Thunbergia laurifolia leaf extract partially recovers lead-induced renotoxicity through modulating the cell signaling pathways

Mohammad Nasiruddin Rana; Naymul Karim; Suksan Changlek; Md Atiar Rahman; Jitbanjong Tangpong; Dina Hajjar; Walla Alelwani; Arwa A Makki

doi:10.1016/j.sjbs.2020.08.016

Thunbergia laurifolia leaf extract partially recovers lead-induced renotoxicity through modulating the cell signaling pathways

Saudi J Biol Sci. 2020 Dec;27(12):3700-3710. doi: 10.1016/j.sjbs.2020.08.016. Epub 2020 Aug 13.

Authors

Mohammad Nasiruddin Rana^{1

2

3}, Naymul Karim^{1

3}, Suksan Changlek^{1

3}, Md Atiar Rahman⁴, Jitbanjong Tangpong^{1

3}, Dina Hajjar⁵, Walla Alelwani⁵, Arwa A Makki⁵

Affiliations

¹ Biomedical Sciences, School of Allied Health Sciences, Walailak University, Nakhon Si Thammarat 80161, Thailand.
² Department of Pharmacology, Zhejiang University School of Medicine, Hangzhou 310058, PR China.
³ Research Excellence Center for Innovation and Health Products (RECIHP), Walailak University, Nakhon Si Thammarat 80160, Thailand.
⁴ Department of Biochemistry and Molecular Biology, University of Chittagong, Chittagong, Bangladesh.
⁵ Department of Biochemistry, College of Sciences, University of Jeddah, Jeddah 80203, Saudi Arabia.

Abstract

This research investigated the reno-protective effect of Thunbergia laurifolia Linn. (TL) in a lead-induced toxicity test through the modulation of cell signaling pathways. The study carried out to evaluate the effect of TL leaf extracts in Swiss Albino mice exposed to lead acetate (PbAc). Prior to in vivo study, a probable kidney-protective effect of the plant leaf extract was presumed through an activity-specific (PASS) molecular docking analysis. In animal model study, albino mice were divided in seven groups and co-treated with PbAc and TL (100, 200 mg/kgBW) or vitamin E (100 mg/kgBW) for 38 days, whereas the untreated control, TL control, and vehicle control groups received sodium acetate, PbAc, sodium acetate plus mineral oil, respectively. At the end of treatment, blood and kidney tissue were collected for investigating Pb concentration, estimating biochemical profile, evaluating oxidative stress and inflammatory parameters. The histopathological change of kidney along with apoptosis was assessed from kidney sections using H & E staining and TUNEL assay. Pb-exposed mice were found to be increased concentration of Pb in the blood and kidney sample, which further led to increased MDA levels in the plasma, blood, and tissue. Followed by kidney damage, increased expression of TNF-α, iNOS, and COX-2 in kidney tissues were noticed, which were related to elevated TNF-α in the systemic circulation of Pb-treated mice. Co-treatment with TL or vitamin E significantly reduced altered structure and apoptosis of kidney tissues. Downregulation of inflammatory markers especially TNF-α, iNOS, and COX-2 with simultaneous improvement of renal function through reduced plasma BUN and creatinine levels demonstrate that TL act as a potential dietary supplement to detoxify Pb in kidney showing an antioxidant and anti-inflammatory effect.

Keywords: Anti-inflammation; BUN, Blood urea nitrogen; BW, body weight; COX-2, Cyclooxygenase-2; DNA, Deoxyribonucleic acid; ELISA, enzyme-linked immunosorbent assay; GFR, Glomerular filtration rate; H&E, Hematoxylin-Eosin; Lead (Pb); MDA, Malondialdehyde; Oxidative stress; Pb, lead; ROS, reactive oxygen species; Renotoxicity; TBARS, Thiobarbituric acid reactive substances; TBS, Tris phosphate saline; TBST, Tris phosphate buffer saline with Tween 20; TL, Thunbergia laurifolia Linn.; TNF-α, Tumor necrosis factor-alpha; TUNEL, Terminal deoxynucleotidyl transferase dUTP nick end labeling; Thunbergia laurifolia Linn.; iNOS, Inducible nitric oxide synthase.