Yi-Zhi-Fang-Dai Formula Protects against Aβ1–42Oligomer Induced Cell Damage via Increasing Hsp70 and Grp78 Expression in SH-SY5Y Cells

Yi-Zhi-Fang-Dai formula (YZFDF) is an experiential prescription used to cure dementia cases like Alzheimer’s disease (AD). In this study, the main effective compounds of YZFDF have been identified from this formula, and the neuroprotective effect againstAβ1–42oligomer of YZFDF has been tested in SH-SY5Y cells. Our results showed that YZFDF could increase cell viability and could attenuate endothelial reticula- (ER-) mediated apoptosis. Evidence indicated that protein folding and endothelial reticula stress (ERS) played an important role in the AD pathological mechanism. We further explored the expression of Hsp70, an important molecular chaperon facilitating the folding of other proteins, and Grp78, the marker protein of ERS in SH-SY5Y cells. Data told us that YZFDF pretreatment could influence the mRNA and protein expression of these two proteins. At last, we also found that YZFDF pretreatment could activate Akt in SH-SY5Y cells. All these above indicate that YZFDF could be a potent therapeutic candidate for AD treatment.

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NEUROPROTECTIVE EFFECTS OF GUARANA (PAULLINIA CUPANA MART.) AGAINST VINCRISTINE IN VITRO EXPOSURE

Journal of Prevention of Alzheimer's Disease ◽

10.14283/jpad.2017.45 ◽

2017 ◽

pp. 1-6

Author(s):

C.F. Veloso ◽

A.K. Machado ◽

F.C. Cadoná ◽

V.F. Azzolin ◽

I.B.M. Cruz ◽

...

Keyword(s):

Cell Viability ◽

Monolayer Culture ◽

Cell Damage ◽

Neuroprotective Effect ◽

In Vitro Study ◽

Oxygen Species ◽

Neuroprotective Effects ◽

Hydroalcoholic Extract ◽

Mice Brain

Background: Vincristine (VCR) is not a specific chemotherapeutic drug, responsible for cause several side effects. In this sense, many natural products have been studied to reduce this problem. Objetives: To examine the guarana neuroprotective effect in mice brain and cerebellum cells against vincristine (VCR) exposition. Design: An in vitro study was performed using mice brain and cerebellum mice in monolayer culture. First, cells were exposed to VCR (0.009 µM for 24 hours and 0.0007 µM for 72 hours) to measure the cytotoxicity effect. Also, the cellular effect of hydroalcoholic extract of guarana (10; 30; 100 and 300 μg/mL) was evaluated in the same cells in 24 and 72 hours. After that, cells were exposed to VCR and guarana extract to evaluate the neuroprotective effect of guarana. Measurements: Cell viability was analyzed by MTT, Free dsDNA and LHD Assays. Moreover, metabolism oxidative profile was evaluated by reactive oxygen species (ROS), lipoperoxidation (LPO) and catalase (CAT) levels through DCFH-DA, TBARS and Catalase Activity Assays, respectively. Results: Our findings revealed that VCR caused neuronal cytotoxicity by reducing cell viability and increasing ROS and LPO levels. On the other hand, guarana did not cause cell damage in none of tested concentrations. In addition, guarana exhibited a notable protective effect on brain and cerebellum cells exposed to VCR by increasing cell viability, stimulating CAT activity, reducing levels of ROS and LPO. Conclusions: In this sense, guaraná is a remarkable antioxidant fruit that could be a target in new therapies development to reduce VCR neurotoxicity.

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Inhibition of the SOCS1-JAK2-STAT3 Signaling Pathway Confers Neuroprotection in Rats with Ischemic Stroke

Cellular Physiology and Biochemistry ◽

10.1159/000484585 ◽

2017 ◽

Vol 44 (1) ◽

pp. 85-98 ◽

Cited By ~ 21

Author(s):

Xiao-Lei Wang ◽

Chun-Mei Qiao ◽

Jiong-Ou Liu ◽

Chun-Yang Li

Keyword(s):

