Puerarin inhibits non-small cell lung cancer cell growth via the induction of apoptosis

Hu, Yefang; Li, Xi; Li, Gang; Liang, Siting; Jiang, Yan

doi:10.3892/or.2018.6234

Cited by 25 publications

(22 citation statements)

References 27 publications

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“…PR has been reported to possess anti-oxidative, hypotensive and hypoglycaemic activities [13][14][15]. Prior studies have demonstrated that PR exerted protective effects on diabetic kidney injury, heart failure, diabetic cardiomyopathy, cardiac fibroblast proliferation, skeletal muscle energy metabolism and liver lipid metabolism [16][17][18][19][20][21][22]. The hypoglycaemic effect of PR on diabetes mellitus was confirmed by previous studies [15,23,24].…”

Section: Discussionmentioning

confidence: 75%

Caspase/AIF/apoptosis pathway: a new target of puerarin for diabetes mellitus therapy

Tao

et al. 2019

Mol Biol Rep

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Pancreatic β cell damage is one of the crucial factors responsible for the development of type 2 diabetes mellitus (T2DM). Previous studies have suggested that puerarin (PR) could regulate the activities of the mitochondrial respiratory chain complex in diabetic nephropathy (DN); however, whether PR can inhibit pancreatic β-cell apoptosis in T2DM remains to be elucidated. In the present study, T2DM mice induced by high-fat diet and streptozotocin (STZ) injection were used as a working model to investigate the mechanism of PR on pancreatic β cell apoptosis. The results showed that PR decreased the serum fasting blood glucose (FBG), total cholesterol (TC), triglyceride (TG) and low-density lipoprotein (LDL) levels but significantly increased the fasting blood insulin (FINS) and high-density lipoprotein (HDL) levels. Furthermore, decreased caspase-3, 8, 9 and apoptosis-inducing factor (AIF) proteins in the pancreas were detected by Western blot analysis. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling (TUNEL) staining demonstrated that the pancreatic β cell apoptosis was inhibited by PR. Furthermore, PR improved the histopathological changes in pancreatic tissue in T2DM mice. Collectively, the data show that PR can protect the β cells from apoptotic death in a mouse model of T2DM through regulating the expression of apoptosis-related protein-AIF and caspase family proteins.

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Section: Discussionmentioning

confidence: 75%

Caspase/AIF/apoptosis pathway: a new target of puerarin for diabetes mellitus therapy

Tao

et al. 2019

Mol Biol Rep

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“…Puerarin (20 µM) also inhibited the growth of NSCLC (NCI-H441) cells by inducing apoptosis and autophagy. The mechanism of action involved the inactivation of PI3K/Akt and ERK pathways [185,336].…”

Section: Isoflavonesmentioning

confidence: 99%

Polyphenol-Mediated Autophagy in Cancer: Evidence of In Vitro and In Vivo Studies

Benvenuto

Albonici

Focaccetti

et al. 2020

IJMS

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One of the hallmarks of cellular transformation is the altered mechanism of cell death. There are three main types of cell death, characterized by different morphological and biochemical features, namely apoptosis (type I), autophagic cell death (type II) and necrosis (type III). Autophagy, or self-eating, is a tightly regulated process involved in stress responses, and it is a lysosomal degradation process. The role of autophagy in cancer is controversial and has been associated with both the induction and the inhibition of tumor growth. Autophagy can exert tumor suppression through the degradation of oncogenic proteins, suppression of inflammation, chronic tissue damage and ultimately by preventing mutations and genetic instability. On the other hand, tumor cells activate autophagy for survival in cellular stress conditions. Thus, autophagy modulation could represent a promising therapeutic strategy for cancer. Several studies have shown that polyphenols, natural compounds found in foods and beverages of plant origin, can efficiently modulate autophagy in several types of cancer. In this review, we summarize the current knowledge on the effects of polyphenols on autophagy, highlighting the conceptual benefits or drawbacks and subtle cell-specific effects of polyphenols for envisioning future therapies employing polyphenols as chemoadjuvants.

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“…However, the effects of PUR on apoptosis are different among various kinds of cells. For example, PUR could suppress apoptosis and reduce myocardial injury induced by ischemia [24], while promoting apoptosis in cancer cells [25,26]. Thus, the specific effects of PUR on the fate of NPMSCs in the development of IDD need to be further clarified.…”

Section: Introductionmentioning

confidence: 99%

“…Consisting of the findings in vitro, PUR applied to a rat model was also found to alleviate deformation and structure disorder in vivo with significant activation of p-Akt. However, a few researches reported the anticancerous effect of PUR by inducing apoptosis through inhibiting the PI3K/Akt signaling pathway [26,56,57]. Since most of the conflicting studies were performed on cancer cell lines, it was curious that PUR could perform completely contrary effects on apoptosis in different cell lines.…”

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confidence: 99%

Puerarin Relieved Compression-Induced Apoptosis and Mitochondrial Dysfunction in Human Nucleus Pulposus Mesenchymal Stem Cells via the PI3K/Akt Pathway

Huang

Peng

et al. 2020

Stem Cells International

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Puerarin (PUR), an 8-C-glucoside of daidzein extracted from Pueraria plants, is closely related to autophagy, reduced reactive oxygen species (ROS) production, and anti-inflammatory effects, but its effects on human nucleus pulposus mesenchymal stem cells (NPMSCs) have not yet been identified. In this study, NPMSCs were cultured in a compression apparatus to simulate the microenvironment of the intervertebral disc under controlled pressure (1.0 MPa), and we found that cell viability was decreased and apoptosis level was gradually increased as compression duration was prolonged. After PUR administration, apoptosis level evaluated by flow cytometry and caspase-3 activity was remitted, and protein levels of Bas as well as cleaved caspase-3 were decreased, while elevated Bcl-2 level was identified. Moreover, ATP production detection, ROS, and JC-1 fluorography as well as quantitative analysis suggested that PUR could attenuate intercellular ROS accumulation and mitochondrial dysfunction. Besides, the rat tail compression model was utilized, which indicated that PUR could restore impaired nucleus pulposus degeneration induced by compression. The PI3K/Akt pathway was identified to be deactivated after compression stimulation by western blot, and PUR could rescue the phosphorylation of Akt, thus reactivating the pathway. The effects of PUR, such as antiapoptosis, cell viability restoration, antioxidation, and mitochondrial maintenance, were all counteracted by application of the PI3K/Akt pathway inhibitor (LY294002). Summarily, PUR could alleviate compression-induced apoptosis and cell death of human NPMSCs in vitro as well as on the rat compression model and maintain intracellular homeostasis by stabilizing mitochondrial membrane potential and attenuating ROS accumulation through activating the PI3K/Akt pathway.

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Puerarin inhibits non-small cell lung cancer cell growth via the induction of apoptosis

Cited by 25 publications

References 27 publications

Caspase/AIF/apoptosis pathway: a new target of puerarin for diabetes mellitus therapy

Caspase/AIF/apoptosis pathway: a new target of puerarin for diabetes mellitus therapy

Polyphenol-Mediated Autophagy in Cancer: Evidence of In Vitro and In Vivo Studies

Puerarin Relieved Compression-Induced Apoptosis and Mitochondrial Dysfunction in Human Nucleus Pulposus Mesenchymal Stem Cells via the PI3K/Akt Pathway

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