Sulfasalazine treatment can cause a positive effect on LPS-induced endotoxic rats

Abstract

The aim of this study, was to determine the effect of sulfasalazine for different periods of time reduces disseminated intravascular coagulation, inflammation and organ damages by inhibiting the nuclear factor kappa beta pathway. The study was performed with 30 Wistar albino rats and the groups were established as Control group, LPS group; endotoxemia was induced with LPS, SL5 group: sulfasalazine (300 mg/kg, single dose daily) was administered for 5 days before the LPS-induced endotoxemia, and LS group: sulfasalazine (300 mg/kg, single dose) was administered similtenously with LPS. Hemogram, biochemical, cytokine (IL-1β, IL-6, IL-10, TNF-α) and acute phase proteins (HPT, SAA, PGE2) analyzes and oxidative status values were measured from blood samples at 3 and 6 h after the last applications in the all groups. The rats were euthanized at 6 h and mRNA levels of BCL2 and BAX genes were examined from liver and brain tissues. Sulfasalazine reduced the increased IL-1β, IL-6, TNF-α and PGE2 levels and significantly increased anti-inflammatory cytokine IL-10 levels. In addition, decreasing of ATIII level was prevented in the SL5 group, and decreasing of fibrinogen levels were prevented in the LS and SL5 groups within first 3 h. In LPS group, leukocyte and thrombocyte levels were decreased, however sulfasalazine application inhibited decreases of leukocyte levels in LS and SL5 groups. In addition, sulfasalazine inhibited the decrease of total antioxidant capacity and unchanged apoptosis in brain and liver. In conclusion, the use of sulfasalazine in different durations reduce the excessive inflammation of endotoxemia cases.

Effect of Tarantula cubensis alcohol extract and Capecitabin combine in Colorectal Cancer rats

“…Complementary DNA (cDNA) was synthesized using the iScript cDNA synthesis kit (Bio-Rad, Hercules, CA, USA) according to the manufacturer's recommended protocol and stored at -20°C until required. The mRNA information and sequences of the primers used to amplify the target genes (Bax), (Bcl-2), and (Cas-3) housekeeping gene (GAPDH) are presented in TABLES I and II, respectively [30,45,46]. In addition, the mRNA and cDNA sequences of the genes were checked with The National Center for Biotechnology Information (NCBI) GenBank database (http://www.ncbi.nlm.nih.gov), and the sequences of their primers were checked with NCBI' s Primer Blast (http://www.ncbi.nlm.…”

Ferroptosis in sepsis: The mechanism, the role and the therapeutic potential

“…If its protective effect in sepsis through the mechanism of ferroptosis is further investigated and confirmed, then we will have the opportunity to investigate effective drugs for sepsis more expeditiously and safely. In accession to exploring the possibility that drugs with proven clinical applications such as artemisinin and rapamycin exert protective effects in sepsis through ferroptosis, other ferroptosis inhibitors such as punicalagin inhibiting Nrf2 and sulfasalazine affecting the Xc-system and GSH synthesis also showed great therapeutic effects in sepsis have been validated accordingly, but whether their mechanism of action is related to the control of ferroptosis remains to be explored (133,134).…”