Journal of Cytology & Histology

Introduction: Cardiotoxicity is one of the most important causes that limit the use of Doxorubicin (DOX) in treatment of the cancer. N-acetylcysteine (NAC) is an antioxidant substance that protects different cellular organelles from free radicals.

The aim of the work: To shed the spot on the role of NAC on cardiotoxicity induced by DOX.

Materials and methods: Forty adult male albino rats were divided into three groups. Group I: it was formed of 20 animals served as a control group. Further, it was divided into two subgroups; Subgroup Ia: formed of 10 animals received physiologic saline and Subgroup Ib: formed of 10 animals received NAC. Group II: formed of 10 animals that received DOX dissolved in normal saline. Group III: formed of 10 animals that received DOX similar togroup II and NAC similar to subgroup Ib. At the end of the second week, all animals were sacrificed; the heart specimens were dissected out and processed to light and electron microscopic examination. Morphometric and statistical analysis was also done.

Results: Light microscopic examination of group II showed deeply stained cardiac muscle fibers and congested coronary vessels. Distorted cardiac muscle fibers and deeply stained nuclei were also observed. Moreover, cellular infiltration was also observed among cardiac muscle fibers. Apparent increase in greenish collagen fibers was seen between cardiac muscle fibers by Masson's trichrome. Electron microscopic examination of group II showed the cardiac muscle with thinning out of some myofibrils, vacuolations of the sarcoplasm and irregular wavy nuclear envelop. Telocytes appeared between cardiac muscle fibers. Group III showed improvement of the cardiac muscle by light and electron microscope with minimal vacuolation in the cardiac muscle. Morphometric and statistical analysis confirmed the histological results.

Conclusion: The present study demonstrated that the administration of N-acetyl cysteine could protect against cardiaotoxicity induced by doxorubicin.

Background: Lungs are susceptible to several types of toxins. Macrophages may play role in lung fibrosis. Mesenchymal stem cells (MSCs) have several valuable functions that make them a promising therapeutic option in the field of regenerative medicine.

Objectives: Investigate possible therapeutic effects of bone marrow (BM)-MSCs on lung injury induced by carbon tetrachloride (CCl₄) in adult rats with reference to role of macrophages plasticity.

Material and methods: Forty-five adult male albino Wistar rats were divided into four groups. Group I (control). Group II (CCl₄): rats received intraperitoneal injection of CCl₄ (0.1 ml/100 g body weight) twice weekly for two weeks. Group III (BM-MSCs treated) received single injection of BM-MSCs after last injection of CCl₄ and were left for further two weeks. Group IV (recovery): were left for two weeks after last injection of CCl₄. At the end of experiment, all rats were sacrificed. Lung specimens were processed and subjected to H&E, Mallory`s trichrome, CD68, toluidine blue, transmission electron microscope and histomorphometric and statistical studies.

Results: CCl₄ and recovery groups showed thickening of interalveolar septa with mononuclear cellular infiltration, dissolved lamellar bodies in pneumocytes type-II and appearance of foamy macrophages. Significant increase in mean area percentage of collagen fibers, and mean number of CD68 macrophages were also noticed. BM-MSCs improved these histological changes with a significant increase number in pneumocyte type-II.

Conclusions: CCl₄ caused lung injury that was associated with inflammation, increased number of macrophages, and collagen fiber deposition. Treatment with BM-MSCs alleviates these changes and could be used in regenerative medicine.

Women after menopause have a lot of complains that negatively distress their life. In the modern years, a lot of conduction methods have been presented to relief undesirable symptoms. Bone marrow mesenchymal stem cells (BM-MSCs) can be recently used as a new therapeutic method treatment of many diseases and avoidance the hormonal therapy symptoms and complications sides effects that happened after menopause.

Aim: The aim of this research is to show a new approach in modification of the structure of vaginal mucosal atrophy by uses of (BM-MSCs) in induced ovariectomized rats.

Methods and results: Fifty female albino rats were used and divided randomly into five groups: control group, ovariectomized group, ovariectomized group plus estrogen (20 ug/kg/day for 4 weeks), ovariectomized with BMMSCs (107 MSCs/rat intravenously) and ovariectomized rats with stem cells/BM-MSCs Intra-vaginal group, the expression of genes for GAPDH, iNOS and TGF-β were done and vaginal biopsies were taken for histological and immunohistochemical studies. In ovariectomized group there was inflammation, ulceration and re-epithelialization with irregularity in collagen fibers, decreased estrogen receptors expression and expression of TGF-β, GAPDH and iNOS were very high. While the rate of healing of epithelium was increased with increased the vasculatures of vaginal mucosa and the estrogen receptors expression was high with decreased expression of GAPDH, iNOS and TGF-β in ovariectomized rats that treated with intra-vaginal group BM-MSCs.

Conclusions: Using the BM-MSCs could be used intravaginal safely in case of vaginal atrophy as they modify the structure of vaginal mucosa than estrogen hormone therapy alone.

RNA-mediated gene silencing is a fundamental mechanism of gene expression regulation. A main component of RNA silencing machinery, the RNase III Dicer enzyme, catalyzes the processing of double-stranded RNAs (dsRNAs) into ≈21-25 nucleotide-long small interfering (si)RNAs and micro (mi)RNAs, an essential step in the biogenesis of small non-coding RNA molecules. In previous report was reported the Dicer localizes with ER and Golgi network in post-mitotic neurons, increasing its expression during the development and maturation in cultured neurons. With the aim to study the components of RNA-induced silencing complex (RISC), it was investigated the effect of Dicer silencing on survival in cultured cerebellar granule neurons (CGNs). In this immnofluorescence study was observed that Dicer silencing by siRNA facilitates the apoptotic neuronal cell death in CGNs