Send to

Choose Destination
Int J Mol Sci. 2018 Jan 7;19(1). pii: E174. doi: 10.3390/ijms19010174.

Chemical Characterization of a Renoprotective Metabolite from Termite-Associated Streptomyces sp. RB1 against Cisplatin-Induced Cytotoxicity.

Author information

School of Pharmacy, Sungkyunkwan University, Suwon 16419, Korea.
College of Korean Medicine, Gachon University, Seongnam 13120, Korea.
Department of Food and Nutrition, Gachon University, Seongnam 13120, Korea.
School of Pharmacy, Sungkyunkwan University, Suwon 16419, Korea.


Platinum-based anticancer drug therapies can cause renal damage and apoptotic kidney cell damage. The development of reno- and kidney-protective molecules is therefore urgently required. To address this challenge, we explored secondary metabolites of termite-associated Streptomyces sp. RB1 isolated from the cuticle of the South African termite, Macrotermes natalensis for their renoprotective ability using bioassay-guided fractionation and LLC-PK1 cells. Chemical investigation of the MeOH extract of Streptomyces sp. RB1 resulted in the isolation and identification of a renoprotective metabolite, 1-O-(2-aminobenzoyl)-α-l-rhamnopyranoside (ABR) (1) from the active fraction, which ameliorated cisplatin-induced cytotoxicity to 80% of the control value at 25 μM. Upregulated phosphorylation of c-Jun N-terminal kinases (JNK) and p38 following cisplatin treatment was markedly decreased after pre-treatment of cells with ABR. In addition, levels of cleaved caspase-3 and the percentage of apoptotic cells were also significantly reduced after pre-treatment with ABR. These findings provide experimental evidence that blocking the MAPK signaling cascade plays a critical role in mediating the renoprotective effect of ABR, which may inspire the development of novel therapeutic substances to prevent anticancer drug-induced nephrotoxicity.


">l-rhamnopyranoside; 1-O-(2-aminobenzoyl)-α-; LLC-PK1 cells; MAPKs; Streptomyces sp. RB1; nephrotoxicity; renoprotective effect

[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Multidisciplinary Digital Publishing Institute (MDPI) Icon for PubMed Central
Loading ...
Support Center