and mRNA decreased significantly ( < 0.05).

Conclusion: High cholesterol concentrations can inhibit the proliferation of ICLCs and promote apoptosis. This decrease in the ICLC proliferation rate might be caused by the inhibition of the stem cell factor/c-Kit signaling pathway.
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http://dx.doi.org/10.4240/wjgs.v12.i5.226DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7289650PMC
May 2020

Cellular and molecular mechanism study of declined intestinal transit function in the cholesterol gallstone formation process of the guinea pig.

Exp Ther Med 2014 Nov 1;8(5):1518-1522. Epub 2014 Sep 1.

Department of the Second General Surgery, Sheng Jing Hospital of China Medical University, Shenyang, Liaoning 110004, P.R. China.

The aim of this study was to investigate the cellular and molecular mechanisms of declined intestinal transit (IT) function in the cholesterol gallstone (CG) formation process. Forty guinea pigs were divided into an experimental group (EG) and a control group (CoG), and the reverse transcription-polymerase chain reaction (RT-PCR) was performed for the analysis of c-kit and stem cell factor (scf) mRNA expression in the small bowel. In addition, immunofluorescence staining and confocal laser microscopy were performed for the observation of the changes in the number of interstitial cells of Cajal (ICCs) in the terminal ileum of each group. RT-PCR showed that, compared with the CoG, the intestinal c-kit and scf mRNA expression levels in the EG were significantly decreased; the average positive area of ICCs in the ileum in the EG was also significantly reduced. During the diet-induced CG formation procedure, the c-kit and scf mRNA expression levels in the small intestine decreased and the number of ICCs decreased. Inhibition of the c-kit/scf pathway may be involved in the declined IT function during the CG formation process.
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http://dx.doi.org/10.3892/etm.2014.1943DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4186406PMC
November 2014

Decreased number of interstitial cells of Cajal play an important role in the declined intestinal transit during cholesterol gallstone formation in guinea pigs fed on high cholesterol diet.

Int J Clin Exp Med 2014 15;7(5):1262-8. Epub 2014 May 15.

Department of The Second General Surgery, Shengjing Hospital of China Medical University Shenyang City, Liaoning Province, China.

To study the changes of interstitial cells of Cajal (ICCs) and expression of c-kt and scf mRNA in terminal ileum tissue during cholesterol gallstone formation in guinea pigs fed on high cholesterol diet, forty guinea pigs were divided into the gallstone group and the control group. The animals in the gallstone group were fed on a high cholesterol diet (HCD), while those in the control group fed on a standard diet (StD). The guinea pigs were sacrificed at the 8th week. The expression of c-kit and scf in terminal ileum were determined by RT-PCR and the morphological characteristics and number of ICCs were observed and calculated by using immunohistochemistry. RT-PCR showed that, compared with the control group, the c-kit and scf mRNA expression levels in the gallstone group were significantly declined. In the animal assay, the decreased number of ICCs was present obviously in the gallstone group. We concluded from the study that decreased number of ICCs, decreased expression of c-kit and scf in terminal ileum are present in guinea pigs fed on high cholesterol diet. The c-kit/scf pathway inhibition might be involved in the decline of intestinal transit function during cholesterol gallstone formation.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4073742PMC
July 2014

[Effect of different concentrations of bortezomib on the expression of ERK, JNK and P38 in daunorubicin-resistant K562 cells].

Zhongguo Shi Yan Xue Ye Xue Za Zhi 2011 Jun;19(3):671-5

Department of Hematology, China Medical University Shengjing Hospital, Shenyang 110022, Liaoning Province, China.

The aim of this study was to investigate the effect of proteasome inhibitor bortezomib on the expression of ERK, JNK, and P38 in daunorubicin (DNR)-resistant K562 cells and its mechanism. MTT method was used to determine the drug-resistant K562 cells and the cellular toxicity of bortezomib; Western blot was used to detect the expression of protein ERK, JNK and P38 in K562 cells after treatment with 100 nmol/L DNR alone or combined with 1 nmol/L and 10 nmol/L bortezomib for 36 hours. Flow cytometry assay was used to detect the apoptosis rate in each group cells. The results indicated that the expression of ERK and P38 were significantly suppressed (p < 0.05) and the expression of JNK was significantly enhanced (p < 0.05) in the cells treated by DNR combined with bortezomib. It is concluded that bortezomib can decrease the expressions of protein ERK and P38 and enhance the expression of JNK, the bortezomib reverses the cellular drug-resistance and promote cell apoptosis through MAPK pathway.
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June 2011

Reversion of Multidrug-Resistance by Proteasome Inhibitor Bortezomib in K562/DNR Cell Line.