Ischemic Stroke ◽

Protein Expression ◽

Cell Viability ◽

Signaling Pathway ◽

Rat Model ◽

Caspase 3 ◽

Neuronal Cells ◽

Stat3 Signaling ◽

Stat3 Signaling Pathway ◽

Mrna And Protein Expression

Background: The present study aims to investigate the protective effects of the SOCS1-JAK2-STAT3 signaling pathway on neurons in a rat model of ischemic stroke. Methods: Our study was conducted using an ischemic stroke rat model. After the microglia were extracted, 40 neonatal Sprague-Dawley (SD) rats were assigned into the blank, AG490, model and negative control (NC) groups. The neurological function of all the rats was evaluated. Histopathological changes were observed. qRT-PCR and western blotting were applied to measure the expression of genes and proteins in the SOCS1-JAK2-STAT3 signaling pathway and related to apoptosis. The TUNEL assay was conducted to calculate the cellular morphology and apoptosis of neuronal cells. Cell viability was detected using the MTT assay. In addition, immunoassays were used to measure the content of superoxide dismutase (SOD), glutathione (GSH) and malondialdehyde (MDA) as well as the levels of oxidative stress. Results: Compared with the blank group, the model and NC groups showed higher neurological function scores—the cytoplasm of the neurons were cavitated, the organelles were reduced with unclear margins, some of the neurons were necrotic, and apoptosis was increased. In addition, the NC and model groups exhibited decreased cell viability, lower mRNA and protein expression of SOCS1 SOCS3 and bcl-2 and reduced SOD and GSH levels but higher mRNA and protein expression levels of AK2, STAT3,Bax and caspase-3 as well as increased protein expression of P-JAK2, P-STAT3 and activated caspase-3 (c-caspase-3). Moreover, the MDA levels were up-regulated in the NC and model groups. In contrast, opposing trends were found in the AG490 group compared with the NC and model groups. Conclusion: These data demonstrate that inhibiting the SOCS1-JAK2-STAT3 signaling pathway can reduce the loss of nerve function and apoptosis of neuronal cells, which provides a new target for the clinical treatment of ischemic stroke.

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The Expression of the ER Stress Sensor GRP78/Bip Is a Target of R-CHOP and Bortezomib Treatments in DLBCL with Prognostic Value. A Rationale for the Use of Proteasome Inhibitors in DLBCL Patients.

Blood ◽

10.1182/blood.v114.22.3734.3734 ◽

2009 ◽

Vol 114 (22) ◽

pp. 3734-3734

Author(s):

Ana Mozos ◽

Gael Roue ◽

Armando López-Guillermo ◽

Pedro Jares ◽

Dolors Colomer ◽

...

Keyword(s):

Stress Response ◽

Combination Therapy ◽

Protein Expression ◽

Cell Viability ◽

Er Stress ◽

Cell Lines ◽

Standard Chemotherapy ◽

Er Stress Response ◽

Mrna And Protein Expression

Abstract Abstract 3734 Poster Board III-670 Introduction The endoplasmic reticulum (ER) stress response is an adaptive signaling pathway that controls cell survival. The activation of the transcription factor Xbp1 is a main event in this response and we have previously shown that Xbp1 activation in DLBCL is associated with aggressive clinical course (Balagué et al. Am J Pathol 2009, 174(6):2337-46). GRP78/Bip is a molecular chaperone that senses ER homeostasis and initiates the ER stress response. The expression of GRP78/Bip in DLBCL has never been addressed before. DLBCL patients are treated with standard doxorubicin-based chemotherapy such as CHOP. Since the introduction of rituximab, no other therapies have shown greater benefit in these patients. The ER stress response may be altered by conventional chemotherapy and it is well known that proteasome inhibition with bortezomib disrupts this response in myeloma. Whether Bip is affected in DLBCL treated with R-CHOP or bortezomib is unknown. Recent evidences suggest that the addition of bortezomib to standard chemotherapy would improve the survival of patients with the DLBCL preferentially of the ABC subtype (Duneleavy et al. Blood 2009, 113(24):6069-76) but the implication of the ER stress in this combination therapy remains unknown. Methods We analyze the mRNA and protein expression of Bip in DLBCL cell lines (OCI-Ly8, SUHDL4, SUDHL6 and SUDHL16) treated with Bortezomib, R-CHOP or their combination. Moreover, we also evaluated the effect of Bip silencing in the response to these treatments by using siRNA assay. Cell viability was analyzed by Annexin V. We also analyze the expression of Bip in 138 DLBCL patients by immunohistochemistry and in 63 of them by mRNA gene expression. Clinical data and follow up were available in 52 patients with a mean follow up of 2.9 years (range 0.02 to 6.7 years). Results All cell lines responded to R-CHOP treatment, with a decrease in cell viability ranging from 20% observed in OCI-LY8 cells to 45% in SUDHL6 cells. Moreover, in parallel with this response we detected a marked decrease in Bip expression both by protein and qPCR analysis. Bortezomib alone was less effective than R-CHOP, with 25% decrease in cell viability in the most sensitive SUDHL6 cells and less than 1% decrease in cell viability in the most resistant OCI-LY8 cells. Bortezomib increased both BiP mRNA and protein expression. The combination of bortezomib plus R-CHOP induces higher rates of cell death in all cell lines ranging between 35% decrease in cell viability in OCI-LY8 cells to 53.7% in SUDHL16 cells. This combination therapy led to an increase of Bip mRNA and protein expression but at much less extent than bortezomib alone. To confirm that BiP plays an antiapoptotic role in DLBCL we performed a siRNA assay for Bip in OCI-LY8 and SUDHL16 cell lines, corresponding to the most resistant and sensitive cell lines. After siRNA transfection, both cell lines reduced 60% to 80% Bip mRNA expression and became sensitive to bortezomib alone and more sensitive to the combination therapy. Bip expression was observed in 96 (69.5%) of newly diagnosed DLBCL tumors independently of Xbp1 activation and ABC subtype. Moreover high Bip mRNA expression (3-4 quartile) was predictive of worse survival (median overall survival 3.34 vs 1.9 years, p=0.048). Conclusions The ER-stress sensor Bip is expressed in DLBCL cell lines and primary tumors and it plays an important prosurvival role. Moreover Bip expression is a target of R-CHOP and bortezomib treatments being responsible for the primary resistance to bortezomib. In addition, the combination of R-CHOP plus bortezomib reduced Bip expression and decreased cell survival providing a rationale for the combination therapy in the clinical settings. Furthermore, high Bip expression is an adverse prognostic factor in newly diagnosed DLBCL patients treated with R-CHOP and may be used to select patients that would benefit from the addition of bortezomib to the standard chemotherapy. Disclosures: No relevant conflicts of interest to declare.

