Edelfosine

Aluminum phosphide (AlP) is widely used in suicide attempts. We evaluated the effects of Diphenylene iodonium (DPI), N- N-acetyl cysteine (NAC), and Nivocasan therapeutics on AlP toxicity. Thirty rats were kept in five groups: control (receiving normal saline); the remaining groups were exposed to oral AlP, and treatments (NAC, DPI, and Nivocasan). Liver function tests (LFTs), serum and liver oxidative markers, insulin, glucose, tumor necrosis factor-α (TNF-α), serum and islets interleukin 1β (IL-1β), and glucose-stimulated insulin secretion through islet isolation were assessed. LFTs significantly increased in AlP poisoned animals, and NAC, DPI, and Nivocasan decreased their levels to near control (P < 0.05). DPI and Nivocasan recovered AlP-induced hypoglycemia. Plasma catalase, GPx, and MDA increased in the AlP group, and NAC, DPI, and Nivocasan had protective effects (P < 0.05). DPI significantly decreased serum TNF-α, and NAC decreased IL-1β levels. NAC reversed AlP-induced lower insulin secretion (P < 0.05). Aluminum phosphide (AlP) induces hypoglycemia and liver damage. AlP-related hypoglycemia is associated with elevated inflammatory and oxidative stress markers and impaired insulin secretion from pancreatic islets which improved by NAC. DPI and Nivocasan treat hypoglycemia. DPI and NAC were effective in reducing inflammatory markers.

The lung, a fragile yet crucial organ for breathing in humans, is susceptible to harm from harmful external elements. This study advances the extraction of Arctium lappa polysaccharide (ALP) by our team, aiming to broaden the possibilities for novel medications targeting lung conditions. The structure of ALP was further analyzed by congo red analysis. Effect of ALP pre-treatment was checked by assessing antioxidant markers, inflammatory cytokines and antiapoptosis in vitro and in vivo. Congo red analysis showed that ALP had a stable three-helical conformation. ALP conferred protection against acute lung injury (ALI) induced by lipopolysaccharide (LPS) through the attenuation of lung tissue injury and inhibition of cell apoptosis. The apoptosis rate in lung tissues was markedly reduced in ALP-treated groups compared to the LPS group (P < 0.01). This protective effect is primarily attributed to dual mechanisms: the suppression of inflammatory cytokine synthesis and the enhancement of antioxidant responses. ALP significantly reduced the levels of LPS-induced inflammatory cytokines (P < 0.05) including tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6) and interleukin-1β (IL-1β) in vitro and in vivo experiments. In addition, ALP alleviated LPS-induced lung injury by reducing malondialdehyde (MDA) and upregulating superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT), and the overall antioxidant capacity (T-AOC) contents. The western blot analysis of mice lung tissues revealed that ALP pretreatment significantly attenuated the LPS-induced upregulation of key inflammatory signaling proteins (P < 0.05), including TLR4, MyD88, p65, P-p65, i-κB, p-i-κB, JNK, and p38 protein levels. The results of RAW264.7 cell experiments further veriffed that ALP inhibited TLR4/NF-κB/MAPK pathway. In conclusion, ALP can reduce LPS-induced ALI by inhibiting inflammation and oxidative stress.