The Effect of Eight Weeks of Continuous and Interval Training with Citrus Aurantium Consumption on Autophagy Markers and MyoD Activation in the Muscle Tissue of Elderly Rats

Introduction: Although exercise training and herbs consumption have protective effects on many diseases, the mechanism of action of exercise training with different intensities and citrus aurantium (CA) extract consumption on the autophagy-dependent MyoD activation pathway is not yet known. The aim of this study was to investigate the effect of eight weeks of moderate intensity continuous training (MICT) and high intensity interval training (HIIT) with CA consumption on the expression of LC3-II, Beclin-1 and MyoD as autophagy related markers in the muscle tissue of elderly rats. Methods: In this experimental study, 42 elderly female rats were randomly assigned to (1) control (C) (2) MICT, (3) HIIT, (4) MICT + CA, (5) HIIT + CA, (6) CA and (7) sham (normal saline) groups. HIIT was performed at 85-110% VO2max intensity and 15-25 m / min speed and MICT at 65% VO2max intensity and 20-25 m / min speed; 300 mg / kg / day CA was received peritoneally. One-way analysis of variance with Tukey's post hoc test was used to analyze the findings. Findings were analyzed using Graph Pad Prism 8.3.0 software (p ≤ 0.05). Results: MICT and HIIT increased LC3II, Bclin1 and MyoD gene expression (p ≤ 0.05); The effect of HIIT on MyoD increase was greater than MICT (p ≤ 0.05). CA increased the expression of LC3II and Bclin1 (p ≤ 0.05). MICT + CA and HIIT + CA increased the expression of LC3II, Bclin1 and MyoD in the muscle tissue of elderly rats (p ≤ 0.05). Conclusion: It seems that exercise training and CA consumption with different mechanism of action activate autophagy in the soleus muscle tissue, however the simultaneous use of HIIT, MICT and CA also has favorable effects on the autophagy-dependent MyoD activation pathway.

Trichloroacetamidate Triggered Expeditious and Novel Synthesis of N-Acylbenzotriazoles

A facile route for the synthesis of diverse range of N-acylbenzotriazole derivatives from corresponding carboxylic acids has been established through carbonyl activation pathway. In this method, trichloroacetonitrile is performed as an effective reagent for an easy access of N-acylbenzotriazoles which was simply proceed through the activation of carboxylic acids via in situ imidate formation in anhydrous 1,2 dichloroethane followed by addition of 1H-benzotriazole at 80 oC for 3-4 hours. Easy handling, one-pot, and metal-free condition demonstrate the notable merits of the devised protocol.

Pathways of IFN-alpha Activation in Patients with Cervical Intraepithelial Neoplasia (CIN)

Objective The aim of the present study was to compare the local and systemic expression of the factors linked to the interferon alpha (IFN-α) activation pathway in different degrees of cervical intraepithelial neoplasia (CIN) and cervical cancer. Methods A total of 128 patients with CIN I, CIN II, CIN III and cervical cancer was evaluated. The real-time polymerase chain reaction (RT-PCR) technique was used to evaluate the gene expression of IFNR1, IFNR2, IFN-α, oligoadenylate synthase (2'5′OAS), cytokine signal suppressor 1 (SOCS) 1, SOCS3, signal transducer and transcription activator 1 (STAT1), and IRF9 from 128 biopsies. A total of 46 out of 128 samples were evaluated by flow cytometry for IFNAR1, IFNAR2, STAT1, IRF7 and IFN-α in peripheral blood cells. Results Patients with CIN II and III (63 samples) had a low local expression of IFNR1, but not IFNR2. Patients with some degree of injury showed high expression of SOCS1 and SOCS3. Systemically, patients with CIN II and III (20 samples) had a significant increase in IFNR1, IFNR2, STAT1, IRF7, and IFN-α in helper, cytotoxic T lymphocytes, and in monocytes. Conclusion Patients with high-grade lesions have increased systemic expression of IFN-α and its activation pathways in helper and cytotoxic T lymphocytes, as well as in monocytes due to an exacerbation of the immune response in these patients. This phenomenon is not accompanied by resolution of the lesion due to a defect in the IFN-α activation pathway that revealed by low local IFNAR1 expression and high local expression of SOCS1 and SOCS3.