Background: There is evidence for an association between major depressive disorder (MDD) and both inflammatory and phosphodiesterase (PDE) pathways. This study aimed to evaluate the adjunct role of the PDE inhibitor pentoxifylline (PTX), a compound with anti-inflammatory properties, in the treatment of adult patients with MDD. Methods: This was a prospective, 12-week, double-blind study of parallel groups. Eighty adult outpatients who met the DSM-IV criteria for MDD participated in the trial. Patients were required to have a baseline Hamilton Rating Scale for Depression (HAM-D) score of at least 18. Patients were allocated randomly: 40 received escitalopram 20 mg/day plus placebo while the other 40 received escitalopram 20 mg/day plus PTX (400 mg b.i.d.). Patients were assessed by a psychiatrist at baseline, and 4, 8, and 12 weeks after the medication had been started. The serum levels of TNF-α, IL-6, IL-10, BDNF, 8-OHdG, and serotonin were measured at baseline and after therapy. Results: After 8 and 12 weeks, the PTX group showed a statistically significantly greater improvement in HAM-D score compared to the control group (least squares mean difference [LSMD] –3.29, p = 0.000 and LSMD –3.49, p = 0.000, respectively). Moreover, the PTX group showed a statistically significantly greater reduction in the serum levels of TNF-α, IL-6, IL-10, and 8-OHdG along with a statistically significant increase in the levels of BDNF and serotonin in comparison with the control group after the treatment. Conclusion: The findings of this study suggest that PTX could be a promising adjunct to antidepressants in the treatment of MDD patients.

Background/Aims: This study aimed to evaluate the efficacy and the immunomodulatory effect of rifaximin as another promising prophylactic therapy against spontaneous bacterial peritonitis (SBP) in cirrhotics. Materials and Methods: Seventy cirrhotic patients with ascites were included in the study. Patients were divided into two groups in a randomized single-blind fashion. Group one (n=40) received rifaximin and group two (n=30) received norfloxacin (control group). The treatment duration was 6 months. Serum levels of tumor necrosis factor alpha (TNF-α), interleukin-6 ( IL-6), and interleukin-10 (IL-10) were the primary inflammatory markers of the study to evaluate the effect of the medications used. Results: Three months after treatment, five cases on norfloxacin therapy showed SBP, whereas all cases on rifaxmine therapy were free from SBP. In addition, there was no significant difference between patients on rifaximin and norfloxacin therapy with respect to TNF-α, IL-6, and IL-10 serum levels (p>0.05). Furthermore, patients on both rifaximin and norfloxacin therapies showed a statistically significant decrease in TNF-α and IL-6 serum levels compared with their baseline levels (p=0.000 and p=0.000, respectively). In contrast, serum IL-10 showed a statistically significant increase in both groups in comparison with its baseline level (p>0.00). Six-month after treatment, patients on rifaximin therapy showed more effective remission from SBP than those on norfloxacin therapy. Conclusion: In conclusion, the use of rifaximin not only prevents bacterial translocation but also modulates the immune response of the inflammatory and the anti-inflammatory cytokines in SBP patients. However, the efficacy and the immunomodulatory effect of rifaximin in the prophylaxis of SBP in cirrhotics needs further prospective large-scale, double-blind studies.

Background: Alzheimer’s disease (AD) is a common neurodegenerative disorder without effective treatment. Thymoquinone (TQ) has demonstrated potential in exhibiting anti-inflammatory, anti-cancer, and antioxidant characteristics. Despite TQ’s neuroprotection effect, there is a scarcity of information regarding its application in AD research, and its molecular trajectories remain ambiguous. Thus, the objective of the current investigation was to examine the potential beneficial effects and underlying mechanisms of TQ in scopolamine (SCOP)-induced neuronal injury to mimic AD in vivo model. Methods: Thirty mice were divided into normal, SCOP, and TQ groups. The Y-maze and pole climbing tests were performed to measure memory and motor performance. Afterwards, histopathological and immunohistochemical examinations were carried out. Furthermore, peroxisome proliferator-activated receptor gamma (PPAR-γ) signaling pathway-related proteins and genes were detected with an emphasis on the role of miR-9. Results: TQ has the potential to ameliorate cognitive deficits observed in SCOP-induced AD-like model, as evidenced by the improvement in behavioral outcomes, histopathological changes, modulation of the expression pattern of PPAR-γ downstream targets with a significant decrease in the deposition of amyloid beta (Aβ). Conclusions: TQ provided meaningful multilevel neuroprotection through its anti-inflammatory and its PPAR-γ agonist activity. Consequently, TQ may possess a potential beneficial role against AD development.