Nutritional status as a predictor of the incidence of pressure injury in adults: A systematic review and meta-analysis.

AIM: Pressure injuries are a significant health care problem worldwide, and many factors influence their occurrence and development. The purpose of this systematic review and meta-analysis was to investigate the role of nutritional status in the development rate of pressure injuries as a potentially modifiable risk factor. METHODS: Study designs included cohort (prospective and retrospective), case-control, and RCTs if the association between nutrition status and pressure injuries was reported. Databases searched included: PubMed, CINAHL, Embase, Scopus, Web of Science, and Cochrane Library on April 20th, 2022. The data were analyzed using OR and random effect model in Revman5.3 and STATA 15 Software. Report this systematic review and meta-analysis according to the PRISMA 2020 statement. RESULTS: A total of 22 separate studies were retained in this systematic review. Of these, 16 articles were included in the meta-analysis. Three studies were assessed as low risk and sixteen as a moderate risk of bias. All RCTs were B quality. The odds ratio of the incidence of pressure injuries in malnourished and non-malnourished patients was 3.66(95% CI: 2.77-4.83). In the three RCTs studies(n = 870), the odds ratio of the incidence of pressure ulcers in patients with standard nutrition to those with specific nutritional interventions was 1.35(95%CI:1.02-1.78). CONCLUSIONS: This systematic review and meta-analysis showed that nutritional status is significantly associated with pressure injuries. Malnutrition can increase the incidence of pressure injuries, and specific nutritional interventions can reduce the incidence of pressure injuries compared to standard nutrition.

CCR2 downregulation attenuates spinal cord injury by suppressing inflammatory monocytes.

Specific elimination of blood-derived macrophages/monocytes following spinal cord injury (SCI) may suppress neurotoxicity without affecting the neuroprotective microglia at the injury sites. We aimed to deplete hematogenous monocytes by downregulating CCR2 through siCCR2-loaded nanoparticles and investigated its outcome in the recovery of locomotor function of SCI mice. We induced SCI in mice and examined the influx of blood-derived monocytes into the injury site. We constructed nanoparticles loaded with siRNA targeting CCR2 and examined its efficiency in downregulating the CCR2 expression in cultured RAW264.7 cells and monocytes in vivo. Finally, we assessed the effects of CCR2 downregulation in pro-inflammatory cytokine production, axon regeneration, and locomotor recovery of the SCI mice. We found that SCI significantly increased the CCL2 expression and number of blood-derived macrophages/monocytes in the lesion area. Nanoparticles loaded with siCCR2 significantly suppressed the CCR2 expression in hematogenous macrophages/monocytes, reduced the number of hematogenous macrophages/monocytes, and reduced pro-inflammatory cytokine production at the injury site. Finally, CCR2 downregulation promoted axon regeneration and improved locomotor recovery in SCI mice. Our study suggests that siCCR2 loading nanoparticles are efficient and specific in downregulating hematogenous macrophages/monocytes without affecting the neuroprotective microglia and its efficacy in promoting locomotor recovery in SCI mice warrants further investigation for its clinical application in SCI.

Ergosterol ameliorates renal inflammatory responses in mice model of diabetic nephropathy.

Ergosterol (ERG) was reported to exhibit anti-inflammatory and anti-oxidative activities. Besides, ERG was found to attenuate kidney injury in the diabetic mouse. However, the protective effect of ERG in diabetic nephropathy-induced inflammation remains unclear. We aimed to study whether ERG could alleviate diabetic nephropathy-induced inflammation and explore the underlying mechanisms. The diabetic nephropathy mice model was induced by intraperitoneal injection of 30 mg/kg Streptozotocin (STZ). The inflammatory cytokines levels, and insulin concentration in the serum of both diabetic nephropathy patients and mouse model were determined by ELISA. mRNA and protein expression were analyzed by RT-PCR and Western blot, respectively. Fasting blood glucose levels were detected using a commercial kit. Blood biochemistry levels were determined by an automatic analyzer. Mesangium proliferation was detected by PAS staining. It was found that serum levels of IL-6, TNF-α, and MCP-1 dramatically increased in the diabetic nephropathy patients. In mice, ERG treatment greatly decreased fasting blood glucose levels, inflammatory cytokine levels, and renal injury, while it enhanced the insulin level. Mechanically, ERG treatment dramatically decreased NF-κB signaling pathway. Our findings highlight the potential of ERG as an effective agent to treat diabetic nephropathy.

Mitofusin-2 ameliorates high-fat diet-induced insulin resistance in liver of rats.

AIM: To investigate the effects of mitofusin-2 (MFN2) on insulin sensitivity and its potential targets in the liver of rats fed with a high-fat diet (HFD). METHODS: Rats were fed with a control or HFD for 4 or 8 wk, and were then infected with a control or an MFN2 expressing adenovirus once a week for 3 wk starting from the 9(th) wk. Blood glucose (BG), plasma insulin and insulin sensitivity of rats were determined at end of the 4(th) and 8(th) wk, and after treatment with different amounts of MFN2 expressing adenovirus (10(8), 10(9) or 10(10) vp/kg body weight). BG levels were measured by Accu-chek Active Meter. Plasma insulin levels were analyzed by using a Rat insulin enzyme-linked immunosorbent assay kit. Insulin resistance was evaluated by measuring the glucose infusion rate (GIR) using a hyperinsulinemic euglycemic clamp technique. The expression or phosphorylation levels of MFN2 and essential molecules in the insulin signaling pathway, such as insulin receptor (INSR), insulin receptor substrate 2 (IRS2), phosphoinositide-3-kinase (PI3K), protein kinase beta (AKT2) and glucose transporter type 2 (GLUT2) was assayed by quantitative real-time polymerase chain reaction and Western-blotting. RESULTS: After the end of 8 wk, the body weight of rats receiving the normal control diet (ND) and the HFD was not significantly different (P > 0.05). Compared with the ND group, GIR in the HFD group was significantly decreased (P < 0.01), while the levels of BG, triglycerides (TG), total cholesterol (TC) and insulin in the HFD group were significantly higher than those in the ND group (P < 0.05). Expression of MFN2 mRNA and protein in liver of rats was significantly down-regulated in the HFD group (P < 0.01) after 8 wk of HFD feeding. The expression of INSR, IRS2 and GLUT2 were down-regulated markedly (P < 0.01). Although there were no changes in PI3K-P85 and AKT2 expression, their phosphorylation levels were decreased significantly (P < 0.01). After intervention with MFN2 expressing adenovirus for 3 wk, the expression of MFN2 mRNA and protein levels were up-regulated (P < 0.01). There was no difference in body weight of rats between the groups. The levels of BG, TG, TC and insulin in rats were lower than those in the Ad group (P < 0.05), but GIR in rats infected with Ad-MFN2 was significantly increased (P < 0.01), compared with the Ad group. The expression of INSR, IRS2 and GLUT2 was increased, while phosphorylation levels of PI3K-P85 and AKT2 were increased (P < 0.01), compared with the Ad group. CONCLUSION: HFDs induce insulin resistance, and this can be reversed by MFN2 over-expression targeting the insulin signaling pathway.