Abstract
Cisplatin is one of the potent chemotherapeutic drugs widely used for the treatment of various types of cancers. However, nephrotoxicity severely restricts the use of this anticancer drug. Alantolactone is a sesquiterpene lactone that exerts a number of biologic properties such as anti-inflammatory, anti-oxidant, and antibacterial activities. This study investigated the role of alantolactone in cisplatin-induced nephrotoxicity and the underlying mechanism. Results showed that alantolactone significantly increased the viability of human renal tubular epithelial cells (HK-2 cells) exposed to cisplatin. Besides, alantolactone inhibited the expression of tumor necrosis factor-a, interleukin-1β, and interleukin-6, as well as the production of nitric oxide. Moreover, alantolactone inhibited the cisplatin-induced increased expression of p-p38/p38, p-JNK/JNK, p-ERK/ERK, and p-p65/p65, which is related to nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), p38, c-Jun N-terminal kinase, and the mitogen-activated protein kinase (MAPK) signaling pathway. This study suggests that alantolactone attenuates cisplatin-induced nephrotoxicity through its anti-inflammatory and antioxidant properties. Thus, alatolactone could be a potential candidate compound for cisplatin-based adjuvant chemotherapy.
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