Chin J Cancer Res 2011 Mar;23(1):69-73

Department of Hematology, Shengjing Hospital, China Medical University, Shenyang 110004, China.

Objective: To observe the reversion of multi-drug resistance by proteasome inhibitor bortezomib in K562/DNR cell line and to analyze the possible mechanism of reversion of multidrug-resistance.

Methods: MTT method was used to determine the drug resistance of K562/DNR cells and the cellular toxicity of bortezomib. K562/DNR cells were cultured for 12 hours, 24 hours and 36 hours with 100 μg/ml DNR only or plus 4 μg/L bortezomib. The expressions of NF-κB, IκB and P-gp of K562/DNR were detected with Western blot method, the activity of NF-κB was tested by ELISA method and the apoptosis rate was observed in each group respectively.

Results: The IC50 of DNR on cells of K562/S and K562/DNR groups were 1.16 μg/ml and 50.43 μg/mL, respectively. The drug-resistant fold was 43.47. The IC10 of PS-341 on Cell strain K562/DNR was 4 μg/L. Therefore, 4 μg/L was selected as the concentration for PS-341 to reverse drug-resistance in this study. DNR induced down-regulation of IκB expression, up-regulation of NF-κB and P-gp expression. After treatment with PS-341, a proteasome inhibitor, the IκB degradation was inhibited, IκB expression increased, NF-κB and P-gp expression decreased in a time dependent manner. Compared to DNR group, the NF-κB p65 activity of DNR+PS-341 group was decreased. Compared to corresponding DNR group, DNR induced apoptosis rate increases after addition of PS-341 in a time dependent manner.

Conclusion: Proteasome inhibitor bortezomib can convert the leukemia cell drug resistance. The mechanism may be that bortezomib decreases the degradation of IκB and the expression of NF-κB and P-gp, therefore induces the apoptosis of multi-drug resistant cells.
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http://dx.doi.org/10.1007/s11670-011-0069-4DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3587529PMC
March 2011

[Effect of bortezomib on MAPK signaling pathway of K562/DNR cells].

Zhongguo Shi Yan Xue Ye Xue Za Zhi 2010 Dec;18(6):1460-3

Department of Hematology, China Medical University, Shenyang 110004, Liaoning Province, China.

The study was aimed to investigate the effects of bortezomib (BTZ) on the expression of ERK, JNK and P38 in daunorubicin (DNR)-resistant K562 cells (K562/DNR) and to clarify the molecular mechanism of BTZ in reversing the drug-resistance in leukemic cells. The K562/DNR cells and the cellular toxicity of BTZ was determined by MTT, then 4 µg/L of BTZ was chosen to do the experiment. The expression of ERK, JNK, p38 and P-gp of K562/DNR cells treated with DNR only or DNR combined with BTZ for 12, 24 and 36 hours was detected by Western blot. The apoptosis rate in each group was assayed by flow cytometry. The results showed that as compared with DNR group, the expression of P-ERK, P-P38 and P-gp was significantly suppressed (p < 0.05) and the expression of P-JNK was significantly enhanced (p < 0.05) in the cells treated with DNR combined with BTZ. There was no change in the expression of total ERK, P38 and JNK. The effect increased with the prolonging of time. Meanwhile, the apoptosis rate in cells treated with DNR combined with BTZ increased compared with DNR only. It is concluded that the BTZ can reverse the drug resistance in K562/DNR cells by MAPK signaling pathway and increase the apoptosis of leukemic cells. The effect shows the characteristics of time-dependent manner.
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December 2010

Possible relationship between intestinal barrier function and formation of pigment gallstones in hamsters.

Hepatobiliary Pancreat Dis Int 2008 Oct;7(5):529-32

Department of General Surgery, Shengjing Hospital, China Medical University, Shenyang 110004, China.

Background: The presence of bacteria in bile is an important factor in the formation of pigment gallstones. The bile of healthy people is sterile and bacteria in the biliary system come from endogenous infection from the gut. Yet, the route of bacterial translocation into the bile duct is still unclear. Theoretically, two routes exist: one is through the intestinal barrier and the other is by direct reflux from the sphincter of Oddi. This study was undertaken to explore the relationship between the effectiveness of intestinal barrier and the formation of pigment gallstones in hamsters.

Methods: Thirty-two hamsters were divided into an experimental and a control group, with 16 hamsters in each group. A low protein and high cellulose diet was given for 6 weeks to induce the formation of pigment gallstones in the experimental group (PS) and a normal diet was given to the control group (CON). Morphological changes, changes in the levels of serum endotoxin and diamine oxidase, and changes in the numbers of B lymphocytes, plasma cells and secretory immunoglobin A (sIgA) in the intestinal mucosa were assessed after 6 weeks.

