Diet and Nutraceutical Supplementation in Dyslipidemic Patients: First Results of an Italian Single Center Real-World Retrospective Analysis.

BACKGROUND: Dyslipidemias are a heterogeneous group of metabolic disorders mainly characterized by an increased risk of atherosclerotic cardiovascular disease (ASCVD) or other conditions, such as acute pancreatitis in hypertriglyceridemia. The aim of this study was to evaluate the effect of diet treatment and nutraceutical (NUTs) supplementation on the plasma lipid profile in outpatient dyslipidemic subjects, considering the influence of several factors (i.e., gender, age, body mass index, alcohol consumption, and smoking habits). METHODS: 487 dyslipidemic patients spanning from 2015 to 2019 were treated with a Mediterranean diet or NUTs in a real-word setting and were retrospectively analyzed. General characteristics and lipid profile at baseline and after the follow-up period were evaluated. RESULTS: Diet alone reduced total cholesterol (-19 mg/dL, -7.7%), LDL cholesterol (-18 mg/dL, -10.1%), and triglycerides (-20 mg/dL, -16.7%). Triglycerides (TG) decreased more in men, while women were associated with higher reduction of LDL cholesterol (LDL-C). Different types of NUTs further ameliorate lipid profiles when associated with diet. Nevertheless, most patients at low ASCVD risk (222 out of 262, 81.6%) did not achieve the 2019 ESC/EAS guidelines recommended LDL-C goals (i.e., LDL-C < 116 mg/dL). CONCLUSION: Lipid-lowering diet improves lipid profile, and NUTs can boost its efficacy, but taken together they are mainly unsatisfactory with respect to the targets imposed by 2019 EAS/ESC guidelines.

Differentiation impairs Bach1 dependent HO-1 activation and increases sensitivity to oxidative stress in SH-SY5Y neuroblastoma cells.

Neuronal adaptation to oxidative stress is crucially important in order to prevent degenerative diseases. The role played by the Nrf2/HO-1 system in favoring cell survival of neuroblastoma (NB) cells exposed to hydrogen peroxide (H2O2) has been investigated using undifferentiated or all-trans retinoic acid (ATRA) differentiated SH-SY5Y cells. While undifferentiated cells were basically resistant to the oxidative stimulus, ATRA treatment progressively decreased cell viability in response to H2O2. HO-1 silencing decreased undifferentiated cell viability when exposed to H2O2, proving the role of HO-1 in cell survival. Conversely, ATRA differentiated cells exposed to H2O2 showed a significantly lower induction of HO-1, and only the supplementation with low doses of bilirubin (0,5-1 µM) restored viability. Moreover, the nuclear level of Bach1, repressor of HO-1 transcription, strongly decreased in undifferentiated cells exposed to oxidative stress, while did not change in ATRA differentiated cells. Furthermore, Bach1 was displaced from HO-1 promoter in undifferentiated cells exposed to H2O2, enabling the binding of Nrf2. On the contrary, in ATRA differentiated cells treated with H2O2, Bach1 displacement was impaired, preventing Nrf2 binding and limiting HO-1 transcription. In conclusion, our findings highlight the central role of Bach1 in HO-1-dependent neuronal response to oxidative stress.