Medicinal plants used in the phytotherapeutical treatment of urolithiasis in dogs – na integrative review

Urolithiasis is a disease in which uroliths form in the urinary tract from individual predisposing factors of each species, and with aggravation, animals can have urethral obstruction and die. In this work, an integrative review of the medicinal plants most used for the treatment of urolithiasis in dogs was carried out. The objective of this work is to collaborate with the veterinary community to expand the use of herbal medicine to treat this pathology, mainly due to its relapsing nature. Its formation can occur in breeds with more evident urinary supersaturation, genetic predisposition, age, reduced daily water intake, metabolic problems, medications that alter urinary pH, inadequate nutrition and predisposition to alterations in the urinary tract. Drug and nutritional treatment is questionable, as there are types of differences in the composition of stones and the response to these can vary a lot and, in more serious cases, surgery is needed. At high rates of recurrence, the use of medicinal plants offers options aimed at the welfare of animals. Therefore, innovative research on their use of these plants informs how they can be consumed safely and with great pharmacological effect. With this, more tutors are looking for professionals who prescribe these plants in a preventive way, avoiding surgical emergencies and possible death of your animal. Urinary system herbal medicines control inflammation and increase diuresis, preventing crystal aggregation and possible growth, in addition to favoring their elimination through the urethra.

TRPV1 Hyperfunction Contributes to Renal Inflammation in Oxalate Nephropathy

Inflammation worsens oxalate nephropathy by exacerbating tubular damage. The transient receptor potential vanilloid 1 (TRPV1) channel is present in kidney and has a polymodal sensing ability. Here, we tested whether TRPV1 plays a role in hyperoxaluria-induced renal inflammation. In TRPV1-expressed proximal tubular cells LLC-PK1, oxalate could induce cell damage in a time- and dose-dependent manner; this was associated with increased arachidonate 12-lipoxygenase (ALOX12) expression and synthesis of endovanilloid 12(S)-hydroxyeicosatetraenoic acid for TRPV1 activation. Inhibition of ALOX12 or TRPV1 attenuated oxalate-mediated cell damage. We further showed that increases in intracellular Ca2+ and protein kinase C α activation are downstream of TRPV1 for NADPH oxidase 4 upregulation and reactive oxygen species formation. These trigger tubular cell inflammation via increased NLR family pyrin domain-containing 3 expression, caspase-1 activation, and interleukin (IL)-1β release, and were alleviated by TRPV1 inhibition. Male hyperoxaluric rats demonstrated urinary supersaturation, tubular damage, and oxidative stress in a time-dependent manner. Chronic TRPV1 inhibition did not affect hyperoxaluria and urinary supersaturation, but markedly reduced tubular damage and calcium oxalate crystal deposition by lowering oxidative stress and inflammatory signaling. Taking all these results together, we conclude that TRPV1 hyperfunction contributes to oxalate-induced renal inflammation. Blunting TRPV1 function attenuates hyperoxaluric nephropathy.