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SIRT3-SOD2-ROS pathway is involved in Linalool-induced glioma cell apoptotic death

Acta Biochimica Polonica ◽

10.18388/abp.2016_1438 ◽

2017 ◽

Vol 64 (2) ◽

Cited By ~ 16

Author(s):

Yanhao Cheng ◽

Chao Dai ◽

Jian Zhang

Keyword(s):

Cell Death ◽

Protein Expression ◽

Cell Viability ◽

Glioma Cell ◽

Apoptotic Cell ◽

Immunoblot Analysis ◽

Apoptotic Cell Death ◽

Dependent Manner ◽

Sod Activity ◽

Mrna And Protein Expression

Glioma is the most prevalent type of adult primary brain tumor and chemotherapy of glioma was limited by drug-resistance. Linalool is an acyclic monoterpene alcohol possessing various pharmacological activities. The present study was conducted to evaluate the effect of Linalool on glioma cell growth. The effect of Linalool on U87-MG cells was investigated and the results showed that Linalool significantly reduced cell viability in U87-MG cells in a concentration and time-dependent manner. In addition, exposure of cells to Linalool resulted in concentration-dependent increase of TUNEL-stained cells, indicating the occurrence of apoptotic cell death. Linalool decreased mitochondrial oxygen consumption rate, increased the expression of Bax and Bcl-2, reduced the expression of Bcl-2 and Bcl-xl, and increased the activities of caspase 3 and caspase 9, leading to increase of apoptosis. Linalool resulted in a concentration-dependent decrease of SOD activity but had no significant effect on the mRNA and protein expression of SOD2. Moreover, Linalool resulted in a significant increase of acetylated SOD2. The mRNA and protein expression of SIRT3 was significantly inhibited by Linalool. Immunoblot analysis showed that there were protein/protein interaction of SOD2 and SIRT3 in control U87-MG cells. Linalool treatment significantly decreased the interaction of SOD2 and SIRT3. Overexpression of SIRT3 significantly inhibited Linalool-induced increase of mitochondrial ROS level, apoptotic cell death and decrease of cell viability. In summary, we found that Linalool exhibited inhibitory effect on glioma cells through regulation of SIRT3-SOD2-ROS signaling.

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Alanyl-glutamine ameliorates lipopolysaccharide-induced inflammation and barrier function injury in bovine jejunum epithelial cells

Biochemistry and Cell Biology ◽

10.1139/bcb-2018-0320 ◽

2019 ◽

Vol 97 (6) ◽

pp. 670-680 ◽

Cited By ~ 4

Author(s):

Xianglun Zhang ◽

Xiuwen Tan ◽

Yifan Liu ◽

Wei You ◽

Guifen Liu ◽

...

