Can a hydrogen sulfide donor protect the liver from cyclophosphamide?
In rats, 10-day NaHS pretreatment lowered CP-driven ALT/AST spikes and suppressed TLR2/4–JNK/NF-κB inflammatory signaling linked to hepatotoxicity.
Source
TLRs-JNK/ NF-κB Pathway Underlies the Protective Effect of the Sulfide Salt Against Liver Toxicity
What they did
They randomized rats into control, CP, NaHS+CP, and PAG+CP groups (n=6 each), gave NaHS or PAG for 10 days, then a single CP 200 mg/kg dose, and measured liver enzymes and TLR pathway markers.
What they found
CP raised ALT/AST; NaHS reduced enzymes (e.g., ALT 33.24 vs 49.57 U/L) and suppressed TLR2/4 with downstream JNK and NF-κB.
The limits
What it doesn't show
Rodent enzyme/pathway changes do not establish a clinical dosing regimen or human oncology safety for NaHS.
Key terms
- NaHS
- Sodium hydrosulfide, used as an H2S donor.
- Cyclophosphamide (CP)
- Alkylating chemotherapy that can injure the liver.
- ALT/AST
- Serum enzymes used as markers of hepatocellular injury.
- TLR2/4
- Toll-like receptors that amplify inflammatory signaling.
- JNK
- c-Jun N-terminal kinase stress pathway.
- NF-κB
- Transcription factor driving inflammatory gene programs.
Flashcards
Research intelligence for this paper
See its role on concept claims, tensions it is part of, placement history, and related discoveries.
Quiz yourself
Rats per group:
Common questions
Animal design?
4 groups of 6 rats; CP ± NaHS or PAG.
CP dose?
Single 200 mg/kg i.p.
Enzyme effect of NaHS?
Lower ALT/AST vs CP alone.
Pathway finding?
TLR2/4, JNK, and NF-κB suppressed by NaHS.
More on pharmacology