Effect of Elaeagnus Angustifolia extract on in vitro wound healing of human dermal fibroblast cells.

AIM: The purpose of this study was to determine the impact of Elaeagnus Angustifolia extract (EA) on human dermal fibroblast (HDF) survival, migration, and wound healing-related genes. METHODS: After preparing the hydroalcoholic extract of EA, MTT and scratch tests were used to determine the effect of EA on the viability and migration of HDFs. In addition, the quantitative polymerase chain reaction (q-PCR) was conducted to evaluate the impact of EA on the expression of wound healing-related genes in HDFs. RESULT: According to the MTT test, a nontoxic concentration of EA (100 µg/ml) was obtained for further investigations. The scratch test results demonstrated that EA improved HDFs' capacity to migrate when compared to the control group. Additionally, q-PCR results revealed that EA could significantly increase wound healing-related genes (VEGF-A, HLA-G5, and IL-6) in comparison with the control group. CONCLUSIONS: The EA could have a significant impact on the viability and migration of HDFs. Also, EA increased the expression of wound healing-related genes.

The importance of hsa-miR-28 in human malignancies.

MicroRNA production in tumorigenesis is dysregulated by a variety of processes, such as proliferation and removal of microRNA genes, aberrant transcriptional regulation of microRNAs, disrupted epigenetic alterations, and failures in the miRNA biogenesis machinery. Under some circumstances, miRNAs may act as tumorigenic and maybe anti-oncogenes. Tumor aspects such as maintaining proliferating signals, bypassing development suppressors, delaying apoptosis, stimulating metastasis and invasion, and promoting angiogenesis have been linked to dysfunctional and dysregulated miRNAs. MiRNAs have been found as possible biomarkers for human cancer in a great deal of research, which requires additional evaluation and confirmation. It is known that hsa-miR-28 can function as an oncogene or tumor suppressor in many malignancies, and it does this by modulating the expression of several genes and the downstream signaling network. MiR-28-5p and miR-28-3p, which originate from the same RNA hairpin precursor miR-28, have essential roles in a variety of cancers. This review outlines the function and mechanisms of miR-28-3p and miR-28-5p in human cancers and illustrates the miR-28 family's potential utility as a diagnostic biomarker for prognosis and early detection of cancers.

The Tumor Suppressor Roles and Mechanisms of MiR-491 in Human Cancers.

MicroRNAs (miRNAs) are short non-coding RNAs that bind to the 3' untranslated region (3'' UTR) of target mRNAs to control gene expression post-transcriptionally. Recent indications have highlighted their important roles in a variety of pathophysiological conditions as well as human malignancies. Dysregulated miRNAs act as tumor suppressor genes or oncogenes in a variety of cancers. MiR-491 has been shown to have a major effect on tumorigenesis in multiple malignancies through binding to specific genes and signaling cascades, thereby preventing cancer progression. This review provides an overview of miR-491 expression in regulatory mechanisms and biological procedures of tumor cells, as well as the prospective possible treatment effects of various types of human cancers.

The altered expression of homing factors in CD34+ hematopoietic stem cells following G-CSF injection and its effects on transplantation quality in ALL patients.

Hematopoietic stem cells (HSCs) transplantation is considered a suitable treatment for malignant or nonmalignant hematological diseases. This study aims to investigate the HSCs homing factors in bone marrow (BM) donors of acute lymphoblastic leukemia (ALL) patients following granulocyte colony-stimulating factor (G-CSF) injection, as well as the G-CSF effects on BM transplantation quality in these patients. To mobilize HSCs into peripheral blood, G-CSF was used for ALL patient's BM donors. For HSCs counting, CD34+ cells were evaluated in analogous and autologous donors using flow cytometry. The expression of stem cell homing factors in CD34+ cells and peripheral blood mononuclear cells (PBMCs) were investigated using a real-time polymerase chain reaction. Finally, hematological factors after BM transplantation in ALL patients were assessed. According to our results, after G-CSF injection, the level of CD34+ HSCs was statistically increased. Besides, autologous donors showed a higher level of CD34+ cells compared to analogous donors before and after G-CSF injection. Additionally, a higher number of CD34+ HSCs was achieved in the autologous samples following G-CSF injection. Furthermore, after G-CSF injection, the expression of matrix metalloproteinase (MMP)-2, MMP-9 was increased; while, stromal cell-derived factor 1, intercellular adhesion molecule-1, and vascular cell adhesion molecule-1 expression were decreased. Moreover, the expression of C-X-C chemokine receptor type 4, lymphocyte function-associated antigen 1, and very late antigen-4 in CD34+ cells and PBMCs were decreased. BM transplantation on Day 90 also caused an increased level of white blood cells, red blood cells, and platelets as compared to the first day; however, no statistical differences were observed in hemoglobin level. In conclusion, G-CSF by altering the expression of HSCs homing factors in ALL donors improves BM transplantation quality in ALL patients.

Ameliorative role of aspirin in paraquat-induced lung toxicity via mitochondrial mechanisms.

Paraquat (PQ) has accounted for numerous suicide attempts in developing countries. Aspirin (ASA) as an adjuvant treatment in PQ poisoning has an ameliorative role. And, it's uncoupling of mitochondrial oxidative phosphorylation role has been well established. The current study aimed at examining the aspirin mechanism on lung mitochondria of rats exposed to PQ. Male rats were randomly allocated in five groups: Control group, PQ group (50 mg/kg; orally, only on the first day), and PQ + ASA (100, 200, and 400 mg/kg; i.p.) groups for 3 weeks. Mitochondrial indices and respiratory chain-complex activities were determined. PQ induced lung interstitial fibrosis; however, ASA (400 mg/kg) led to decrease in this abnormal alteration. In comparison with PQ group, complex II and IV activity, and adenosine triphosphate content in ASA groups had significantly increased; however, reactive oxygen species production, mitochondrial membrane permeabilization, and mitochondrial swelling were significantly reduced. In conclusion, aspirin can alleviate lung injury induced by PQ poisoning by improving mitochondrial dynamics.