Keyword(s):

Epithelial Cells ◽

Protein Expression ◽

Tight Junction ◽

Cell Viability ◽

Barrier Function ◽

Intestinal Inflammation ◽

Inflammatory Factors ◽

Tight Junction Proteins ◽

Mrna And Protein Expression ◽

Junction Proteins

The aim of this study was to investigate the effects of alanyl-glutamine (Ala-Gln) on the regulation of lipopolysaccharide (LPS)-induced inflammation and barrier function in bovine jejunum epithelial cells (BJECs). BJECs were exposed (or not) to 1 μg/mL LPS for 24 h to generate a pro-inflammatory model. The cells were then treated with different concentrations of Ala-Gln (0.25, 0.5, 1.0, 2.0, or 4.0 mmol/L) to detect any regulatory effects on the inflammation and barrier function of BJECs. LPS decreased cell viability and enhanced the production of the pro-inflammatory cytokines interleukin (IL)-6 and IL-8. LPS induced inflammation and damaged the barrier function of BJECs, as evidenced by up-regulated mRNA and protein expression of inflammatory factors and down-regulated expression of tight junction proteins. Conversely, Ala-Gln rescued the decrease in cell viability and prevented the accumulation of ILs after LPS exposure by reducing the mRNA and protein expression levels of inflammatory factors. In addition, Ala-Gln induced the mRNA and protein expression of multiple tight junction proteins, and thus reconstituted the barrier function of BJECs. In conclusion, Ala-Gln attenuates injury from inflammation and repairs damaged intestinal barrier induced with LPS, suggesting its potential as a therapeutic agent against intestinal inflammation in mammals.

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Silibinin Inhibits TGF-β-induced MMP-2 and MMP-9 Through Smad Signaling Pathway in Colorectal Cancer HT-29 Cells

Basic & Clinical Cancer Research ◽

10.18502/bccr.v12i2.5752 ◽

2021 ◽

Author(s):

Zahra Zare ◽

Tina Nayerpour dizaj ◽

Armaghan Lohrasbi ◽

Zakieh Sadat Sheikhalishahi ◽

Amirhooman Asadi ◽

...

Keyword(s):

Colorectal Cancer ◽

Protein Expression ◽

Cell Viability ◽

Cancer Cells ◽

Cell Line ◽

Dependent Manner ◽

Smad2 Phosphorylation ◽

Mrna And Protein Expression ◽

Dose Dependent ◽

Ht 29

Background: Metastasis of cancer cells is the primary responsible for death in patients with colorectal cancer (CRC). Transforming growth factor-β (TGF-β)-induced matrix metalloproteinases (MMPs) are essential for the metastasis process. Silibinin is a natural compound extracted from the Silybum marianum that exhibits anti-neoplastic activity in cancer cell lines. In this study, we evaluated the effects of silibinin on MMP-2 and MMP-9 induced by TGF-β in human HT-29 CRC cell line and the potential mechanism underlying the effects. Methods: The present in vitro study was done on the HT-29 cell line. The HT-29 cell line was cultured in RPMI1640 and exposed to TGF- β (5 ng/ml) in the absence and presence of different concentrations of silibinin (10, 25, 50, and 100 μM). The effect of silibinin on HT-29 cell viability was measured with the MTT assay. A real-time polymerase chain reaction (Real-Time PCR) determined the relative mRNA expression of MMP-2 and MMP-9. Western blotting was employed to examine MMP-2 and MMP 9 protein expression and Smad2 phosphorylation. Results: Silibinin inhibits cell viability of HT-29 cell line at 24 hours in a dose-dependent manner. TGF-β increased the mRNA and protein expression of MMP-2, MMP-9, and phosphorylated Smad2 compared to controls. Pharmacological inhibition with silibinin markedly blocked TGF-β–induced MMP-2 and MMP-9 mRNA and protein expression and Smad2 phosphorylation. Conclusion: Silibinin decreased the cell viability of HT-29 cancer cells in a dose-dependent manner. Silibinin also inhibited TGF-β-stimulated MMP-2 and MMP-9 expression in HT-29 cells, possibly mediated with the Smad2 signaling pathway.

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Tert-Butylhydroquinone Prevents Oxidative Stress-Mediated Apoptosis and Extracellular Matrix Degradation in Rat Chondrocytes

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2021/1905995 ◽

2021 ◽

Vol 2021 ◽

pp. 1-12

Author(s):

Bo Yang ◽

Haisheng Huang ◽

Qisong He ◽

Wei Lu ◽

Lu Zheng ◽

...

