Superoxide dismutase(Ube Industries Ltd.)

A Liposomal delivery system is a novel and distinguishing way of organized medicine administration. The advancements in liposomal technology allow for controlled drug distribution to treat rheumatoid arthritis effectively. Liposomes are microscopic lipid-based vesicles that have shown promise in transporting substances, such as superoxide dismutase, hemoglobin, erythrocyte interleukin-2, gamma interferon, and smaller compounds.

Liposomes are biocompatible, nontoxic, biodegradable, non-immunogenic, and flexible, with sizes ranging from 0.025 to 2.5 micrometers. LDS is normally employed to distribute drugs through topical conduits, but fresh investigation has shown that it offers promise for oral, ocular, and parenteral administration. Our major objective is to gather information about liposomes, focusing on their applicability in rheumatoid arthritis treatment.

In the current review, we have tried to cover the preparation techniques, clinical trials, patents, marketed formulations, vesicle types, formulations used to treat rheumatoid arthritis and other ailments, and layered liposomal formulations with improved characteristics.

Research has established LDS as a biocompatible, sustainable, non-toxic, adaptable material. Researchers working on LDS technology in rheumatoid arthritis will find this review particularly useful as it may unclutter novel ways for therapeutic intercessions in treating the disease.

We have previously reported a failure of recovery of synaptic function in the CA1 region of acute hippocampal slices from mice with a conditional neuronal knockout (KO) of GLT‐1 (EAAT2, Slc1A2) driven by synapsin‐Cre (synGLT‐1 KO). The failure of recovery of synaptic function is due to excitotoxic injury. We hypothesized that changes in mitochondrial metabolism contribute to the heightened vulnerability to excitotoxicity in the synGLT‐1 KO mice. We found impaired flux of carbon from 13C‐glucose into the tricarboxylic acid cycle in synGLT‐1 KO cortical and hippocampal slices compared with wild‐type (WT) slices. In addition, we found downregulation of the neuronal glucose transporter GLUT3 in both genotypes. Flux of carbon from [1,2‐13C]acetate, thought to be astrocyte‐specific, was increased in the synGLT‐KO hippocampal slices but not cortical slices. Glycogen stores, predominantly localized to astrocytes, are rapidly depleted in slices after cutting, and are replenished during ex vivo incubation. In the synGLT‐1 KO, replenishment of glycogen stores during ex vivo incubation was compromised. These results suggest both neuronal and astrocytic metabolic perturbations in the synGLT‐1 KO slices. Supplementing incubation medium during recovery with 20 mM D‐glucose normalized glycogen replenishment but had no effect on recovery of synaptic function. In contrast, 20 mM non‐metabolizable L‐glucose substantially improved recovery of synaptic function, suggesting that D‐glucose metabolism contributes to the excitotoxic injury in the synGLT‐1 KO slices. L‐lactate substitution for D‐glucose did not promote recovery of synaptic function, implicating mitochondrial metabolism. Consistent with this hypothesis, phosphorylation of pyruvate dehydrogenase, which decreases enzyme activity, was increased in WT slices during the recovery period, but not in synGLT‐1 KO slices. Since metabolism of glucose by the mitochondrial electron transport chain is associated with superoxide production, we tested the effect of drugs that scavenge and prevent superoxide production. The superoxide dismutase/catalase mimic EUK‐134 conferred complete protection and full recovery of synaptic function. A site‐specific inhibitor of complex III superoxide production, S3QEL‐2, was also protective, but inhibitors of NADPH oxidase were not. In summary, we find that the failure of recovery of synaptic function in hippocampal slices from the synGLT‐1 KO mouse, previously shown to be due to excitotoxic injury, is caused by production of superoxide by mitochondrial metabolism. image