ArticleCell biochemistry and biophysics2026
Modulation of Nrf2/TNF-α and TLR4/TGF-β1 Signaling Pathways by Nigella Sativa Oil and Echinacea Purpurea Extract Attenuates Cyclosporine A-Induced Nephrotoxicity and Immunotoxicity.
Article in Cell biochemistry and biophysics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cyclosporine A (CSA), a critical immunosuppressant, induces nephrotoxicity through oxidative stress and inflammatory pathways, limiting its clinical utility. Natural compounds like Nigella sativa oil (NSO) and Echinacea purpurea extract (EPE) possess antioxidant and immunomodulatory properties, but their combined mechanistic action against CSA toxicity is unexplored. This study investigated the protective mechanisms of NSO and EPE, individually and in combination, against CSA-induced renal and immunological toxicity in rats. Fifty male Wistar rats were divided into five groups (n = 10/group): Control, CSA (cyclosporine A, 15 mg/kg/day, i.p.), CSA + NSO (Nigella sativa oil, 200 mg/kg/day, p.o.), CSA + EPE (Echinacea purpurea extract, 200 mg/kg/day, p.o.), and CSA + NSO+EPE (100 mg/kg/day each, p.o.). After 30 days, renal and bone marrow tissues were analyzed for oxidative stress and redox status markers (malondialdehyde, MDA; reduced glutathione, GSH; oxidized glutathione, GSSG) and the antioxidant transcription factor Nrf2 (nuclear factor erythroid 2-related factor 2), alongside the pro-inflammatory mediator TNF-α (tumor necrosis factor-alpha). Gene expression of renal injury biomarkers (Tlr4, toll-like receptor 4; Tgfb1, transforming growth factor-β1; Lcn2, lipocalin-2; Kim1, kidney injury molecule-1) and bone marrow immunomodulatory cytokines (Il2, interleukin-2; Il6, interleukin-6; Il17a, interleukin-17 A; Ifng, interferon-γ) was also assessed. Serum hepatic (AST, aspartate aminotransferase; ALT, alanine aminotransferase) and renal (creatinine, urea) function parameters, along with hematological parameters, were also evaluated. CSA significantly (p < 0.05) induced oxidative stress (↑MDA, ↑GSSG; ↓GSH, ↓Nrf2) and inflammation (↑TNF-α) in kidney and bone marrow. It upregulated renal pro-fibrotic and injury genes (Tlr4, ~ 2.9-fold; Tgfb1, ~ 4.9-fold; Lipocalin-2, ~ 3.9-fold; Kim1, ~ 4.3-fold) and severely downregulated bone marrow cytokines (Il2, Il6, Il17a, Ifng; up to ~ 80%). Co-treatment with NSO and EPE, particularly in combination, potently reversed these effects. The combination therapy most effectively normalized oxidative balance, suppressed TNF-α, enhanced Nrf2, mitigated the expression of renal injury genes, and significantly restored the expression of key bone marrow cytokines towards control levels, concurrently improving serum creatinine, urea, and hematological profiles. NSO and EPE confer protection against CSA toxicity through a multi-mechanistic approach: potentiation of the Nrf2 antioxidant pathway and concomitant suppression of TLR4-mediated inflammatory and TGF-β1-driven fibrotic signaling. Their combination offers a superior therapeutic strategy to harness CSA's immunosuppressive benefits while alleviating its detrimental renal and immunological side effects.
Indexed as
Identifiers
42758440What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.