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Xanthones protects lead-induced chronic kidney disease (CKD) via activating Nrf-2 and modulating NF-kB, MAPK pathway.

ABSTRACT: Xanthones from a tropical fruit of Garcinia mangostana L. is known to possess a wide spectrum of pharmacologic properties, including antioxidant, anti-bacterial, anti-inflammatory, and antidiabetic activities. The current study aimed to assess the possible protective effects of xanthones against lead acetate (PbAc)-induced chronic kidney disease (CKD). To accomplish, in vitro antioxidant assays of xanthones, in vivo oxidative stress parameters, histopathology, inflammatory parameters were evaluated using PbAc-induced IRC male mice. The study was supported by in silico molecular docking of respective organ receptor protein-ligand interaction. Results revealed that xanthones potentially scavenged the DPPH, superoxide, hydroxyl, and nitric oxide radicals. Oxidative stress, kidney dysfunction, inflammatory markers, and kidney apoptosis increased by PbAc were attenuated with the co-treatment of xanthones. The treatment remarkably improved the tissue architecture. Of note, in silico prediction of activity study showed that protective role of xanthones could be due to its efficacy to activate the Nrf-2, regulate the intracellular [Ca2+], as well as downregulate the NF-kB, MAPK pathway. In a nutshell, xanthones could be a potential candidate for the management of PbAc-induced kidney damage.

SUBMITTER: Rana MN

PROVIDER: S-EPMC6920509 | biostudies-literature | 2020 Mar

REPOSITORIES: biostudies-literature

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Xanthones protects lead-induced chronic kidney disease (CKD) via activating Nrf-2 and modulating NF-kB, MAPK pathway.

Rana Mohammad Nasiruddin MN Tangpong Jitbanjong J Rahman Md Atiar MA

Biochemistry and biophysics reports 20191210

Xanthones from a tropical fruit of Garcinia mangostana L. is known to possess a wide spectrum of pharmacologic properties, including antioxidant, anti-bacterial, anti-inflammatory, and antidiabetic activities. The current study aimed to assess the possible protective effects of xanthones against lead acetate (PbAc)-induced chronic kidney disease (CKD). To accomplish, in vitro antioxidant assays of xanthones, in vivo oxidative stress parameters, histopathology, inflammatory p ...[more]

PMID: 31886417

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Project description:Background: Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is a common respiratory disease characterized by persistent hypoxemia and an uncontrolled inflammatory response. Valsartan, an angiotensin II type 1 receptor antagonist, is clinically used to treat hypertension and has anti-inflammatory and antioxidant effects on gefitinib-induced pneumonia in rats. However, the potential therapeutic effects of valsartan on lipopolysaccharide (LPS)-induced ALI remain unclear. This study investigated the protective role of valsartan in LPS-induced ALI and its underlying mechanisms. Methods: LPS-treated BEAS-2B cells and ALI mouse model were established. BEAS-2B cells were treated with LPS (10 μg/mL) for 24h, with or without valsartan (20, 40, and 80 µM). For ALI mouse models, LPS (5 mg/kg) was administered through intratracheal injection to treat the mice for 24h, and valsartan (10 or 30 mg/kg) was injected intraperitoneally twice 2 h before and 12 h after the LPS injection. Pulmonary functional parameters were examined by an EMKA pulmonary system. Hematoxylin and eosin staining, flow cytometry, CCK-8 assay, qRT-PCR, ELISA, immunofluorescence, Western blotting, and related commercial kits were used to assess the pathological damage to the lungs, neutrophil recruitment in the lung tissue and bronchoalveolar lavage fluid (BALF), cell viability, inflammation, oxidative activity, and mucus production, respectively. Potential mechanisms were further explored using network pharmacology and Western blotting. Results: Valsartan rescued LPS-reduced cell viability of BEAS-2B cells, improved the pulmonary function, ameliorated pathological lung injury in mice with ALI, ameliorated LPS-induced neutrophil recruitment in BALF and lung tissue of mice, attenuated oxidative stress by increasing the level of SOD and decreasing that of MDA and GSSG, inhibited LPS-induced MUC5AC overproduction, decreased the LPS-induced increase in expression of pro-inflammatory cytokines/chemokines including TNF-α, IL-6, IL-1β, CXCL-1 and CXCL-2, and restored the expression of anti-inflammatory IL-10. Mechanistic studies showed that valsartan inhibits LPS-induced phosphorylation of nuclear factor-kappa B (NF-κΒ) and mitogen-activated protein kinases (MAPKs) including P38, extracellular signal-regulated kinase (ERK), and c-Jun N-terminal kinase (JNK) in both LPS-treated cells and the mouse model of ALI. Conclusion: Valsartan protects against LPS-induced ALI by attenuating oxidative stress, reducing MUC5AC production, and attenuating the inflammatory response that may involve MAPK and NF-κΒ pathways.

Dataset Information

Xanthones protects lead-induced chronic kidney disease (CKD) via activating Nrf-2 and modulating NF-kB, MAPK pathway.

Publications

Xanthones protects lead-induced chronic kidney disease (CKD) via activating Nrf-2 and modulating NF-kB, MAPK pathway.

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