Genistein sodium dihydrate(Axcentua Pharmaceuticals AB)

This study aims to investigate the effect of essential oil of Acori Tatarinowii Rhizoma on microglial pyroptosis and decipher the underlying mechanism. BV-2 cells were treated with 1 μg·mL~(-1) lipopolysaccharide(LPS) and 10 μmol·L~(-1) nigericin sodium salt for the modeling of pyroptosis. The cells were treated with different doses of essential oil of Acori Tatarinowii Rhizoma, and then the cell viability and apoptosis were examined by the CCK-8 assay and flow cytometry, respectively. The levels of tumor necrosis factor-α(TNF-α), interleukin-1β(IL-1β), and interleukin-18(IL-18) were measured by ELISA. The mRNA levels of nucleotide-binding domain, leucine-rich repeat, and pyrin domain-containing protein 3(NLRP3), apoptosis-associated speck-like protein containing CARD(ASC), and cysteine proteinase-1(caspase-1) were determined by qRT-PCR. The immunofluorescence assay was used to detect the expression of ionized calcium-binding adapter molecule 1(Iba-1) and NLRP3. Western blot was employed to determine the protein levels of B lymphocytoma-2(Bcl-2), Bcl-2 associated X protein(Bax), Iba-1, κB-inhibitor kinase beta(IKKβ), p-IKKβ(Y188), nuclear factor-κB p65(NF-κB p65), p-NF-κB(S536), NLRP3, ASC, caspase-1, cleaved caspase-1, gasdermin D(GSDMD), and GSDMD-N. The results showed that 8, 16, and 32 μg·mL~(-1) essential oil of Acori Tatarinowii Rhizoma increased the viability, increased the expression of Bcl-2/Bax, and reduced the apoptosis of the cells exposed to LPS and nigericin sodium salt. In addition, the essential oil inhibited the expression of Iba-1, lowered the levels of TNF-α, IL-1β, and IL-18, and down-regulated the mRNA levels of NLRP3, ASC, and caspase-1 as well as the protein levels of NLRP3, ASC, caspase-1, p-IKKβ(Y188)/IKKβ, p-NF-κB(S536)/NF-κB p65, cleaved caspase-1, and GSDMD-N. The results indicated that the essential oil of Acori Tatarinowii Rhizoma inhibited the NLRP3 inflammasome-mediated pyroptosis of microglia.

Most pain studies have been based on a postsurgical, third molar model using ibuprofen (IBU)/acetaminophen (APAP). Studies have found quicker onset of pain relief with a newer formulation of IBU - ibuprofen sodium dihydrate (ISD). The purpose of this study was to compare pain reduction of ISD/APAP to ISD in an acute endodontic pain model of untreated patients experiencing moderate to severe pain with symptomatic apical periodontitis.

In this double-blind randomized study, 64 adult emergency patients in acute moderate to severe pain, a pulpal diagnosis of symptomatic irreversible pulpitis or necrosis, and symptomatic apical periodontitis participated. Each patient randomly received either one dose of 768 mg ISD/1000 mg APAP or one dose of 768 mg ISD. Pain intensity scores were recorded every 15 minutes over 240 minutes using the Heft-Parker VAS along with time to first sign of pain relief, time to meaningful pain relief, and time to 50% pain relief also recorded. The data were analyzed statistically.

Both ISD and ISD/APAP groups showed a progressive decrease in pain from baseline to 120 minutes after medication administration. Afterward, a relative plateau was seen in the patients' pain. There was no difference in the VAS scores between the ISD and ISD/APAP at any given time point, time to first sign of pain relief, time to meaningful pain relief, and time to 50% pain relief.

The addition of APAP to ISD for pain control in an untreated endodontic pain model did not differ significantly from ISD alone.