Morin hydrate ameliorates cisplatin-induced ER stress, inflammation and autophagy in HEK-293 cells and mice kidney via PARP-1 regulation

Singh, Mahendra; Chauhan, Anil Kumar; Kang, Sun Chul

doi:10.1016/j.intimp.2018.01.031

Cited by 65 publications

(37 citation statements)

References 42 publications

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“…These doses could clinically be achievable (35). Previous studies have demonstrated that a low dose of morin reduced the cisplatin-induced toxicity of 293 cells and mouse kidney cells (36) and showed neuroprotective effect of morin in lead acetate-induced apoptosis in the rat brain (37). The induction of tumor cell apoptosis in response to morin at higher doses has been further confirmed in our current data.…”

Section: Discussionsupporting

confidence: 86%

Antitumor activity of the plant extract morin in tongue squamous cell carcinoma cells

Jia

Zhang

et al. 2018

Oncol Rep

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Morin is a naturally occurring bioflavonoid originally isolated from members of the Moraceae family of flowering plants and it possesses antitumor activity in various human cancer cells. The present study explored the antitumor effects of morin in tongue squamous cell carcinoma (TSCC) cells in vitro and investigated the underlying molecular events. A TSCC cell line was treated with different doses of morin for up to 48 h. Analyses of cell viability, using Cell Counting Kit‑8 (CCK‑8), EdU incorporation, colony formation, flow cytometric analysis of cell cycle distribution and apoptosis, wound healing assay, western blot analysis and qRT‑PCR assays, were then performed. The data revealed that morin treatment reduced Cal27 cell proliferation and reduced the migration capacity of tumor cells in a dose‑dependent manner. Morin treatment also significantly upregulated mammalian sterile 20‑like 1 (MST1) and MOB kinase activator 1 (MOB1) phosphorylation in CAL27 cells, but suppressed nuclear translocation of yes‑associated protein (YAP) through the induction of YAP phosphorylation in Cal27 cells. Moreover, the expression of YAP‑targeting genes, such as CTGF, CYR61 and ANKRD, was downregulated in morin‑treated TSCC cells, indicating that morin was able to activate the Hippo signaling pathway to inhibit YAP nuclear translocation and YAP‑related transcriptional activity in TSCC cells. In conclusion, the data from the present study demonstrated that morin produces anti‑TSCC activity in vitro through activation of the Hippo signaling pathway and the downstream suppression of YAP activity in TSCC cells. Future studies should assess the clinical antitumor effects of morin.

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Section: Discussionsupporting

confidence: 86%

Antitumor activity of the plant extract morin in tongue squamous cell carcinoma cells

Jia

Zhang

et al. 2018

Oncol Rep

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“…Autophagy is closely related to cell death and plays an important role in embryonic development and ovarian diseases. CDDP induces a large number of cell apoptosis and tissue damage by stimulating oxidative stress [7,44,45], which activates autophagy through AMPK/mTOR signaling pathway [36]. Therefore, we determined whether the apoptosis of TICs in CDDPinduced POI rats involves changes of autophagy levels stimulated by oxidative stress.…”

Section: Discussionmentioning

confidence: 99%

“…We chose CCK-8 and mRFP-GFP-LC3 assays to determine the autophagy levels. Concentrations of CDDP assessed using CCK-8 and exposures time were selected based on previous reports [34][35][36]. TICs were incubated with varying concentrations of CDDP (0, 5, 10, 15, 20, 40, or 60 μM) for 24 h (Fig.…”

Section: Effects Of Cddp Treatment On Autophagy In Ticsmentioning

confidence: 99%

hUMSC transplantation restores ovarian function in POI rats by inhibiting autophagy of theca-interstitial cells via the AMPK/mTOR signaling pathway

