Notoginsenoside R1 protects oxygen and glucose deprivation‐induced injury by upregulation of miR‐21 in cardiomyocytes

Liu, Zengjia; Wang, Haiyang; Hou, Guoliang; Cao, Honglei; Zhao, Yan; Yang, Baofa

doi:10.1002/jcb.28194

Cited by 20 publications

(26 citation statements)

References 48 publications

(106 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…For example, the expression of miR‐133b was observed to be declined in peripheral blood of patients with VMC and overexpression of miR‐133b inhibited the proliferation of cardiomyocytes and the production of cytokines interleukin 6 (IL‐6) and tumor necrosis factor (TNF)‐α, thus alleviating CVB3 infection‐induced myocardial injuries (Zhang et al, ). Besides that, Liu et al reported that Notoginsenoside R1 protected against oxygen–glucose deprivation‐induced cardiomyocytes damage by rescuing cell viability and suppressing cell apoptosis through up‐regulating miR‐21 expression (Liu et al, ). In addition, Goldberg and his colleagues revealed that the expression of cardiac‐ and inflammatory‐related miR‐21 was remarkably enhanced during the acute phase (Goldberg et al, ).…”

Section: Introductionmentioning

confidence: 99%

Retracted: Baicalin relieves lipopolysaccharide‐evoked inflammatory injury through regulation of miR‐21 in H9c2 cells

Liu

Wang

Zhao

2020

Phytotherapy Research

View full text Add to dashboard Cite

Myocarditis is a common heart disease which lacks effective treatment till now.Baicalin possesses plenty of activities, including anti-inflammation. In this investigation, we attempted to investigate the influences of Baicalin on Lipopolysaccharide (LPS)-evoked H9c2 cells.Cells viability, apoptosis, and expressions of apoptosisassociated proteins were, respectively, measured utilizing CCK-8 assay, flow cytometry and western blot. The levels of IL-6 and TNF-α were detected through enzyme-linked immunosorbent assay, western blot and qRT-PCR. miR-21 expression was detected through qRT-PCR and was silenced using cell transfection. The expressions of NF-κB and PDCD4/JNK pathways related proteins were measured through western blot. We found that LPS stimulation induced cell apoptosis and upregulation of IL-6 and TNF-α. Baicalin treatment effectively suppressed LPS-induced inflammation and apoptosis. The NF-κB and PDCD4/JNK pathways were blocked by Baicalin. Additionally, the enhanced expression of miR-21 triggered by LPS was further elevated by Baicalin. Further study revealed that the inhibiting effects of Baicalin on LPS-evoked injury were largely attenuated by knockdown of miR-21. Moreover, the associated NF-κB and JNK pathways, which were suppressed by Baicalin treatment, were then activated by knockdown of miR-21. Our present study revealed that Baicalin alleviated LPS-evoked inflammatory injury via suppressing the NF-κB and PDCD4/JNK pathways through regulating miR-21 expression. K E Y W O R D S apoptosis, Baicalin, inflammatory injury, MiR-21, myocarditis

show abstract

Section: Introductionmentioning

confidence: 99%

Retracted: Baicalin relieves lipopolysaccharide‐evoked inflammatory injury through regulation of miR‐21 in H9c2 cells

Liu

Wang

Zhao

2020

Phytotherapy Research

View full text Add to dashboard Cite

show abstract

“…Then secondary screening was conducted by reading the full text of the remaining 52 studies; 28 studies were excluded because of at least one of the following reasons: 1) failed to obtain full text; 2) non-NGR1 treatment; 3) inappropriate cell model; 4) compared with Chinese herbal medicine or herbal active compounds; 5) no control group; 6) master dissertation or doctoral dissertation; and 7) no available data. Finally, 11 papers (He et al, 2014; Meng et al, 2014; Wan et al, 2015; Yu et al, 2016; Zhou et al, 2016; Wang et al, 2016; Hou et al, 2017; Wang et al, 2017; Zhou et al, 2017; Liu et al, 2019; Tu et al, 2018) were included ( Figure 2B ).…”

Section: Resultsmentioning

confidence: 99%

“…Eleven studies involved in cell experiments between 2014 and 2018 were included, of which four studies (Wan et al, 2015; Zhou et al, 2016; Hou et al, 2017; Zhou et al, 2017) were published in Chinese and seven studies (He et al, 2014; Meng et al, 2014; Wang et al, 2016; Yu et al, 2016; Wang et al, 2017; Liu et al, 2019; Tu et al, 2018) in English. Wistar Suckling mice cardiomyocytes were used in three studies (Wan et al, 2015; Zhou et al, 2016; Zhou et al, 2017), and embryonic cardiomyoblast-derived cardiomyocytes (H9C2) of rat were used in two studies (He et al, 2014; Yu et al, 2016).…”

