Search Results (3)

Diabetes mellitus (DM) is a chronic metabolic disorder characterized by impaired glycemic regulation and persistent hyperglycemia, which drives the onset of microvascular complications such as diabetic neuropathy and nephropathy. Chronic hyperglycemia activates oxidative stress pathways and alters gut microbiota composition, both of which contribute to disease progression. In this context, probiotics have emerged as promising therapeutic agents due to their ability to modulate oxidative stress, improve glycemic control, and influence gut microbial balance. This review summarizes preclinical and clinical evidence supporting the antioxidant potential of probiotics in DM management, with a focus on underlying mechanisms. Strains from the Lactobacillus and Bifidobacterium genera are the most extensively studied and have demonstrated hypoglycemic and antioxidant effects, including the enhancement of key antioxidant enzymes and reductions in lipid peroxidation and nitrosative stress markers. Probiotics have also shown beneficial effects in DM-associated complications, particularly diabetic neuropathy and nephropathy. While clinical data are still limited, recent findings underscore oxidative stress as a critical therapeutic target influenced by probiotic interventions. Overall, current evidence supports probiotics as a complementary strategy for managing DM and its complications, highlighting the need for further well-designed clinical trials exploring diverse strains, formulations, and dosing regimens. Full article

Neuropathic pain (NP) is the most prevalent and debilitating form of chronic pain, caused by injuries or diseases of the somatosensory system. Since current first-line treatments only provide poor symptomatic relief, the search for new therapeutic strategies for managing NP is an active field of investigation. Multiple mechanisms contribute to the genesis and maintenance of NP, including damage caused by oxidative stress. The naturally occurring antioxidant alpha-lipoic acid (ALA) is a promising therapeutic agent for the management of NP. Several pre-clinical in vitro and in vivo studies as well as clinical trials demonstrate the analgesic potential of ALA in the management of NP. The beneficial biological activities of ALA are reflected in the various patents for the development of ALA-based innovative products. This review demonstrates the therapeutic potential of ALA in the management of NP by discussing its analgesic effects by multiple antioxidant mechanisms as well as the use of patented ALA-based products and how technological approaches have been applied to enhance ALA’s pharmacological properties. Full article

Although the mouse model of incisional pain is broadly used, the mechanisms underlying plantar incision-induced nociception are not fully understood. This work investigates the role of Na_v1.8 and Na_v1.9 sodium channels in nociceptive sensitization following plantar incision in mice and the signaling pathway modulating these channels. A surgical incision was made in the plantar hind paw of male Swiss mice. Nociceptive thresholds were assessed by von Frey filaments. Gene expression of Na_v1.8, Na_v1.9, TNF-α, and COX-2 was evaluated by Real-Time PCR in dorsal root ganglia (DRG). Knockdown mice for Na_v1.8 and Na_v1.9 were produced by antisense oligodeoxynucleotides intrathecal treatments. Local levels of TNF-α and PGE₂ were immunoenzymatically determined. Incised mice exhibited hypernociception and upregulated expression of Na_v1.8 and Na_v1.9 in DRG. Antisense oligodeoxynucleotides reduced hypernociception and downregulated Na_v1.8 and Na_v1.9. TNF-α and COX-2/PGE₂ were upregulated in DRG and plantar skin. Inhibition of TNF-α and COX-2 reduced hypernociception, but only TNF-α inhibition downregulated Na_v1.8 and Na_v1.9. Antagonizing NF-κB and p38 mitogen-activated protein kinase (MAPK), but not ERK or JNK, reduced both hypernociception and hyperexpression of Na_v1.8 and Na_v1.9. This study proposes the contribution of the TNF-α/p38/NF-κB/Na_v1.8 and Na_v1.9 pathways to the pathophysiology of the mouse model of incisional pain. Full article