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
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Can a hydrogen sulfide donor protect the liver from cyclophosphamide?
These passages occur verbatim in the stored paper text. They support the points listed below; they do not verify every statement in the explanation.
4 groups of 6 rats each.
animals were divided randomly into 4 groups each of 6 rats.
CP 200 mg/kg raised ALT/AST (p<0.05).
As presented in Figure 1 , administration of a single CP dose (200 mg/kg, i. p.) significantly elevated ( p < 0.05) both serum ALT ( Figure 1A ) and AST levels ( Figure 1B ) compared to the control group.
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.
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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.
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