Keyword(s):

Oxidative Stress ◽

Extracellular Matrix ◽

Matrix Metalloproteinase ◽

Protein Expression ◽

Cell Viability ◽

Cell Counting ◽

Expression Levels ◽

Extracellular Matrix Components ◽

Mrna And Protein Expression

Oxidative stress-induced chondrocyte apoptosis and degradation of the extracellular matrix (ECM) play an important role in the progression of osteoarthritis (OA). In addition, tert-butylhydroquinone (TBHQ) is an activator of the nuclear factor erythroid derived-2-related factor 2 (Nrf2). The present study aimed to determine the effectiveness of TBHQ in preventing the apoptosis of chondrocytes and degradation of the extracellular matrix, induced by oxidative stress, in vitro. Therefore, rat chondrocytes were exposed to 20 μM tert-butyl hydroperoxide (TBHP) for 24 h to establish an oxidative damage model, in vitro. Thereafter, cell viability was evaluated using the Cell Counting Kit-8 assay. Moreover, the level of ROS was determined through 2′,7′-dichlorofluorescein diacetate staining. The mitochondrial membrane potential of chondrocytes was also measured using JC-1. Furthermore, cell apoptosis was assessed through Annexin V-fluorescein isothiocyanate/propidium iodide staining. The study also performed Western blotting and qPCR to evaluate the expression of extracellular matrix components, matrix catabolic enzymes, and changes in signalling pathways. The results showed that 2.5 and 5 μM of TBHQ reduced the TBHP-induced generation of excessive ROS and improved cell viability. Additionally, 2.5 and 5 μM of TBHQ prevented mitochondrial damage and apoptosis in rat chondrocytes. Treatment with TBHQ also increased the mRNA and protein expression levels of aggrecan and collagen II. However, TBHQ reduced the mRNA and protein expression levels of matrix metalloproteinase 3 (MMP3) and matrix metalloproteinase 13 (MMP13) in rat chondrocytes. In addition, treatment with TBHQ enhanced the protein expression levels of Nrf2, NADPH quinone oxidoreductase 1 (NQO-1), and hemeoxygenase-1 (HO-1) in rat chondrocytes. The current study showed that TBHQ was not only effective in protecting against TBHP-induced oxidative stress but also inhibited the apoptosis of rat chondrocytes and degradation of the ECM by activating the Nrf2 pathway. The results therefore suggest that TBHQ holds potential for use in the treatment of OA.

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Downregulation of CYP39A1 Serves as a Novel Biomarker in Hepatocellular Carcinoma with Worse Clinical Outcome

Oxidative Medicine and Cellular Longevity ◽

10.1155/2021/5175581 ◽

2021 ◽

Vol 2021 ◽

pp. 1-18

Author(s):

Dan Li ◽

Tao Yu ◽

Junjie Hu ◽

Jie Wu ◽

Shi Feng ◽

...

Keyword(s):

Hepatocellular Carcinoma ◽

Overall Survival ◽

Cell Growth ◽

Protein Expression ◽

Cell Viability ◽

Suppressor Gene ◽

Metabolic Enzyme ◽

Poor Overall Survival ◽

Mrna And Protein Expression ◽

Growth Changes

Background. CYP39A1 is a poorly characterized metabolic enzyme that has been investigated in a few tumors. However, the role of CYP39A1 in hepatocellular carcinoma (HCC) has not yet been clarified. In this study, the expression and clinical significance of CYP39A1 in HCC were explored. Methods. CYP39A1 protein expression was detected in Akt/c-Met-induced HCC mice and 14 paired fresh HCC samples as well as another 159 HCC and matched noncancerous tissues. Meanwhile, the mRNA expression was analyzed by GEO and TCGA analysis and validated in 14 paired fresh HCC tissues. Furthermore, the relationships between CYP39A1 expression and clinicopathologic features as well as prognosis were analyzed. HCC cell growth changes were analyzed by cell viability assays after CYP39A1 overexpression and then validated after CYP39A1 knockout by DepMap database analysis. Results. CYP39A1 protein expression was lower expressed in HCC mouse models, and its mRNA and protein expression were also downregulated in HCC compared with noncancerous liver tissues. Higher CYP39A1 expression was associated with well differentiation. Moreover, survival analysis indicated that lower CYP39A1 expression was associated with poorer overall survival. In addition, HepG2 and SMMC-7721 cell viability were inhibited after CYP39A1 overexpression. Genome-wide CRISPR/Cas9 proliferation screening indicated that knockout of CYP39A1 could promote HCC cell growth. Likewise, p-NF-κB and Nrf2 were suppressed after CYP39A1 overexpression. It is worth mentioning that total bile acid, total bilirubin, and direct bilirubin were significantly increased in the patients with low CYP39A1 expression. Conclusions. Downregulation of CYP39A1 is associated with HCC carcinogenesis, tumor differentiation, and poor overall survival, suggesting that CYP39A1 may serve as a tumor suppressor gene and novel biomarker for HCC patients.

