Preventive Impacts of Black Tea, Green Tea and Bidens pilosa on Renal Stone Formation in Rats: Antioxidant and Anti-inflammatory Pathways.

Previous in vivo studies demonstrated that oxalate loading motivate free radical generation and inflammation, thereafter renal tubular cells damage. This study purposed to discover the efficacy of black tea (BT), green tea (GT), and B. pilosa tea (PT) aqueous extracts to prevent kidney stone formation. Thirty rats were separated into five groups, (I) fed a balanced diet (control normal, CN). (II) fed potassium oxalate rich diet (KOx) to cause hyperoxaluria, without any treatment. Groups III, IV, and V were fed high oxalate diets concomitantly to tea extracts BT, GT, and PT, in that order. Protein, albumin, creatinine, urea, electrolytes (sodium and potassium) were measured in serum, whereas, oxidative markers and some inflammatory cytokines were measured in kidney homogenates. Total phenolic, total flavonoids and antioxidant capacity tests were assessed in all tea extracts. The PT and GT extract had the highest values of total phenolic and total flavonoids, respectively. Moreover, PT extract showed the highest antioxidant capacity among all tea types. The high oxalate diet (KOx) group altered reduced glutathione (GSH) redox balance, notably lowered serum protein, albumin, sodium, and antioxidant enzymes, but significantly increased malondyaldehyde (MDA) level, creatinine, urea, potassium and nitric oxide (NO) in serum. All inflammation markers were notably (p<0.05) elevated in KOx rats. Interestingly, The BT, GT and PT treatment substantially prevented the biochemical changes and restored the observed histological alterations in fed KOx rats. The PT had the strongest influence among other tea extracts. Briefly, these findings suggest that B. pilosa tea aqueous extract, among all studied tea extracts, has an ability to reduce inflammation, glutathione redox equilibrium, prevent peroxidative damage, and replenish renal tissue antioxidants. It can be regarded as functional drink agent to protect from the renal oxalate crystallization.