Biomarkers of Orthodontic Patients After Use of 1% Brazilian Red Propolis Toothpaste: A Randomized Clinical Study.

Aim: To evaluate the salivary biomarkers and plaque index after a treatment with a propolis-contained toothpaste. Materials and Methods: This is a longitudinal, randomized, double-blind study where 76 participants were randomized into two groups: Group I: Fluoridated Red Propolis toothpaste; Group II: Fluoridated toothpaste. The participants were selected in a municipality without fluoridated public water. All participants received standardized oral hygiene instructions from the same instructor for 3 daily brushings (after breakfast, after lunch, and before bed) for a period of 2 min; Saliva samples were collected before (D0) and after 28 days (D28) of treatment for analysis of pH and total protein, amylase, and IL-10. Saliva was collected in the initial consultation and on return, totaling two collections. All samples were collected under the same conditions, by the same operator and between 9:00 AM and 11:00 AM in order to minimize the influence of circadian rhythm on salivary flow. Results: On D0 and D28, the various treatments had no effect on total salivary proteins (G1: P = 0.0746; G2: P = 0.2144), and the pH stayed about the same. Additionally, there was no change in the amylase activity in G1 (P = 0.1877) or G2 (P = 0.4674). Significant decreases in G1 (P < 0.0001) and G2 (P = 0.03) were observed with IL-10. There was no statistically significant difference in the salivary flow between the BRP toothpaste-treated group (P = 0.172) and the commercial fluoridated toothpaste-treated group (P = 0.329). Compared to G2 (P = 0.03), G1 showed a superior decline in the plaque index (P = <0.0001). Conclusions: After 28 days of using the toothpastes, there were no changes in the amylase, pH, or total protein indicators. After 28 days, there was a decrease in the propolis group's IL-10 dose and plaque index.

Anti-Inflammatory, Antinociceptive, and Antioxidant Properties of Anacardic Acid in Experimental Models.

Anacardic acid (AA), a compound extracted from cashew nut liquid, exhibits numerous pharmacological activities. The aim of the current investigation was to assess the anti-inflammatory, antinociceptive, and antioxidant activities of AA in mouse models. For this, Swiss albino mice were pretreated with AA (10, 25, 50 mg/kg, intraperitoneally, ip) 30 min prior to the administration of carrageenan, as well as 25 mg/kg of prostaglandin E2, dextran, histamine, and compound 48/80. The antinociceptive activity was evaluated by formalin, abdominal, and hot plate tests, using antagonist of opioid receptors (naloxene, 3 mg/kg, ip) to identify antinociceptive mechanisms. Results from this study revealed that AA at 25 mg/kg inhibits carrageenan-induced edema. In addition, AA at 25 mg/kg reduced edema and leukocyte and neutrophilic migration to the intraperitoneal cavity, diminished myeloperoxidase activity and malondialdehyde concentration, and increased the levels of reduced glutathione. In nociceptive tests, it also decreased licking, abdominal writhing, and latency to thermal stimulation, possibly via interaction with opioid receptors. Taken together, these results indicate that AA exhibits anti-inflammatory and antinociceptive actions and also reduces oxidative stress in acute experimental models, suggesting AA as a promising compound in the pharmaceutical arena.

Preventive effect of bergenin against the development of TNBS-induced acute colitis in rats is associated with inflammatory mediators inhibition and NLRP3/ASC inflammasome signaling pathways.

Ulcerative colitis is an idiopathic inflammatory bowel disease characterized by intestinal inflammation; blocking this inflammatory process may be the key to the development of new naturally occurring anti-inflammatory drugs, with greater efficiency and lower side effects. The objective of this study is to explore the effects of bergenin (BG) in TNBS (2,4,6-trinitrobenzenesulfonic acid)-induced acute colitis model in rats in order to assist in the studies for the development of novel natural product therapies for inflammatory bowel disease. 48 Wistar rats were randomized into six groups: (i) Control and (ii) TNBS control; (iii) 5-ASA 100 mg/kg/day (iv) BG 12 mg/kg/day (v) BG 25 mg/kg/day and (vi) BG 50 mg/kg/day. Colitis was induced by instillation of TNBS. Colitis was evaluated by an independent observer who was blinded to the treatment. Our results revealed that bergenin decreased the macroscopic and microscopic damage signs of colitis, and reduced the degree of neutrophilic infiltration in the colon tissue; also, it was capable to down-regulate COX-2, iNOS, IkB-α, and pSTAT3 protein expression. Similarly, using a protocol for indirect ELISA quantification of cytokines, bergenin treatment reduced IL-1ß, IFN-γ and IL-10 levels, and inhibited both canonical (IL-1) and non-canonical (IL-11) NLRP3/ASC inflammasome signaling pathways in TNBS-induced acute colitis. Conclusion: Our study has provided evidence that administration of bergenin reduced the damage caused by TNBS in an experimental model of acute colitis in rats, reduced levels of pro-inflammatory proteins and cytokines probably by modulation of pSTAT3 and NF-κB signaling and blocking canonical and non-canonical NLRP3/ASC inflammasome pathways.