Tag Archives: Bax

Localization and level of proapoptotic protein regulators in a rat lung tissue during development of acute experimental bronchopneumonia

D. S. Ziablitsev1*, A. O. Tykhomyrov2, O. O. Dyadyk3,
S. V. Kolesnikova1, S. V. Ziablitsev1

1Bogomolets National Medical University, Kyiv, Ukraine;
2Palladin Institute of Biochemistry, National Academy of Sciences of Ukraine, Kyiv;
3Shupyk National Healthcare University of Ukraine, Kyiv;
*e-mail: denis898@ukr.net

Received: 20 July 2022; Revised: 13 September 2022;
Accepted: 04 November 2022; Available on-line: 14 November 2022

Apoptosis plays an important role in the development of acute inflammatory lung injury (AILI) and its consequences, which can be realized in different cells with distinct intensity and rate. The aim of this study was to determine the distribution and expression intensity of apoptosis markers in the lungs of rats in the AILI model with endotracheal introduction of capron thread and LPS. Immunoblotting and immunohistochemical studies were performed using monoclonal antibodies against Bax and caspase-3 proteins. It was shown that Bax level increased significantly with the peak on the 7th day. The second peak of Bax 40 dimeric form was noted on the 21st day. The level of both pro-caspase-3 and active caspase-3 was also dramatically increased with a maximum on the 5th day and the second peak of active caspase-3 content was observed on the 21st day. These changes reflected the activation of apoptosis in key trigger periods of AILI during the development of exudative hemorrhagic pneumonia and subsequent fibrotic remodeling of the lungs.

Effect of N-acetyl cysteine on oxidative stress and Bax and Bcl2 expression in the kidney tissue of rats exposed to lead

M. Gholami1, A. B. Harchegani2, S. Saeedian3,
M. Owrang4, M. R. Parvizi1*

1Department of Physiology, Faculty of Medicine, AJA University of Medical Sciences, Tehran, Iran;
2Department of Medical Genetics, Faculty of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran;
3Medical Genomic Research Center, Tehran Medicine Sciences Islamic Azad University, Tehran, Iran;
4Faculty of Medicine, Sari Branch, Islamic Azad University, Sari, Iran;
*e-mail: mparvizi@alumnus.tums.ac.ir

Received: 30 May 2020; Accepted: 17 December 2021

This study aimed to consider the lead-induced oxidative damage of the kidney of male rats and the role of antioxidant N-acetylcysteine (NAC) in preserving cells against Pb toxicity. Rats were randomly divided into five groups including G1 (control), G2 (single 70 mg/kg dose of Pb), G3 (continuous daily 2 mg/kg dosing of Pb for 4 weeks), G4 (single dose of Pb + 50 mg/kg NAC), and G5 (continuous daily dosing of Pb + 50 mg/kg NAC). The level of malonic dialdehyde (MDA) and total antioxidant capacity were measured spectrophotometrically.The level of Pb in  serum and kidney tissue was measured by atomic absorption spectroscopy. Expression of Bax and Bcl2 genes was estimated using RT-PCR.  It was shown that single and continuous exposure to Pb caused a considerable increase of Pb content in serum and kidney tissue of rats in G2 and G3 groups compared to other groups. NAC treatment significantly improved TAC values and decreased MDA values in the serum of rats exposed to Pb. Single and continuous Pb dosing caused a 3.9- and 13.1-fold increase in Bax expression and 1.5-fold and 2.1-fold decrease in Bcl2 expression in a kidney tissue respectively. The current study revealed that single and  especially continuous Pb exposure  was strongly associated with Pb accumulation, antioxidant depletion, oxidative stress and kidney cells apoptosis. NAC can help protect kidney tissue against Pb by elevating antioxidant capacity, mitigating oxidative stress and normalizing Bax and Bcl2 genes expression.

Leptin and curcumin affect renal ischemia-reperfusion injury via modulation of P65 and Bax genes expression

M. M. Ragy1, M. M. Ramzy2*

1Physiology Department, Faculty of Medicine, Minia University, Misr-Aswan Road, Egypt;
2Biochemistry Department, Faculty of Medicine, Minia University, Misr-Aswan Road, Egypt;
*e-mail: maggiemaher24@gmail.com

Received: 01 June 2020; Accepted: 17 December 2020

Ischemia and reperfusion are natural steps during kidney transplantation, and ischemia-reperfusion injury is a critical condition in which physicians must preserve organ function and control cell damage. As leptin is thought to play an important role in the regulation of the immune system and inflammation and curcumin is a potent anti-fibrotic agent, both agents are promising to have therapeutic impact on renal damage. The present study was designed to evaluate the effects of leptin and curcumin on renal ischemia-reperfusion injury. Forty adult male albino rats were divided into four groups: control; ischemia-reperfusion (I/R), leptin-treated (leptin was injected intraperitoneally at a dose 100 μg/kg for 3 days prior to ischemia) and curcumin-treated (curcumin was given orally at a dose of 50 mg/kg/day for 5 days before ischemia). All rats were sacrificed 24 hours after reperfusion. Serum urea and creatinine, renal malondialdehyde and total antioxidant capacity were measured. Renal TNF-α was assayed by ELISA and P65 and Bax mRNA expression were determined using RT-PCR. Our results demonstrated a significant increase in P65 and Bax mRNA expression after renal ischemia-reperfusion injury compared to control group. Both leptin and curcumin prevented oxidative damage of the renal tissues as they lowered MDA and nitric oxide levels, increased antioxidant capacity and decreased TNF-α level. It was shown that protective leptin and curcumin effect against kidney IR-induced oxidative injury was associated with a down-regulation of P65 and Bax expression. These results show that ischemia-reperfusion leads to renal damage and also they reveal that both leptin and curcumin have protective implications which may be promising agents for avoiding various adverse effects.