such as kidney disfunction, reproductive system disturbances, and hematotoxicity , which restrict their clinical use. Therefore, safety therapeutic window of Tripterysium glycosides is very narrow. Furthermore, Min Ma et al.  showed that Tripterysium glycoside administration at the dose of 50 mg kg−1 d−1 for 35 days could induce the biochemical changes in oxidative stress in premature ovarian insufficiency in KM mice. Recently, another research showed that oral administration of Tripterysium glycosides (270 mg kg−1) can induce liver injury and deteriorate the hepatic oxidative stress injury in male KM mice . Those researches consistently showed that high doses of Tripterysium glycosides did harm to the antioxidative system in the model of rodent. Therefore, it still needs to be tested further that whether low and safe doses of Tripterysium glycosides administration could play an important role to anti-oxidative stress or not. It was worth mentioned that the authors of the letter “The effects of oxidative stress following ischemia–reperfusion injury” to editors proposed a new and interesting potential protective mechanism of Tripterysium glycosides preconditioning on the model of ischemia reperfusion injury in rodent model, which was beneficial for uncovering the whole and more comprehensive effect of Tripterysium glycosides.
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