Somayeh Dehghanipour; Sara Saadatmand; Nasim Hayati Roodbari; Mahdi Mahdavi
Volume 24, Issue 8 , 2022
Abstract
Background: Breast cancer is extensively studied for its resistance to chemotherapy. Therefore, finding efficient therapeutic agents is vital to increasing the survival rate of patients.
Objectives: Here, we conducted an in vitro study on the anti-tumor properties of Vinca herbacea extract on SKBR3 ...
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Background: Breast cancer is extensively studied for its resistance to chemotherapy. Therefore, finding efficient therapeutic agents is vital to increasing the survival rate of patients.
Objectives: Here, we conducted an in vitro study on the anti-tumor properties of Vinca herbacea extract on SKBR3 cells.
Methods: Apoptotic and anti-invasive activity of V. herbacea extract was studied using Annexin FITC-V kit and Matrigel invasive assay, respectively. The expression of angiogenesis genes (VEGFR-1, VEGFR-2, and VEGF-A), apoptotic-related genes (Bcl-2 and BAX), as well as metastatic genes (MMP2 and MMP9) were studied using real-time polymerase chain reaction.
Results: Vinca herbacea extract showed significant antiproliferative and cytotoxic effects on human breast cancer cells, compared to human embryonic kidney cells 293. Vinca herbacea extract had a great apoptosis-inducing potential in breast cancer cells by activating caspase-3 and increasing the BAX/Bcl-2 ratio. Vinca herbacea extract prevented cancer cell angiogenesis, marked by decreasing the expression level of angiogenesis-related genes, including VEGF, VEGFR-1, and VEGFR-2. In addition, V. herbacea extracts reduced cancer cell invasion and noticeably decreased the expression level of metastasis-associated genes, including MMP2 and MMP9.
Conclusion: Vinca herbacea extracts exhibited vigorous cytotoxic effects on SKBR3 cells by the alteration of apoptosis, cell adhesion, invasion, and angiogenesis.
Miran Gholami; Paria Ghahremani; Zhaleh Mohsenifar; Mohammad Mahdi Jaafarzadeh; Ali Momeni; Mohammad Reza Parvizi
Volume 24, Issue 1 , 2022
Abstract
Background: Lead, as the most important toxic heavy element, has several devastating effects on human health and influences most biochemical and physiological functions. It is widely accepted that lead can adversely affect the cardiovascular system since it can be quickly absorbed and recycled in the ...
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Background: Lead, as the most important toxic heavy element, has several devastating effects on human health and influences most biochemical and physiological functions. It is widely accepted that lead can adversely affect the cardiovascular system since it can be quickly absorbed and recycled in the blood strain.
Objectives: This survey scrutinized the effects of N-acetylcysteine (NAC) on the oxidative damage, inflammation, and expression of protein kinase C-alpha (PKC-?) and ankyrin repeat domain 1 (ANKRD1) genes in the heart tissue of rats exposed to lead (Pb).
Methods: The rats were incidentally divided into five groups, including four study groups for the investigation of the effects of the single and continuous doses of lead were examined with and without NAC and a control group (G1). The levels of malondialdehyde (MDA), total antioxidant capacity (TAC), interleukin (IL)-10, and tumor necrosis factor alpha (TNF-?) were analyzed. A reverse transcription polymerase chain reaction was applied to investigate the expression of PKC-? and ANKRD1 genes.
Results: Continuous exposure to Pb significantly decreased serum levels of TAC and IL-10; however, it increased MDA and TNF-? contents (P<0.001). The continuous dose of Pb also dramatically increased the expression of PKC-? and ANKRD1 genes in the cardiac tissue by 4.27-fold and 3.07-fold, respectively (P<0.001). N-acetylcysteine treatments not only improved morphological changes, oxidative stress, and inflammatory biomarkers but also compensated antioxidant capacity and the expression of PKC-? and ANKRD1 genes in cardiac tissues.
Conclusion: Lead exposure is remarkably related to cardiotoxicity mainly by inducing oxidative stress, inflammation, and antioxidant discharge. N-acetylcysteine ameliorates Pb-induced cardiotoxicity by improving the antioxidants capacity, mitigating oxidative stress, and down expressing PKC-? and ANKRD1 genes.
