ABSTRACT
Objective To analyze the association between serum uric acid (SUA)level and diabetic peripheral neuropathy(DPN)in the elderly patients with type 2 diabetes mellitus(T2DM).Methods A total of 1 091 cases of elderly T2DM in-and out-patients in our hospital from January 2012 to December 2015 were enrolled in this study.The patients with DPN was diagnosed by neuropathy disability score.All the subjects were divided into two groups according to whether the patients with DPN:NDPN(n=574)and DPN group(n=517).The differences in clinical manifestations and biochemical parameters were compared between the two groups,meanwhile the mobidity rates of hyperuricemia between the two groups were calculated.Logistic regression analysis was used to analyze odds ratios between SUA and the prevalence of DPN.Results The mean serum uric acid of DPN group was(338.79±93.76)μmol/L versus NDPN group's(301.82± 58.94)μmol/L(P＜0.05).The prevalence of hyperuricemia was 20.12％ in DPN group,higher than that in NDPN group(13.24％)(x2 =15.962,P =0.000).Compared with NDPN group,age,duration of diabetes,history of cerebral infarction and the levels of SUA,HbA1C and TG in DPN group were significantly increased,and the levels of eGFR and TBIL decreased(P＜0.05),and there were no significant differences in the other indexes between the two groups (P＞ 0.05).Logistic regression analysis showed that increased SUA level was an independent risk factor for DPN,OR =2.293 (95 ％ CI:1.497-3.824) (P ＜ 0.05).Conclusions It has closely correlation between SUA level and DPN,and SUA is one of the independent impact factors for DPN in the elderly patients with type 2 diabetes mellitus.
ABSTRACT
Oxaliplatin is a key drug in chemotherapy of colorectal cancer (CRC). However, its efficacy is unsatisfied due to drug resistance of cancer cells. In this study, we tested whether a natural agent, ursolic acid, was able to enhance the efficacy of oxaliplatin for CRC. Four CRC cell lines including SW480, SW620, LoVo, and RKO were used as in vitro models, and a SW620 xenograft mouse model was used in further in vivo study. We found that ursolic acid inhibited proliferation and induced apoptosis of all four cells and enhanced the cytotoxicity of oxaliplatin. This effect was associated with down-regulation of Bcl-xL, Bcl-2, survivin, activation of caspase-3, 8, 9, and inhibition of KRAS expression and BRAF, MEK1/2, ERK1/2, p-38, JNK, AKT, IKKα, IκBα, and p65 phosphorylation of the MAPK, PI3K/AKT, and NF-κB signaling pathways. The two agents also showed synergistic effects against tumor growth in vivo. In addition, ursolic acid restored liver function and body weight of the mice treated with oxaliplatin. Thus, we concluded that ursolic acid could enhance the therapeutic effects of oxaliplatin against CRC both in vitro and in vivo, which offers an effective strategy to minimize the burden of oxaliplatin-induced adverse events and provides the groundwork for a new clinical strategy to treat CRC.