Hyperuricemia is an abnormal metabolic condition characterized by an increase in uric acid levels in the blood. It is the cause of gout, manifested by inflammatory arthritis, pain and disability. This study examined the possible ameliorative impacts of parsley (PAR) and celery (CEL) as hypouricemic agents at biochemical, molecular and cellular levels. PAR and CEL alone or in combination were orally administered to hyperuricemic (HU) mice and control mice for 10 consecutive days. Serum levels of uric acid and blood urea nitrogen (BUN), xanthine oxidase activity, antioxidants, inflammatory (IL-1β and TNF-α) and anti-inflammatory cytokines (IL-10) were measured. mRNA expression of urate transporters and uric acid excretion genes in renal tissues were examined using qRT-PCR (quantitative real time PCR). Normal histology and immunoreactivity of transforming growth factor-beta 1 (TGF-β1) in kidneys was examined. Administration of PAR and CEL significantly reduced serum BUN and uric acids in HU mice, ameliorated changes in malondialdehyde, catalase, and reduced glutathione, glutathione peroxidase (GPX), IL-1β, TNF-α and IL-10 in hyperuricemic mice. Both effectively normalized the alterations in mURAT-1, mGLUT-9, mOAT-1 and mOAT-3 expression, as well as changes in TGF-β1 immunoreactivity. Interestingly, combined administration of PAR and CEL mitigated all examined measurements synergistically, and improved renal dysfunction in the hyperuricemic mice. The study concluded that PAR and CEL can potentially reduce damaging cellular, molecular and biochemical effects of hyperuricemia both individually and in combination. Hyperuricemia (HU) is defined as an increase in the levels of uric acid over normal ranges (6 mg/dL in females and 7 mg/dL in males) 1,2. HU is associated with meat and seafood ingestion, hypertension and obesity 2-4. Advanced HU is associated with gout 5. Gout results in deposition of urate in soft tissues and joints, and arthritis in men over 40 years old 5. Uric acid (UA) is the end product of the catabolism of purine compounds in the liver. UA is excreted mainly by the kidneys and to a lesser extent by the gastrointestinal tract 6,7. It is degraded by gut microbiota (one third) in a process known as intestinal uricolysis 8. The remaining two thirds depends on interchange between UA secretion and reabsorption in the kidney tubules 8-10. Treatment of gout mainly depends on allopurinol (ALP). ALP is an inhibitor of xanthine oxidase and stimulates renal excretion of UA 10,11. Other anti-inflammatory drugs (indomethacin) can be used, but these may cause side effects 11. Therefore, identifying safe herbal medications is the goal for both patients and physicians. The use of organic drugs and therapies is cost-effective 12. The positive and promising effects of medicinal herbs on renal diseases, infertility, liver disorders and diabetes are clearly established and are accepted by patients and clinicians as a safe medication for these disorders 13-17 .