Paeonol, a major compound of moutan cortex, attenuates cisplatin-induced nephrotoxicity in mice
Lee Hj, Lee Gy, Kim Hs, Bae Hs. Evidence-Based Complementary and Alternative Medicine. Volume 2013 (2013), http://dx.doi.org/10.1155/2013/310989
Cisplatin is an effective chemotherapeutic agent that is used for the treatment of a variety of cancers; however, its nephrotoxicity limits the use of this drug. In the present study, we examined whether paeonol, a major compound of Moutan Cortex, has protective effects on cisplatin-induced acute renal failure in mice.
To accomplish this, Balb/c mice (6 to 8?wk of age, weighing 20 to 25?g) were administered, Moutan Cortex (300?mg/kg) or paeonol (20?mg/kg) once a day.
At day 4, mice received cisplatin (30, 20, or 10?mg/kg) intraperitoneally. The paeonol-treated group showed marked attenuation of serum creatine and blood urea nitrogen levels as well as reduced levels of proinflammatory cytokines and nitric oxide when compared to the control group. In addition, the paeonol-treated group showed prolonged survival and marked attenuation of renal tissue injury.
Taken together, these results demonstrated that paeonol can prevent the renal toxic effects of cisplatin.
Moutan Cortex, the root bark of Paeonia suffruticosa Andrews, has been used extensively as a traditional medicine for treatment of various diseases such as atherosclerosis, infection, and inflammation. Previous studies have revealed that the extracts of Moutan Cortex can inhibit nitric oxide and TNF-? in activated mouse peritoneal macrophages (Chung et al, 2007).
A variety of compounds including paeonoside, paeonolide, apiopaeonoside, paeoniflorin, oxypaeoniflorin, benzoyloxypaeoniflorin, benzoylpaeoniflorin, paeonol, and sugars have been identified in Moutan Cortex (Chen et al, 2006). Paeonol, a major phenolic component of Moutan Cortex, has various biological activities such as antiaggregatory, antioxidant, anxiolytic-like, and anti-inflammatory functions (Ishiguro et al, 2006). In this study, paeonol treatment significantly reduced the elevated levels of serum creatinine and BUN.
In addition, the role of proinflammatory cytokines in cisplatin-induced acute renal failure has been well documented (Faubel et al, 2007; Ramesh & Reeves, 2002), and elevation of the proinflammatory cytokines TNF-? and IL-1? as well as that of IL-6 has been demonstrated in humans with acute renal failure (Simmons et al, 2004).
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