Impact of folic acid supplementation on ischemia‒reperfusion-induced kidney injury in rats: folic acid prophylactic role revisited.

Folic acid (FA), with its anti-inflammatory and antioxidant properties, may offer protection against ischemia-reperfusion (IR) injury. This study investigated whether FA safeguards rat kidneys from IR by targeting high mobility group box-1 (HMGB1), a key inflammatory mediator. Fifty adult male Wistar rats were randomly allocated into four groups: control, IR, IR + FA pretreatment, and FA alone. Compared to controls, IR significantly impaired renal function and elevated levels of malondialdehyde, HMGB1, NF-κB, and caspase 3. FA pretreatment effectively reversed these detrimental changes, protecting renal function and minimizing tissue damage. The FA-alone group showed no significant differences compared to the control group, indicating no adverse effects of FA treatment. Mechanistically, FA inhibited HMGB1 expression and its downstream activation of NF-κB and caspase 3, thereby quelling inflammation and cell death. FA shields rat kidneys from IR-induced injury by suppressing HMGB1-mediated inflammation and apoptosis, suggesting a potential therapeutic avenue for IR-associated kidney damage.

Possible role of l-carnitine in improvement of metabolic and hepatic changes in hyperuricemic and hyperuricemic-Fructose-supplemented rats.

Hyperuricemia was linked to diabetes mellitus, metabolic syndrome, and oxidative stress, and could be induced by higher fructose consumption through altering energy status in liver. l-Carnitine is an antioxidant, affecting mitochondria and cellular energetics; however, little is known about its effects in hyperuricemic states. This study investigated metabolic and hepatic effects of hyperuricemia and fructose feeding, and demonstrated the role of l-Carnitine in such states. Fifty adult male Wistar rats were randomly divided into control, untreated hyperuricemic, fructose-supplemented hyperuricemic, l-Carnitine-treated hyperuricemic, and l-Carnitine-treated fructose-supplemented hyperuricemic groups. The separated plasma was used for determination of the glycemic control, lipid profile, liver function tests, uric acid level, and oxidative stress markers. Atherogenic index, HOMA-IR, and body mass index (BMI) were calculated. Left liver lobe and left kidney specimen from all groups were used for histopathological studies. Hyperuricemic rats exhibited significantly hypoalbuminemia, dyslipidemia, insulin resistance, and oxidative stress compared to the controls. Fructose-supplemented hyperuricemic group showed obesity and more deleterious effects, as well as, steatosis, and renal tubular damage compared to the hyperuricemic rats. Concomitant l-Carnitine treatment with hyperuricemia improved such effects, despite causing adiposity. While combined l-Carnitine treatment and fructose supplementation in hyperuricemia limited the aggressive hyperuricemic picture of fructose supplementation. It is concluded that hyperuricemia has detrimental metabolic and hepatic effects. Artificial fructose supplementation worsened such effects, while l-Carnitine was efficient in ameliorating these hyperuricemia and/or excess fructose-induced hyperuricemia effects, through its anti-inflammatory, antisteatotic, and antioxidant properties.