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Biatractylolide Modulates PI3K-Akt-GSK3β-Dependent Pathways to Protect against Glutamate-Induced Cell Damage in PC12 and SH-SY5Y Cells

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2017/1291458 ◽

2017 ◽

Vol 2017 ◽

pp. 1-9 ◽

Cited By ~ 3

Author(s):

Li Zhu ◽

Ning Ning ◽

Yu Li ◽

Qiu-Fang Zhang ◽

Yong-Chao Xie ◽

...

Keyword(s):

Protein Expression ◽

Inhibitory Concentration ◽

Antioxidant Activities ◽

Cell Damage ◽

Neuroprotective Effect ◽

Neuroblastoma Cell ◽

Neuroblastoma Cell Line ◽

Pharmacological Activities ◽

Adrenal Pheochromocytoma ◽

Atractylodes Macrocephala

Biatractylolide, isolated from the ethyl acetate extract of Atractylodes macrocephala, has shown various pharmacological activities such as antitumor and antioxidant activities. In this work, we aim to study the protective effect of biatractylolide on glutamate-induced rat adrenal pheochromocytoma cell (PC12) and human bone marrow neuroblastoma cell line (SH-SY5Y) injury and preliminarily explore its mechanism. The results showed that glutamate was cytotoxic with an inhibitory concentration 50% (IC50) of 8.5 mM in PC12 and 10 mM in SH-SY5Y cells. In this work, the preincubation with biatractylolide (10, 15, and 20 μM) observably improved cell viability, inhibited the apoptosis of cells induced by glutamate, and reduced the activity of LDH. AO staining revealed that apoptosis of cells was decreased. Additionally, the results of western blotting manifested that pretreatment with biatractylolide could downregulate GSK3β protein expression and upregulate p-Akt protein expression, thereby protecting PC12 and SH-SY5Y cells from injury. All these findings indicate that biatractylolide has a neuroprotective effect on glutamate-induced injury in PC12 and SH-SY5Y cells through a mechanism of the PI3K-Akt-GSK3β-dependent pathways.

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Effect of Huangkui on mouse podocytes under high glucose environment

Boletin Latinoamericano y del Caribe de Plantas Medicinales y Aromaticas ◽

10.37360/blacpma.21.20.5.38 ◽

2021 ◽

Vol 20 (5) ◽

pp. 515-523

Author(s):

Chun-Li Yu ◽

◽

Xiu-Li Fei ◽

Ding-Zhong Tang ◽

Kun Liu ◽

...

Keyword(s):

Cell Cycle ◽

Flow Cytometry ◽

Diabetic Nephropathy ◽

Protein Expression ◽

Cell Viability ◽

Mtt Assay ◽

High Glucose ◽

Group Iv ◽

Normal Glucose ◽

Mrna And Protein Expression

To explore a new underlying molecular mechanism of Huangkui Extract Powder (HKEP) in the alleviation of diabetic nephropathy (DN). Murine immortalized podocytes were divided into (i) normal glucose (NG, 5.6 mM), (ii) NG + HKEP (0.45 g/L), (iii) HG, and (iv) HG + HKEP (0.45 g/L) groups. MTT assay and flow cytometry were used to detect the podocyte proliferation, apoptosis and cell cycle. Cell viability was inhibited, and apoptosis increased in (iii) HG group compared with (i) NG group (p<0.05). mRNA and protein expression of nephrin and podocin significantly decreased in (iii) HG group compared with (i) NG group (p<0.05). When compared with (iii) HG group, (iv) HG + HKEP group had higher cell viability, lower apoptotic rate and higher mRNA and protein expression of nephrin and podocin (p<0.05). HKEP can attenuate HG-induced podocyte damage, which may be one of the mechanisms of HKEP for attenuating DN.

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