Bao

Cui

et al. 2020

Stem Cell Res Ther

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Background: Previous studies of primary ovarian insufficiency (POI) have focused on granulosa cells (GCs) and ignored the role of theca-interstitial cells (TICs). This study aims to explore the mechanism of the protective effects of human umbilical cord-derived mesenchymal stem cells (hUMSCs) on ovarian function in POI rats by regulating autophagy of TICs. Methods: The POI model was established in rats treated with cisplatin (CDDP). The hUMSCs were transplanted into POI rats by tail vein. Enzyme-linked immunosorbent assay (ELISA) analysis, hematoxylin and eosin (HE) staining, and immunohistochemistry were used to measure the protective effects of hUMSCs. The molecular mechanisms of injury and repairment of TICs were assessed by immunofluorescence, transmission electron microscope (TEM), flow cytometry (FCM), western blot, and quantitative real-time polymerase chain reaction (qRT-PCR). Results: In vivo, hUMSC transplantation restored the ovarian function and alleviated the apoptosis of TICs in POI rats. In vitro, hUMSCs reduced the autophagy levels of TICs by reducing oxidative stress and regulating AMPK/mTOR signaling pathway, thereby alleviating the apoptosis of TICs. Conclusion: This study indicates that hUMSCs protected ovarian function in POI by regulating autophagy signaling pathway AMPK/mTOR.

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“…caspase-12, a marker of apoptosis, is localized on the ER and is specifically activated via erS, and not via membrane or mitochondrial signals. it has been reported that erS-mediated apoptosis is important in cP-induced nephrotoxicity, suggesting that er is a target of cP, and that GrP78, caspase-12 and cHoP are important molecules (9,40,41).…”

Section: Discussionmentioning

confidence: 99%

Dexmedetomidine alleviates cisplatin‑induced acute kidney injury by attenuating endoplasmic reticulum stress‑induced apoptosis via the α2AR/PI3K/AKT pathway

Chai

Zhu

et al. 2020

Mol Med Report

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cisplatin (cP) is an effective antineoplastic agent; however, cP-induced acute kidney injury (aKi) seriously affects the prognosis of patients with cancer. endoplasmic reticulum (er) stress (erS)-induced apoptosis serves a pivotal role in the pathogenesis of cP-induced aKi. dexmedetomidine (dex), a potent α 2 adrenergic agonist, has been reported to exert protective effects against aKi. However, the protective effects of dex against cP-induced aKi and the potential molecular mechanisms remain unknown. in the present study, male Sprague-dawley rats were divided into four groups (n=10/group), as follows: control group; cP group, rats received an intraperitoneal (i.p.) injection of 5 mg/kg cP; dex + cP group, rats received an i.p. injection of 25 µg/kg dex immediately after cP treatment; and dex + cP + atipamezole (atip) group, rats received an i.p. injection of 250 µg/kg atip, an α 2 adrenoreceptor (α 2 ar) antagonist, and then received the same treatment as the dex + cP group. rats were anesthetized and sacrificed 96 h after CP injection. Subsequently, serum blood urea nitrogen (Bun) and serum creatinine (Scr) were analyzed, and kidney samples were collected for analyses. Pathological changes were examined using hematoxylin and eosin staining, and protein expression levels were assessed using western blotting and immunohistochemical staining. in addition, apoptosis was examined using a terminal deoxynucleotidyl transferase duTP nick-end labeling assay. The present results suggested that dex protected against cP-induced aKi by attenuating histological changes in the kidney, serum Bun and Scr production. Furthermore, the expression levels of 78-kda glucose-regulated protein, c/eBP homologous protein and caspase-12, and the apoptotic rate in the kidney were decreased following dex treatment. in addition, the expression levels of phosphorylated (p)-Pi3K and p-aKT in the dex + cP group were significantly increased. Conversely, the renoprotective effects of dex were attenuated following the addition of atip. in conclusion, dex may alleviate cP-induced aKi by attenuating erS-induced apoptosis, at least in part, via the α 2 ar/Pi3K/aKT signaling pathway.

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Morin hydrate ameliorates cisplatin-induced ER stress, inflammation and autophagy in HEK-293 cells and mice kidney via PARP-1 regulation

Cited by 65 publications

References 42 publications

Antitumor activity of the plant extract morin in tongue squamous cell carcinoma cells

Antitumor activity of the plant extract morin in tongue squamous cell carcinoma cells

hUMSC transplantation restores ovarian function in POI rats by inhibiting autophagy of theca-interstitial cells via the AMPK/mTOR signaling pathway

Dexmedetomidine alleviates cisplatin‑induced acute kidney injury by attenuating endoplasmic reticulum stress‑induced apoptosis via the α2AR/PI3K/AKT pathway

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