Lycium barbarum polysaccharide attenuates chemotherapy-induced ovarian injury by reducing oxidative stress.

AIM: We aimed to examine the effects of Lycium barbarum polysaccharide (LBP) on ovarian damage induced by cyclophosphamide (CTX) and to investigate the underlying mechanism. METHODS: A total of 240 female Sprague-Dawley rats were randomly divided into five groups: the control group, the CTX-induced ovarian injury (OI) group, and three LBP groups. Different concentrations of LBP solution were administered to the LBP groups by gastric infusion for 15 days, and the OI group and LBP groups were then subjected to CTX treatment for another 15 days. On days 7, 14, and 28 after CTX injection, femoral vein blood and ovarian tissues were collected for the measurements of antioxidant enzymes and oxidation products. Serum indicators were measured by enzyme-linked immunosorbent assay; and Nrf2, heme oxygenase-1, and quinone oxidoreductase 1 protein levels were detected by Western blot analysis. RESULTS: LBP attenuated CTX-induced ovarian damage and reversed associated adverse effects. LBP reduced oxidative stress by enhancing the potency of antioxidant enzymes and attenuating elevated levels of oxidation products following CTX injection. Furthermore, LBP upregulated Nrf2, heme oxygenase-1, and quinone oxidoreductase 1 protein expression. CONCLUSION: LBP exerts protective effects against CTX-induced ovarian injury by reducing oxidative stress and activating the Nrf2/ARE-signaling pathway.

Preparation, characterization, and in vivo evaluation of mitoxantrone-loaded, folate-conjugated albumin nanoparticles.

Folic acid was covalently conjugated to bovine serum albumin nanoparticles (BSANP) to target the nanoparticles to SKOV3 cells expressing folate receptors. Mitoxantrone was incorporated into the folate-conjugated albumin nanoparticles, and the final nanoparticle size was 68 nm, as measured by a laser light scattering particle analyzer. The cytotoxic activity of mitoxantrone- loaded, folate-conjugated albumin nanoparticles (MTO-BSANP-folate), which was quantitated by (3)H-thymidine incorporation, was higher than mitoxantrone-loaded BSANP (MTO-BSANP) and MTO solution, and could be inhibited by free folic acid. MTO-BSANPfolate may be endocytosed via the folate receptor on the surface of SKOV3 cells. MTO-BSANPfolate also inhibited tumor growth better than the MTO-BSANP and MTO solution in vivo. These results indicate that folate-conjugated BSANP may have therapeutic potential as a vector for anticancer drugs in cancer chemotherapy.