Results: Four hamsters died during lithogenesis and body weight decreased in the PS group. Pigment gallstones were found in 11 hamsters at the end of the experiment, giving a lithogenesis rate of 91.67%. The serum endotoxin level before and after gallstone formation in the PS group was 0.2960+/-0.1734 U/ml and 8.2964+/-4.6268 U/ml, respectively (P<0.05). The blood diamine oxidase level before and after gallstone formation in the PS group was 2.6333+/-0.8037 U/ml and 3.3642+/-0.9545 U/ml, respectively (P<0.05). The numbers of B lymphocytes, plasma cells and sIgA in the intestinal mucosa in the PS group were 71.56+/-2.89, 68.65+/-2.09 and 27.56+/-1.07, respectively, and were significantly decreased compared with the corresponding values in the CON group (94.25+/-3.69, 93.47+/-3.98 and 42.57+/-1.96, respectively, P<0.05).

Conclusions: A low protein and high cellulose diet can markedly reduce intestinal barrier function and facilitate the formation of pigment gallstones. The decrease of intestinal barrier function may take part in the formation of pigment gallstones.
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October 2008

Effect of intestinal transit on the formation of cholesterol gallstones in hamsters.

Hepatobiliary Pancreat Dis Int 2007 Oct;6(5):513-5

Department of General Surgery, Second Affiliated Hospital (Shengjing Hospital), China Medical University, Shenyang 110004, China.

Background: The effect of "intestinal transit" has become a new field of interest in the study of the pathogenesis of cholesterol gallstones. This study was undertaken to further test this notion and ascertain the relationship between impaired intestinal transit function and cholesterol gallstones.

Methods: A total of 64 hamsters were divided into 2 groups, experimental and control. Each was subdivided into 4 subgroups for sacrifice at different time. A high-cholesterol diet and a standard diet were fed to each group. The geometric center, which represents the intestinal transit function was calculated.

Results: The growth of all hamsters was normal. Cholesterol gallstones were found in 2 hamsters at the end of the 4th week. The geometric center values for the experimental and control groups were 2.3891+/-0.3923 vs. 2.7730+/-0.5283, at the end of week 3; 1.8148+/-0.4312 vs. 3.2294+/-1.1613 at week 4; 1.8451+/-0.3700 vs. 2.9075+/-0.3756 at week 5; and 1.8025+/-0.3413 vs. 3.0920+/-0.5622 at week 6.

Conclusion: A high cholesterol diet can significantly reduce the intestinal transit function and facilitate the formation of cholesterol gallstones.
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October 2007

Systemic delivery of full-length C/EBP beta/liposome complex suppresses growth of human colon cancer in nude mice.

Cell Res 2005 Oct;15(10):770-6

State Key Laboratory of Molecular Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China.

C/EBP beta (CCAAT/enhancer-binding protein beta) is an important transcription factor involved in cellular proliferation and differentiation. Overexpression of the full-length C/EBP beta protein results in cellular growth arrest and apoptosis. Using a nonviral liposome as carrier, we delivered the full-length C/EBP beta expression plasmid, pCN, into nude mice bearing CW-2 human colon cancer tumors via tail vein. Southern blots revealed that the major organs and tumors were transfected. Experimental gene therapy showed that a strong suppression of tumor growth was observed in the pCN-treated mice, and such suppression was due to the overexpression of C/EBP beta, leading to the increased apoptosis in tumors of pCN-treated mice. No apparent toxic effects of pCN/liposome complex were observed in the animals. Thus, C/EBP beta has tumor suppression effect in vivo and may be used in gene therapy for cancers.
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http://dx.doi.org/10.1038/sj.cr.7290346DOI Listing
October 2005

Gene expression profile favoring phenotypic reversion: a clue for mechanism of tumor suppression by NF-IL6 3'UTR.

Cell Res 2003 Dec;13(6):509-14

State Key Laboratory of Molecular Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China.

Transfection of cDNA in 3'untranslated region of human nuclear factor for interleukin-6 (NF-IL6 3'UTR) induced tumor suppression in a human hepatoma cell line. cDNA array analysis was used to reveal changes in gene expression profile leading to tumor suppression The results indicate that this suppression was not due to activation of dsRNA-dependent protein kinase, nor to inactivation of oncogenes; rather, all the changes in expression of known genes, induced by NF-IL6 3'UTR cDNA may be ascribed to the suppression of cellular malignancy. Therefore, our results imply that this 3'untranslated region may have played role of a regulator of gene expression profile.
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http://dx.doi.org/10.1038/sj.cr.7290195DOI Listing
December 2003
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