Objective To investigate the effects of curcumin on UVB-induced elevation of cellular ROS level and cell death and to explore the involvement of transcription factor Nrf2.Methods Mouse embryonic fibroblasts (MEFs) were pretreated with or without curcumin then irradiated with UVB.The cell viability,cellular ROS level and protein levels of Nrf2 and HO1 were determined by MTT assay,DCFH fluorescence and Western blotting,respectively.These measurements were also performed in Nrf2 (-/-) MEFs.Results UVB irradiation elevated cellular ROS level and decreased cell viability of MEFs(t =16.65,15.89,P ＜ 0.05),while the curcumin pretreatment significantly attenuated the deleterious effects of UVB(t =11.88,3.77,P ＜ 0.05).UVB irradiation moderately increased the protein levels of Nrf2 and HO1 and activated JNK and ERK.The curcumin pretreatment led to more remarked elevation of Nrf2 and HO1 proteins,while inhibited UVB-activated JNK and ERK,but it had little effect on p38MAPK.In contrast,Nrf2 (-/-) MEFs showed significantly decrease in Nrf2 and HO1 expressions and were more susceptible to UVB-induced damages.Interestingly,the protective effects of curcumin were also greatly compromised in Nrf2 (-/-) MEFs (t =16.73,-8.23,P ＜ 0.05).Conclusions Curcumin can attenuate UVB-induced oxidative damages in MEFs by activating Nrf2 signaling.

Objective: To improve the understanding of rare anti-myelin-associated glycoprotein (MAG) positive IgM monoclonal gammopathy related peripheral neuropathy (IgM-PN) . Methods: Eleven cases of IgM paraproteinemia and anti-MAG antibody positive neuropathy diagnosed since 2014 in Peking Medical Union College Hospital were summarized. The medical records including clinical manifestation, lab results, treatment and prognosis were analyzed. Results: Among the 11 patients (8 male and 3 female) , the median onset age is 63 years old (range from 52 to 77 years old) . The peripheral neuropathy of 9 patients were characterized by distal onset of numbness, 6 patients suffered from muscle weakness. The nerve conduction velocity study indicated that all 11 patients had demyelinating peripheral nerve damage, which was sensory predominant and more severe in lower limbs, 6 of them had secondary axonal damage. Monoclonal IgM gammopathy was identified in all 11 patients, among which 6 were IgM κ, 2 IgG κ and IgM κ bi-clonal, 3 IgM λ. Three patients were diagnosed with Waldenström’s macroglobulinaemia. The anti-MAG-IgM antibody was positive in all 11 cases. After diagnosis, 9 patients received combination chemotherapy including rituximab or rituximab treatment alone. The monoclonal IgM level declined significantly in 7 patients. The neuropathy was stable or improved. Conclusions Anti-MAG antibody positive IgM-PN is a rare M protein related disease. In peripheral neuropathy with undetermined etiology, we suggest to screen M protein and anti-MAG antibody. Chemotherapy including rituximab or rituximab alone is recommended as first-line therapy.