Neuroprotective effects of sinapic acid involve the iron regulatory role on the rotenone-induced Parkinson's disease model

Abstract In the last decades, ferroptosis and its relationship with Parkinson's disease have gained significant attention. Compounds that affect ferroptosis and iron-dependent pathways in particular, have possible candidates for study in this context.Sinapic acid is an iron-chelator and high antioxidant bioactive phenolic acid. Its neuroprotective action, due to the antioxidant capacity, has been shown in several experimental models.However, the relationship between iron and antioxidant actions is still misunderstood and therefore, in the current study, we tried to investigate the effects of sinapic acid in rotenone-induced Parkinson's disease with the aspect of ferroptosis and iron-dependent alterations.The Parkinson's disease model was induced by a single dose intrastriatal and intrategmental rotenone (5µg/µl) injection.Sinapic acid (30mg/ kg) was orally administered during a 28-day period after the Parkinson's disease model was validated.Our results demonstrated that sinapic acid treatment attenuated rotenone-induced increase of serum transferrin and iron levels.Furthermore, sinapic acid inhibited rotenone-induced heme oxygenase-1(HO-1) increase and decrease of glutathione peroxidase-4 (GPx-4) levels in brain tissue. Also, sinapic acid treatment decreased motor impairment, likely as a result of the ameliorative effects on the tyrosine hydroxylase immunoreactivity loss after the rotenone insult.Our study suggests that the iron regulatory role of sinapic acid possibly plays a role in the protective effect on rotenone-induced neuronal damage.

The effect of ellagic acid on the repair process of periodontal defects related to experimental periodontitis in rats

Abstract Objective This study aims to evaluate the effect of ellagic acid (EA) by measuring the levels of alveolar bone resorption and inflammatory and oxidative stress markers in the periodontal tissues and serum on the periodontal repair process related to experimental periodontitis in rats. Methodology Forty Wistar rats were divided into four study groups as follows: Group 1=healthy control (n=10); Group 2=EA control (15 mg/kg)(n=10); Group 3=periodontitis (n=10); Group 4=periodontitis+EA (15 mg/kg) (n=10). The periodontitis model was established by ligating bilateral mandibular first molars for 14 days. Then, rats were given normal saline or EA for another 14 days by gavage administration. Serum and gingiva myeloperoxidase (MPO) activity, 8-hydroxydeoxyguanosine(8-OHdG), and glutathione (GSH) levels were analyzed by ELISA. İmmunohistochemical analysis was used to detect Interleukin (IL)-6, IL-10, and tumor necrosis factor-alpha (TNF-α) immunoreactivities in the periodontal tissues. Alveolar bone loss (ABL) and attachment loss (AL) was evaluated by histomorphometry analysis. Results ABL and AL were statistically higher in group 3 than in groups 1, 2 and 4 and in group 4 than in groups 1 and 2 (p<0.05). MPO activities in gingival tissue and serum were significantly increased in group 3 compared to groups 1 and 2 (p<0.05). Significantly higher serum GSH levels, lower gingiva, and serum 8-OHdG levels, and MPO activity were observed in group 4 compared to group 3 (p<0.05). Rats with periodontitis (group 3) expressed significantly higher immunoreactivities of IL-6 and TNF-α and lower IL-10 immunoreactivity compared to those other groups (p<0.05). IL-6 and TNF-α immunoreactivities significantly decreased and IL-10 immunoreactivity increased in group 4 after the use of EA compared to group 3 (p<0.001). Conclusions Our findings showed that EA provides significant improvements on gingival oxidative stress and inflammatory markers and alveolar bone resorption in the repair process associated with experimental periodontitis. Therefore, EA may have a therapeutic potential on periodontitis.

Gingival crevicular fluid oxidative stress level in patients with periodontal disease and hyperlipidemia

Abstract: This study aimed to assess the impact of hyperlipidemia on healthy and diseased periodontal tissue by evaluating oxidative stress biomarkers in gingival crevicular fluid (GCF). Clinical periodontal parameters and blood serum lipid, GCF malondialdehyde (MDA), protein carbonyl (PC), and total antioxidant capacity (TAOC) levels were evaluated in six age and sex-matched groups (n = 15 each) of normolipidemic and hyperlipidemic individuals as follows: normolipidemic + periodontally healthy (H), normolipidemic + gingivitis (G), normolipidemic + chronic periodontitis (CP), hyperlipidemic + periodontally healthy (HH), hyperlipidemic + gingivitis (HG), and hyperlipidemic + CP (HCP). GCF MDA, and PC levels varied among groups, with patients with periodontitis having the highest MDA and PC levels [CP > G > H (p < 0.01) and HCP > HG > HH (p < 0.01)] and the lowest TAOC levels [CP < G < H (p < 0.01) and HCP < HG < HH (p < 0.01)]. Furthermore, paired comparisons showed MDA and PC levels to be higher and TAOC levels to be lower in HCP compared with NCP (p < 0.01). In patients with hyperlipidemia, GCF, MDA, and PC levels positively correlated with clinical assessments and serum triglycerides (TG), total cholesterol (TC), and low-density lipoprotein cholesterol (LDL) levels and negatively correlated with serum high-density lipoprotein cholesterol (HDL) levels, whereas GCF TAOC levels negatively correlated with clinical assessments and serum TG, TC, and LDL levels, but positively correlated with serum HDL levels (p < 0.01). In normolipidemic patients, GCF, MDA, and PC levels positively correlated with clinical assessments and serum TG levels and negatively correlated with serum HDL levels, whereas GCF TAOC levels negatively correlated with clinical assessments and serum TG levels and positively correlated with serum HDL levels (p < 0.01). In conclusion, abnormal serum lipid subfractions could be considered a risk factor for enhancing oxidative stress in GCF in the presence of periodontal disease.