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Objective To investigate whether umbilical cord mesenchymal stem cells (UC-MSCs) can exert kidney protection in diabetes rats through regulating autophagy. Methods Type 2 diabetes rats model was induced by a high-fat diet combined with a low dosage of streptozotocin (STZ) intraperitoneal injection. After successful modeling, those rats were fed with a high-fat diet for another eight weeks, and the control group (10) was given a normal chow diet. The treatment group (MSCs group, 10) was infused UC-MSCs (3x106 suspended in 0.5 ml PBS) via tail vein once every two weeks, for a total of eight weeks of treatment. The diabetes control group (T2DM group, 10) was infused 0.5 ml PBS solution via tail vein and the control group did not receive any treatment at the same time. Random blood glucose and body weight were monitored every two weeks. One week after the fourth treatment, intraperitoneal glucose tolerance test (IPGTT) was performed in all rats, and later on they were sacrificed and their kidneys were collected for histopathological examinations and autophagy-related protein examinations. Data was measured using two independent sample mean t tests, one-way ANOVA and repeated measures analysis of variance. Results Compared to T2DM group, random blood glucose decreased [(23.9±3.7) vs (28.7±2.1) mmol/L, t=3.568, P<0.01], and glucose tolerance improved (t=3.07-6.64, P<0.01) in MSCs group. The pathological results showed that in the MSCs group the degree of glomerular sclerosis was reduced (P<0.01, t=17.28), the glomerular basement membrane thickening was relieved (P<0.01, t=12.00),and the degree of renal interstitial fibrosis was improved (P<0.01, t=2.83-17.28). Examinations of autophagy-related proteins showed that the MSCs group exhibited increased expression of LC3[(78.3±5.3)% vs(33.4±8.3)%,t=10.22, P<0.01] and reduced expression of P62[(24.1±4.2)% vs (93.3±4.9)%, t=24.13, P<0.01],which indicated that the level of autophagy in rat kidneys were significantly increased after MSCs infusion. Conclusion UC-MSCs therapy has the function of kidney protection and delay the development of diabetic nephropathy, which may be related to the enhancement of autophagy in renal tissues. [ABSTRACT FROM AUTHOR]

Cervical cancer is a leading cause of cancer death among women in the world. The specific etiopathogenesis of cervical cancer is indeed complex. Even so, we should make arduous efforts to have a precise understanding of the complicate cellular/molecular mechanisms underlying initiation, progression and/or prevention of the cervical cancer. The high-risk human papillomavirus (hrHPV) is considered as the major causative agent of cervical cancer. But with the existence of hrHPV only is not sufficient, autophagy plays a vital character in the development of cervical cancer. Autophagy is the endogenous, tightly regulated cellular "housekeeping" process responsible for the degradation of damaged and dysfunctional cellular organelles and protein aggregates. Our aims in this review were (1) to provide a brief synopsis of process of autophagy (including an overview of the key molecular mediators of this catabolic process and its relationship with hrHPV infection) and (2) most importantly, summarize the current evidence for autophagy-mediated cervical carcinogenesis. One of the latest opinions about the etiopathogenesis is that hrHPV leads to the occurrence of cervical cancer via inhibiting the host's autophagy. The infection of hrHPV will cause the autophagy of cancerous cells, resulting in autophagic cell death, which will suppress the further infection of HPV in return. But the autophagy would be knocked down by the hrHPV, which means the protecting action would end with failure. What's worse, the negative denouement will enhance the infectivity of HPV ultimately, which leads to accelerate cervical carcinogenesis.