Section: Resultsmentioning

confidence: 99%

“…The dosages of NGR1 were 10 μmol/L in two studies (Zhou et al, 2016; Zhou et al, 2017), 20 μmol/L in one study (Yu et al, 2016), and 100 μmol/L in two studies (He et al, 2014; Wan et al, 2015). Cell viability and TUNEL-positive rate were used as outcome measures in six studies (He et al, 2014; Wan et al, 2015; Zhou et al, 2016; Yu et al, 2016; Zhou et al, 2017; Liu et al, 2019), LDH in seven studies (He et al, 2014; Meng et al, 2014; Wang et al, 2016; Zhou et al, 2016; Zhou et al, 2017; Hou et al, 2017; Tu et al, 2018), SOD in three studies (Wan et al, 2015; Zhou et al, 2016; Zhou et al, 2017), and MDA in four studies (Meng et al, 2014; Wan et al, 2015; Zhou et al, 2016; Zhou et al, 2017). The detailed characteristics of the included studies were generalized in Table 2 .…”

Section: Resultsmentioning

confidence: 99%

See 1 more Smart Citation

Notoginsenoside R1 for Organs Ischemia/Reperfusion Injury: A Preclinical Systematic Review

et al. 2019

View full text Add to dashboard Cite

Notoginsenoside R1 (NGR1) exerts pharmacological actions for a variety of diseases such as myocardial infarction, ischemic stroke, acute renal injury, and intestinal injury. Here, we conducted a preclinical systematic review of NGR1 for ischemia reperfusion (I/R) injury. Eight databases were searched from their inception to February 23rd, 2019; Review Manager 5.3 was applied for data analysis. CAMARADES 10-item checklist and cell 10-item checklist were used to evaluate the methodological quality. Twenty-five studies with 304 animals and 124 cells were selected. Scores of the risk of bias in animal studies ranged from 3 to 8, and the cell studies ranged from 3 to 5. NGR1 had significant effects on decreasing myocardial infarct size in myocardial I/R injury, decreasing cerebral infarction volume and neurologic deficit score in cerebral I/R injury, decreasing serum creatinine in renal I/R injury, and decreasing Park/Chiu score in intestinal I/R injury compared with controls (all P < 0.05 or P < 0.01). The multiple organ protection of NGR1 after I/R injury is mainly through the mechanisms of antioxidant, anti-apoptosis, and anti-inflammatory, promoting angiogenesis and improving energy metabolism. The findings showed the organ protection effect of NGR1 after I/R injury, and NGR1 can potentially become a novel drug candidate for ischemic diseases. Further translation studies are needed.

show abstract

“…notoginsenoside r1 (nTr1) is the main functional ingredient derived from Panax notoginseng, a traditional chinese herbal medicine (8). Previous studies have shown that NTR1 has cardio-protective and neuro-protective effects (9)(10)(11). in addition, nTr1 has the function of promoting osteoblastogenesis through regulating runt-related transcription factor 2 (runX2) and activating the Smad-independent signaling pathway p38/MAPK (12).…”

Section: Introductionmentioning

confidence: 99%

Notoginsenoside R1 promotes differentiation of human alveolar osteoblasts in inflammatory microenvironment through inhibiting NF‑κB pathway and activating Wnt/β‑catenin pathway

Huang

2020

Mol Med Rep

View full text Add to dashboard Cite

alveolar bone is vital for dental implantation and periodontal treatment. notoginsenoside r1 (nTr1) may promote the differentiation of human alveolar osteoblasts (HaoBs), but the underlying molecular mechanisms remain unclear. The present study investigated the pro-differentiation function of NTR1 on HAOBs in order to find new methods of dental treatment. HAOBs were surgically obtained from dental patients and the cells were isolated, cultured and identified under an inverted phase contrast microscope. The cells were treated with different concentrations of NTR1 alone or further stimulated by TnF-α. an alkaline phosphate (alP) activity assay and alizarin red staining were performed to detect alP activity and mineralization of the cells, respectively. Cell viability was assayed using an MTT assay. The expressions of osteogenic-related factors and the factors associated with the NF-κB and Wnt/β-catenin pathways were examined by reverse transcription-quantitative PCR or western blot analysis. Successfully passaged HaoBs presented blue granules and red calcium deposits after staining. The viability of HAOBs was unchanged following treatment with NTR1 at ≤20 µmol/l and/or TnF-α, but slightly reduced by 40 µmol/l nTr1. TnF-α-induced decreases of calcium nodules and ALP activity were decreased by NTR1 in HAOBs. TNF-α also regulated the expressions of runt-related transcription factor 2, osteopontin (oPn), osteocalcin (ocn), p50, phosphorylated p65, aXin2, dickkopf-related protein 1 and β-catenin, while the regulatory effect was reversed by NTR1. NTR1 promoted the differentiation of HaoBs in the TnF-α-induced inflammatory microenvironment through inhibiting the nF-κB pathway and activating the Wnt/β-catenin pathway.

show abstract

Notoginsenoside R1 protects oxygen and glucose deprivation‐induced injury by upregulation of miR‐21 in cardiomyocytes

Cited by 20 publications

References 48 publications

Retracted: Baicalin relieves lipopolysaccharide‐evoked inflammatory injury through regulation of miR‐21 in H9c2 cells

Retracted: Baicalin relieves lipopolysaccharide‐evoked inflammatory injury through regulation of miR‐21 in H9c2 cells

Notoginsenoside R1 for Organs Ischemia/Reperfusion Injury: A Preclinical Systematic Review

Notoginsenoside R1 promotes differentiation of human alveolar osteoblasts in inflammatory microenvironment through inhibiting NF‑κB pathway and activating Wnt/β‑catenin pathway

Contact Info

Product

Resources

About