Nystatin導(dǎo)致所有六個(gè)念珠菌屬種類的頰上皮細(xì)胞粘附的顯著減少。^[1] Nystatin是抗生素，增加血漿膜對(duì)小的一價(jià)離子的滲透性，包括氯離子。Nystatin增加心尖氯離子滲透，跨上皮氯離子的運(yùn)輸是由運(yùn)輸橫跨氣管上皮細(xì)胞的基底膜，這主要反映了共轉(zhuǎn)運(yùn)子的活性。Nystatin（400 unit/mL）增加了跨上皮36Cl流量基礎(chǔ)水平約1.5倍，并消除了UTP對(duì)流量的刺激作用。Nystatin治療還消除UTP刺激的可飽和的基底外側(cè)的結(jié)合的發(fā)揮作用的Na-K-CL共轉(zhuǎn)運(yùn)子，isoproterenol刺激的結(jié)合僅被 Nystatin輕度抑制。^[2] 通過(guò)調(diào)控endostatin內(nèi)化介導(dǎo)網(wǎng)格蛋白，Nystatin顯著增強(qiáng)內(nèi)皮細(xì)胞攝取endostatin。Nystatin增強(qiáng)endostatin內(nèi)化，也增加了其對(duì)內(nèi)皮細(xì)胞管形成和遷移的抑制作用。^[3]

Nystatin combined with endostatin selectively enhances endostatin uptake and biodistribution in tumor blood vessels and tumor tissues but not in normal tissues of tumor-bearing mice, ultimately resulting in elevated antiangiogenic and antitumor efficacies of endostatin in vivo. ^[3] Liposomal Nystatin, at doses as low as 2 mg/kg of body weight/day, protects neutropenic mice against Aspergillus-induced death in a statistically significant manner at the 50-day time point compared to either the no-treatment, the saline, or the empty-liposome group. ^[4]