Introduction:Inflammatory responses in celiac disease (CD) may lead to immune dysregulation and sleep disturbance.Additionally, impaired tryptophan (Trp) metabolism in the gastrointestinal tract has been linked to chronic intestinal inflammation.This study aimed to investigate the relationship between sleep disorders, Trp levels, and cytokine profiles in patients with CD.Methods: A cohort study involving 76 adults with CD (mean age 40.3 years) was conducted from March to December 2022.Sleep quality was assessed using the Pittsburgh sleep quality index (PSQI) questionnaire.Plasma Trp levels were measured using high-performance liquid chromatography (HPLC), and serum tumor necrosis factor-alpha (TNF-) and interleukin (IL)-10 levels were determined using enzyme-linked immunosorbent assay (ELISA).IL-2 and IL-4 expression was evaluated using quantitative real-time polymerase chain reaction (qPCR).Results: A significant proportion (63.2%) of patients with CD experienced poor sleep quality.Additionally, increasing age was positively correlated with sleep disturbances.Importantly, patients with CD and poor sleep quality had lower plasma Trp levels than those with good sleep quality (P<0.0001).Moreover, individuals with poor sleep quality exhibited elevated IL-2 levels (P=0.03)compared to those with good sleep quality.Conversely, no significant difference was observed in IL-4, IL-10, and TNF- levels between individuals with poor and good sleep quality. Conclusion: LowTrp levels may indicate the potential for Trp supplementation to alleviate sleep disturbances in patients with CD.However, further research is required to understand the underlying mechanisms and evaluate potential interventions.

Introduction: Genotropin, a recombinant human growth hormone (GH), has been proposed as a potential repositioning drug to treat neurological disorders.However, its efficacy in managing neuropathic pain remains unclear.This study aimed to evaluate the analgesic effects of Genotropin and investigate its potential mechanisms of action.Methods: Two weeks after chronic constriction injury (CCI) of the sciatic nerve, adult male rats were randomly assigned to three main groups: Control, vehicle (normal saline [NS]), and treatment.The treatment group received Genotropin at doses of 0.3 and 0.6 mg/kg, either alone or in combination with L-arginine, L-NAME, or glutamate (n=8 per group).Pain-related behaviors were assessed using Von Frey filaments, the plantar test, and the Randall-Selitto test.Blood samples were collected to analyze oxidative and antioxidative markers.Results: Genotropin significantly reduced mechanical allodynia (P<0.05,F=2.7) and mechanical (P<0.01,F=3.4) and thermal hyperalgesia (P<0.001,F=2.5).Pretreatment with 0.3 mg/kg GH abolished the pronociceptive effects of L-arginine (500 mg/kg) and glutamate (1000 nmol) (P<0.01;F=2, F=3) while enhancing the antinociceptive effect of L-NAME (P<0.05,F=2.8).GH also significantly reduced lipid peroxidation (P<0.01,F=3.7) and restored levels of glutathione, glutathione peroxidase (GPx), and superoxide dismutase (SOD) (P<0.01;F=11, F=10.52,F=5, respectively).Additionally, catalase (CAT) levels were significantly increased (P<0.01,F=5). Conclusion:These results suggest that exogenous GH alleviates neuropathic pain and enhances antioxidant defenses in a model of peripheral neuropathic pain.The involvement of glutamate and nitric oxide (NO) pathways in GH's antinociceptive effects was also demonstrated.Therefore, Genotropin holds potential as a repositioned therapeutic agent for treating neuropathic pain.

Introduction: Opioid dependence significantly disrupts cognitive activities such as learning and memory, which may be the reason for a return to drug use.Morphine (MOR) can increase oxidative damage in the brain.We aim to investigate the effect of coenzyme Q10 (CoQ10) on cognitive impairment, cue-related reinstatement, and expression of brain-derived neurotrophic factor (BDNF) in MOR-dependent rats.Methods: In this study, 40 male Wistar rats (200-220 g) were divided into 5 experimental groups (n=8) as follows: Oil group, MOR+oil group, MOR+CoQ10-100 group, MOR+CoQ10-200 group, and MOR+CoQ10-400 group.The rats were administered increasing doses of MOR (25 to 100 mg/kg, SC) once daily.After 21 days of addiction, CoQ10 treatment is administered by gavage at doses of 100, 200, and 400 mg/kg once daily for one month.CoQ10 is dissolved in 1 mL of sesame oil and administered.Behavioral assessments were performed using a novel object recognition (NOR) test, working memory in the Y-maze, social interaction, and conditioned place preference (CPP).The expression of BDNF was assessed in the hippocampus through immunohistochemistry. Results:Treatment with CoQ10 at a dosage of 100, 200, and 400 mg/kg within 4 weeks resulted in a significant improvement in the NOR task (P<0.01,P<0.001), working memory in the Y-maze (P<0.01,P<0.001), social interaction (P<0.001),cue-related reinstatement in the CPP (P<0.01,P<0.001) and significantly increased expression of BDNF (P<0.001) in the hippocampus of male rats. O Conclusion:CoQ10 could improve cognitive impairment and reduce reinstatement in MORaddicted male rats.Histologic examination confirmed the neuroprotective effects of CoQ10 in the hippocampus.CoQ10 could be a potential therapeutic agent for MOR-induced cognitive impairment and relapse.