IntroductionRelevant aspects of Alzheimer's disease (AD) can be modeled by aluminium-maltolate injection into specific regions of the brain. The possible role of berberine chloride (BC) as an anti-inflammatory agent in the brain has been previously addressed.Material and methodsRabbits were divided into control (C), untreated lesion (L) and BC-treated + lesion (L + BC) groups. Animals in L + BC received BC (50 mg/ kg) orally 1 day after surgery and daily for 2 weeks. The lesion was induced by injection of 100 µl of either vehicle or water containing 25 mM aluminium-maltol into intraventricular fissure. Weight loss, ataxia, paralysis and tremor were monitored. For histopathology, Bielschowsky silver and H&E staining were employed. β-Secretase activity in hippocampus was finally assessed.ResultsAll L animals died on days 12-15 after lesion. Seven to 10 days after lesion, abnormal symptoms as well as cachexia were seen in over 90% of cases. L rabbits lost an average of 0.5 kg which was significant on days 10 and 12 (p < 0.05); this was not completely prevented by BC. Up to day 15, all L animals had lost their lives (p < 0.001). BC treatment protected the hippocampus from degeneration, altered the behavior and decreased the activity of β-site amyloid precursor protein cleaving enzyme-1 (BACE-1).ConclusionsConsidering the findings in regard to physiological abilities, histological changes and BACE-1 activity in hippocampus changes, it is concluded that BC treatment could be an effective therapy in restoring Al maltol-induced behavioral derangements in the rabbit model of AD.

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Asthma is one of the most common chronic diseases in the world, affecting over 300 million people. It is an inflammatory disorder characterized by bronchoconstriction and airway hyperresponsiveness, followed by inflammatory manifestations in the respiratory system. The prevalence of asthma is rising and there is a clinical need to develop more effective treatments. While corticosteroids (glucocorticosteroids) remain the mainstay of asthma therapy, they have limitations because of their potentially severe side-effects and the presence of corticosteroid resistance in some patients. This review discusses current strategies in the treatment of asthma and considers new therapeutic regimens of asthma in the drug development pipeline.

Hypothyroidism may reduce, whereas hyperthyroidism may aggravate, asthma symptoms. The mechanisms underlying this relationship are largely unknown. Since thyroid hormones have central roles in cell growth and differentiation, we hypothesized that airway remodeling, in particular increased airway smooth muscle (ASM) mass, may be involved. To address this hypothesis, we investigated the effects of triiodothyronine (T3) and l-thyroxine (T4) in the absence and presence of the profibrotic transforming growth factor (TGF)-β1 on human ASM cell phenotype switching. T3 (1-100 nM) and T4 (1-100 nM) did not affect basal ASM proliferation. However, when combined with TGF-β1 (2 ng/ml), T4 synergistically increased the proliferative response, whereas only a minor effect was observed for T3. In line with a switch from a contractile to a proliferative ASM phenotype, T4 reduced the TGF-β1-induced contractile protein expression by ∼50%. Cotreatment with T3 reduced TGF-β1-induced contractile protein expression by ∼25%. The synergistic increase in proliferation was almost fully inhibited by the integrin αvβ3 antagonist tetrac (100 nM), whereas no significant effects of the thyroid receptor antagonist 1-850 (3 μM) were observed. Inhibition of MEK1/2, downstream of the integrin αvβ3, also inhibited the T4- and TGF-β1-induced proliferative responses. Collectively, the results indicate that T4, and to a lesser extent T3, promotes a proliferative ASM phenotype in the presence of TGF-β1, which is predominantly mediated by the membrane-bound T4 receptor αvβ3. These results indicate that thyroid hormones may enhance ASM remodeling in asthma, which could be of relevance for hyperthyroid patients with this disease.

Background and aims: Several pharmacological and biological activities have been attributed to Cuminum cyminum L. (CC), including analgesic, antioxidant, anti-inflammatory, and anti-epileptic effects. In this regard, the present study evaluated the antidepressant-like effects of the CC essential oil (EO) on the forced swim test (FST) and tail suspension test (TST) in male mice. Materials and Methods: The gas chromatography-mass spectrometry (GC-MS) apparatus was used for detecting the chemical compounds of CC EO. In the present study, 72 male NMRI mice were randomly allocated to 12 groups (each containing 6 animals) including control or vehicle (10 mL/kg, i.p.), fluoxetine (20 mg/kg, i.p.), imipramine (30 mg/kg, i.p), and the CC EO (100, 200, and 300 mg/kg, i.p.). Then, several parameters were measured and recorded, including immobility time, swimming time, and climbing time in FST, along with immobility time in TST, respectively. Results: Cuminaldehyde followed by cymene, γ-terpinene, phenylglycol, 2-caren-10-al, 2-β-pinene, acoradiene, and cuminic acid were the major components of the CC EO. Based on the results, all doses of the CC, fluoxetine, and imipramine reduced immobility time in both FST (P<0.001) and TST (P<0.001). On the other hand, all doses of the CC and fluoxetine increased swimming time (P<0.001) although climbing time was only increased by 200 and 300 mg/kg of the EO (P<0.01 and P<0.001, respectively) and imipramine (P<0.001). Conclusion: Based on the findings of the present study, the components of the CC induced antidepressant-like activity similar to that of fluoxetine and imipramine in both tests. However, further studies are required to confirm the role of different active components and the exact mechanism of action.