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

Overview

Rana and colleagues tested whether an aqueous Thunbergia laurifolia leaf extract altered lead-acetate-induced kidney toxicity in mice. This is lane a4 toxicology and co-treatment evidence, not vitamin/mineral supplement occurrence evidence: Pb acetate was deliberately supplied in drinking water, and blood/kidney Pb were measured as exposure-confirmation endpoints. The paper reports exact blood Pb, kidney Pb, kidney-weight, renal-function, and histopathology values.

Key numbers

• Study design: seven experimental groups, n = 6 mice per group, treated for 38 days.
• Lead exposure: PbAc at 1% in DW (drinking water) in the PbAc, Pb + TL, and Pb + vitamin E groups.
• Co-treatments: Thunbergia laurifolia leaf extract at 100 mg/kgBW or 200 mg/kgBW; vitamin E at 100 mg/kgBW in the comparator group.
• Blood Pb, untreated control vs PbAc vs Pb + TL 100 vs Pb + TL 200 vs Pb + vitamin E: 1.83 ± 0.26, 65.35 ± 0.83, 63.12 ± 1.59, 62.96 ± 1.25, and 64.89 ± 2.45 mg/dL.
• Kidney Pb, untreated control vs PbAc vs Pb + TL 100 vs Pb + TL 200 vs Pb + vitamin E: 1.43 ± 0.08, 52.70 ± 0.27, 45.45 ± 2.14, 42.50 ± 0.97, and 52.90 ± 2.13 mg/g protein.
• Relative kidney weight, untreated control vs PbAc vs Pb + TL 100 vs Pb + TL 200 vs Pb + vitamin E: 0.81 ± 0.03, 1.12 ± 0.04, 1.04 ± 0.04, 0.92 ± 0.04, and 1.01 ± 0.06.
• Plasma renal-function markers, untreated control vs PbAc vs Pb + TL 100 vs Pb + TL 200 vs Pb + vitamin E: BUN 32.80 ± 1.01, 45.04 ± 4.49, 20.33 + 0.41, 23.00 + 0.71, and 23.33 + 1.02 mg/dL; creatinine 0.23 ± 0.03, 0.38 ± 0.05, 0.33 + 0.05, 0.36 + 0.03, and 0.27 + 0.04 mg/dL.
• Urine endpoints, untreated control vs PbAc vs Pb + TL 100 vs Pb + TL 200 vs Pb + vitamin E: protein 20.80 ± 0.02, 27.60 ± 0.05, 24.10 ± 0.02, 22.20 ± 0.05, and 19.50 ± 0.04 mg/dL; creatinine 15.20 ± 1.17, 9.60 ± 1.62, 11.07 ± 0.14, 18.80 ± 3.04, and 22.10 ± 0.96 mg/dL; protein/creatinine ratio 1.36, 2.88, 2.18, 1.18, and 1.13.
• Histopathology scores: PbAc group scored +++ for hydropic degeneration in tubules, glomerular damage, and inflammatory cellular infiltration; Pb + TL 100 scored ++ for all three; Pb + TL 200 and Pb + vitamin E scored 0 for all three.
• Apoptosis: the text states the PbAc group had a 5.75-fold increase in kidney cell death versus untreated control, and TL 200 mg/kgBW reduced dead cells by 2.97-fold vs PbAc.

Methods (brief)

The authors combined in silico PASS and molecular-docking work with an in vivo Swiss Albino mouse experiment. Thunbergia laurifolia leaves were collected in Nakhon Si Thammarat, Thailand, oven-dried, pulverized, water-extracted, autoclaved, filtered, and freeze-dried. Blood and kidney Pb were measured by atomic absorption spectrophotometry using a Z-5000 Hitachi instrument at 283.3 nm; the paper reports Pb as total lead without speciation. Oxidative-stress, inflammatory, renal-function, H&E histopathology, and TUNEL apoptosis endpoints were assessed after 38 days of treatment.

Implications

Certification: This paper should not enter any consumer-product occurrence pool. It records controlled mouse lead-acetate exposure and kidney toxicity endpoints, with a botanical co-treatment that reduced kidney Pb relative to PbAc controls but did not normalize blood Pb.

Courses: Useful for teaching the difference between exposure confirmation, tissue retention, and injury mitigation. The paper shows why a co-treatment can improve renal injury markers while leaving high systemic Pb exposure largely intact.

App: Supports lead toxicology and remediation-context notes on the metal and mitigation pages. It does not support a vitamin/mineral supplement occurrence row.

Microbiome: No microbiome endpoints.

Wiki pages this source may touch

• Lead
• Remediation evidence — drivers and interventions
• Health

Verification notes

• Recovered under the 2026-06-10 inclusion-by-default rule, lane a4 exposure and health effect, with adjacent a2 co-treatment context. Prior skip was skip:no-occurrence-data because the paper had no consumer-product concentration table.
• DOI, title, authors, journal, open-access license, treatment structure, n = 6 group size, PbAc drinking-water dose, Table 1 Pb and kidney-weight values, Table 2 kidney-function values, Table 3 histopathology grades, and method details were checked against the extracted PDF text on 2026-06-11.
• Units are preserved exactly as printed in the source, including mg/dL, mg/g protein, mg/kgBW, and 1% in DW. The BUN and creatinine rows use the source’s printed + notation for several Pb co-treatment cells.
• Speciation: the source reports Pb and PbAc exposure; no lead speciation is reported.
• Products and ingredients are intentionally empty because this is an animal toxicology/co-treatment paper, not a botanical supplement occurrence study.

Update history

The five most recent substantive edits to this page, classified major (evidence or structure moved), correction (a published value or statement was wrong and has been fixed), or minor (narrative rewritten without changing the underlying evidence). Each description is derived from what the edit did to this page; the linked commit is the authoritative record, routine regeneration passes are excluded, and the full version history lives in git. When DOI minting comes online (see schema docs), each entry below will also link to a version-pinned DataCite DOI.