Investigation of the cytotoxicity, antioxidative and immune-modulatory effects of Ligusticum porteri (Osha) root extract on human peripheral blood lymphocytes

Nguyen, Khanh; Sparks, Jean; Omoruyi, Felix O.

doi:10.1016/s2095-4964(16)60280-7

Cited by 12 publications

(10 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A previous report demonstrated an elevation in KCNQ1OT1 expression levels in cataract tissue specimens ( 30 ). Ectogenic TGF-β2 is widely used in cataract-associated research, particularly in LEC-associated EMT ( 16 , 31 , 32 ). In the same manner, the present study employed TGF-β2-treated SRA01/04 cells to generate a cataract cell model.…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA KCNQ1OT1 promotes proliferation and epithelial‑mesenchymal transition by regulation of SMAD4 expression in lens epithelial cells

Chen

et al. 2018

Mol Med Report

View full text Add to dashboard Cite

Long noncoding RNAs (lncRNAs) are associated with various diseases including cataracts. The role of lncRNA potassium voltage-gated channel subfamily Q member 1 opposite strand/antisense transcript 1 (KCNQ1OT1) on lens epithelial cell (LEC) proliferation and epithelial-mesenchymal transition (EMT) in cataracts disease remains unclear. In the present study, KCNQ1OT1 and mothers against decapentaplegic homolog (SMAD)4 expression levels were upregulated in human cataract lens posterior capsular samples and in transforming growth factor (TGF)-β2-treated SRA01/04 cells, as demonstrated by reverse transcription-quantitative polymerase chain reaction, immunohistochemical staining and western blot analyses. A further loss of function test revealed that suppression of KCNQ1OT1 inhibited the proliferation and EMT of TGF-β2-treated SRA01/04 cells. Additionally, the present study reported that increase and decrease of KCNQ1OT1 regulated SMAD4 expression, which indicated that SMAD4 may be a downstream gene of KCNQ1OT1. Finally, a constructed SMAD4 RNA interference experiment confirmed that the function of KCNQ1OT1 was to act on LEC proliferation and EMT, and this was achieved via the SMAD4 signaling pathway. The findings of the present study may provide a novel target for molecular therapy of cataracts disease.

show abstract

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA KCNQ1OT1 promotes proliferation and epithelial‑mesenchymal transition by regulation of SMAD4 expression in lens epithelial cells

Chen

et al. 2018

Mol Med Report

View full text Add to dashboard Cite

show abstract

“…In recent years, a growing number of studies has found that TCMs have immunomodulatory effect ( 32 , 33 ). The aim of the present study was to further explore the efficacy and mechanism of BSNXD as a potential osteoimmunological regulator in the therapy of PMO.…”

Section: Introductionmentioning

confidence: 99%

Bu‑Shen‑Ning‑Xin decoction suppresses osteoclastogenesis by modulating RANKL/OPG imbalance in the CD4+ T lymphocytes of ovariectomized mice

