Identification of Renoprotective Phytosterols from Mulberry (<i>Morus alba</i>) Fruit against Cisplatin-Induced Cytotoxicity in LLC-PK1 Kidney Cells
The aim of this study was to explore the protective effects of bioactive compounds from the fruit of the mulberry tree (<i>Morus alba</i> L.) against cisplatin-induced apoptosis in LLC-PK1 pig kidney epithelial cells. <i>Morus alba</i> fruit is a well-known edible fruit commo...
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| Autores principales: | , , , , , , , |
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| Formato: | article |
| Lenguaje: | EN |
| Publicado: |
MDPI AG
2021
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| Materias: | |
| Acceso en línea: | https://doaj.org/article/65844ca2131c42c59a6f874886c4e904 |
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| Sumario: | The aim of this study was to explore the protective effects of bioactive compounds from the fruit of the mulberry tree (<i>Morus alba</i> L.) against cisplatin-induced apoptosis in LLC-PK1 pig kidney epithelial cells. <i>Morus alba</i> fruit is a well-known edible fruit commonly used in traditional folk medicine. Chemical investigation of <i>M. alba</i> fruit resulted in the isolation and identification of six phytosterols (<b>1</b>–<b>6</b>). Their structures were determined as 7-ketositosterol (<b>1</b>), stigmast-4-en-3β-ol-6-one (<b>2</b>), (3β,6α)-stigmast-4-ene-3,6-diol (<b>3</b>), stigmast-4-ene-3β,6β-diol (<b>4</b>), 7β-hydroxysitosterol 3-O-β-<span style="font-variant: small-caps;">d</span>-glucoside (<b>5</b>), and 7α-hydroxysitosterol 3-O-β-<span style="font-variant: small-caps;">d</span>-glucoside (<b>6</b>) by analyzing their physical and spectroscopic data as well as liquid chromatography/mass spectrometry data. All compounds displayed protective effects against cisplatin-induced LLC-PK1 cell damage, improving cisplatin-induced cytotoxicity to more than 80% of the control value. Compound <b>1</b> displayed the best effect at a relatively low concentration by inhibiting the percentage of apoptotic cells following cisplatin treatment. Its molecular mechanisms were identified using Western blot assays. Treatment of LLC-PK1 cells with compound <b>1</b> decreased the upregulated phosphorylation of p38 and c-Jun N-terminal kinase (JNK) following cisplatin treatment. In addition, compound <b>1</b> significantly suppressed cleaved caspase-3 in cisplatin-induced LLC-PK1 cells. Taken together, these findings indicated that cisplatin-induced apoptosis was significantly inhibited by compound <b>1</b> in LLC-PK1 cells, thereby supporting the potential of 7-ketositosterol (<b>1</b>) as an adjuvant candidate for treating cisplatin-induced nephrotoxicity. |
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