Isaac Zamora-Bello

Background: Tartrazine (TZ) has been linked to hyperactivity in children, as well as to kidney and liver damage. Furthermore, naringenin (NG) is a flavonoid with antioxidant and anti-inflammatory properties that may mitigate the damage caused by TZ. Methods: Four independent groups were used, each consisting of seven male Wistar rats—vehicle VEH (saline solution/DMSO, 0.600 mL; IP), TZ (150 mg/kg; IP), NG (100 mg/kg; IP), and TZ + NG (150 mg/kg; 100 mg/kg; IP). For 28 days, treatments were administered every 24 h, and the behavioral effects were evaluated via the open field and Rotarod tests. At the end of the behavioral tests, biochemical and histological analyses of the liver, kidney, and intestine were performed. Results: In the open field test, TZ decreased the number of crossings and rearing behaviors, which was attenuated in NG. The number of grooming behaviors was significantly reduced by TZ, while the duration of this behavior did not significantly differ between the treatment groups. In Rotarod, the TZ group presented less coordination than the other groups. In the TZ group, all parameters included in the liver and kidney function tests showed a significant increase compared to normal levels, reflecting a pathological condition in those organs. On the other hand, groups TZ + NG were within the reference intervals. Treatment with NG reduced the damage caused by TZ. Finally, in the histological analysis, damage to liver, kidney, and intestinal tissues was observed in the TZ groups, whereas treatment with NG mitigated the cellular damage caused by TZ. Conclusions: Naringenin exhibited a protective effect as it restored liver and kidney parameters to normal levels and demonstrated a predominant preservation of the histological architecture of the liver, kidney, and intestine. In this regard, the protective effect observed could be related to the antioxidant, anti-inflammatory, and anti-apoptotic properties described for naringenin. However, further research is still needed to validate the use of naringenin as a potential candidate for improving renal and hepatic function, based on mechanistic studies.

Introduction: Spontaneous and recurrent epileptic seizures cause neuroinflammation, whereas the chronic administration of antiepileptic drugs may lead to hepatotoxicity and nephrotoxicity. Investigating natural compounds such as naringenin, which exhibits antioxidant, anti-inflammatory, and neuroprotective properties, could mitigate these toxic effects. However, whether naringenin delays seizure onset through anti-inflammatory mechanisms remains unclear. Objective: We evaluated the anticonvulsant effect of subchronic naringenin administration and its impact on inflammatory biomarkers in rats. Methods: Thirty-two male Wistar rats were divided into four groups (n = 8 each): vehicle (10% DMSO), naringenin (50 mg/kg), naringenin (100 mg/kg), and diazepam (4 mg/kg). Treatments were administered once daily for ten days through the intraperitoneal route. On day 11, status epilepticus (SE) was induced via the lithium-pilocarpine model. One hour after SE onset, cardiac blood was collected, and the serum was analyzed via ELISA to quantify the following inflammatory markers: superoxide dismutase (SOD), C-reactive protein (CRP), carbonyl protein, and nitrite/nitrate. Results: We found that 100 mg/kg naringenin increased the latency to SE and the first generalized seizure and shortened the duration of generalized seizures. Fifty percent of the rats in the 100 mg/kg naringenin group did not develop SE. The group treated with 100 mg/kg naringenin demonstrated reduced levels of CRP, protein carbonyls, and nitrates; conversely, the inhibition of SOD activity increased. Conclusions: Naringenin exerted anticonvulsant activity associated with a reduction in oxidative stress and inflammatory plasma biomarkers, suggesting its potential utility in the future development of alternative treatments to reduce epilepsy symptoms.

Objectives: To evaluate the effects of chronic oral administration of commercial guava (Psidium guajava L.) leaf extract on biochemical markers and liver histology in a model of metabolic syndrome in rats. Methods: Thirty-five Wistar rats were assigned to five independent groups (n=7 per group): the control group (CG), which received a diet with standard rodent food (Nutri-Cubos ^® ) and water ad libitum ; the metabolic syndrome group (MS), MS + P . guajava (Pg) low-dose (PgL; 100 mg/kg), MS + Pg medium-dose (PgM; 200 mg/kg), and MS + Pg high-dose (PgH; 300 mg/kg) groups. MS was induced with a rich diet of fat and carbohydrates, in addition to the intake of a 30 % sucrose solution ad libitum for 14 weeks. From week 15 onward, guava leaf extract or vehicle was administered orally every 24 h for 30 consecutive days without changing the experimental diet. At the end of the treatment, biochemical tests, liver histopathological analysis and adipose tissue analysis were performed. Results: The MS group presented levels above the reference ranges for biochemical tests, weight gain, waist circumference gain, arterial hypertension, atypical liver cells and aberrant appearance in adipose rat tissue. The PgM and PgH groups presented opposite effects of MS on biochemical parameters, such as increased blood pressure and liver damage. Conclusions: Chronic treatment with Pg leaf extract attenuated MS in Wistar rats, restoring the levels of biochemical parameters and exerting hepatoprotective effects. These findings suggest that guajava extract could be used in the development of therapeutic agents to improve the biochemical and histological alterations induced by MS.

Epilepsy is a chronic neurological disorder that lacks a cure. The use of plant-derived antioxidant molecules such as those contained in turmeric powder and resveratrol may produce short-term anticonvulsant effects. A total of 42 three-month-old male Wistar rats were divided into six groups (n = 7 in each group): Vehicle (purified water), turmeric (150 and 300 mg/kg, respectively), and resveratrol (30 and 60 mg/kg, respectively), administered per os (p.o.) every 24 h for 35 days. Carbamazepine (300 mg/kg/5 days) was used as a pharmacological control for anticonvulsant activity. At the end of the treatment, status epilepticus was induced using the lithium–pilocarpine model [3 mEq/kg, intraperitoneally (i.p.) and 30 mg/kg subcutaneously (s.c.), respectively]. Seizures were evaluated using the Racine scale. The 300 mg/kg of turmeric and 60 mg/kg of resveratrol groups had an increased latency to the first generalized seizure. The groups treated with 150 and 300 mg/kg of turmeric and 60 mg/kg of resveratrol also had an increased latency to status epilepticus and a decreased number of generalized seizures compared to the vehicle group. The chronic administration of turmeric and resveratrol exerts anticonvulsant effects without producing kidney or liver damage. This suggests that both of these natural products of plant origin could work as adjuvants in the treatment of epilepsy.