Zhang

Tang

et al. 2018

Int J Mol Med

View full text Add to dashboard Cite

Postmenopausal osteoporosis (PMO) has been recognized as an inflammatory condition. CD4+ T cells serve a key role in the interaction between bone metabolism and the immune system. Bu-Shen-Ning-Xin decoction (BSNXD), a traditional Chinese medicine, has been ultilized as a remedy for PMO. In the present study, the aim was to investigate the immune modulatory effects of BSNXD on CD4+ T cells, receptor activation of nuclear factor κB ligand (RANKL)/osteoprotegerin (OPG) imbalance, skeletal parameters and osteoclastogenesis. Ovariectomized (OVX) mice were treated with a series of concentrations of BSNXD and then autopsied. The bone phenotype was analyzed by micro computed tomography. CD4+ T cells were isolated and their percentage was measured using flow cytometry (FCM). RANKL and OPG expression by the CD4+ T cells at the transcriptional and translational levels were quantified by reverse transcription-quantitative polymerase chain reaction, ELISA and FCM. CD4+ T cells were cultured with blood serum derived from BSNXD-treated OVX mice (BSNXD-derived serum) and the apoptosis rate was quantified by FCM. CD4+ T cells were co-cultured with bone marrow-derived macrophages and exposed to BSNXD-derived serum to whether CD4+ T cells are involved in BSNXD-modulated osteoclastogenesis and the results were quantified via tartrate-resistant acid phosphatase staining. The results revealed that BSNXD ameliorated OVX-induced bone loss, prevented the expansion of CD4+ T cells and restored the RANKL/OPG imbalance in the CD4+ T cells of OVX mice. In vitro, BSNXD-derived serum promoted the apoptosis of CD4+ T cells. The co-culture system demonstrated that CD4+ T cells from OVX mice increase osteoclastogenesis, while this effect was suppressed by BSNXD administration. The findings of the study collectively suggest that BSNXD exerts an immunoprotective effect on the bone phenotype of OVX mice by ameliorating RANKL/OPG imbalance in CD4+ T cells and attenuating osteoclastogenesis.

show abstract

“…Cell proliferation was assessed using a Cell Counting Kit-8 (CCK-8, Dojindo, Japan) according to the published article [ 6 ]. HT-29 cells in the logarithmic phase were harvested and resuspended at a final concentration of 5 × 10 4 cells/ml, then were seeded into 96-well tissue plates with 100 μl of cell solution each well in triplicate.…”

Section: Methodsmentioning

confidence: 99%

Insulin promotes progression of colon cancer by upregulation of ACAT1

et al. 2018

View full text Add to dashboard Cite

BackgroundInsulin resistant and the progression of cancer is closely related. The aim of this study was to investigate the effect of insulin on the proliferation and migration of colon cancer cells and its underlying mechanism.MethodsColon carcinoma tissues from the 80 cases of colon cancer patients were collected. Immunohistochemistry was used to detect the expression of acyl coenzyme A: cholesterol acyltransferase1 (ACAT1), and we analyzed the correlation between hyperglycemia and ACAT1, hyperglycemia and metastasis. CCK8 assay and transwell assay were used to investigate the effect of different concentrations of insulin and ACAT1siRNA on human colon cancer cell line HT-29. ACAT1 mRNA expression and protein level in HT-29 cells were determined by real-time quantitative PCR and western blotting, respectively.ResultsBiopsies from patients with colon carcinoma showed hyperglycemia links ACAT1, lymph nodes metastasis and distant metastasis. Insulin markedly promoted cell proliferation and migration in human colon cancer HT-29 cells. Moreover, ACAT1mRNA expression and protein level were increased by insulin. ACAT1siRNA resulted in a complete inhibition of the ACAT1 mRNA expression. Consequently insulin-triggered cell proliferation and migration on colon cancer cells were inhibited.ConclusionThe progression of colon cancer has a positive correlation with hyperinsulinemia. Insulin-triggered cell proliferation and metastatic effects on colorectal cancer cells are mediated by ACAT1. Therefore, insulin could promote colon cancer progression by upregulation of ACAT1, which maybe is a potential therapeutic target for colon cancer.

show abstract

Investigation of the cytotoxicity, antioxidative and immune-modulatory effects of Ligusticum porteri (Osha) root extract on human peripheral blood lymphocytes

Cited by 12 publications

References 24 publications

Long noncoding RNA KCNQ1OT1 promotes proliferation and epithelial‑mesenchymal transition by regulation of SMAD4 expression in lens epithelial cells

Long noncoding RNA KCNQ1OT1 promotes proliferation and epithelial‑mesenchymal transition by regulation of SMAD4 expression in lens epithelial cells

Bu‑Shen‑Ning‑Xin decoction suppresses osteoclastogenesis by modulating RANKL/OPG imbalance in the CD4+ T lymphocytes of ovariectomized mice

Insulin promotes progression of colon cancer by upregulation of ACAT1

Contact Info

Product

Resources

About