Oxidative stress and the inflammatory process are involved in ischemia–reperfusion (I/R) injury. Juglans mollis has been reported as having antioxidant activity, which could attenuate the damage caused by I/R. We evaluated whether a methanolic extract of Juglans mollis (JM) exhibits nephroprotective activity in a Wistar rat model of I/R injury. Four groups of six rats were used: Sham, I/R, JM, and JM + I/R. Two groups were dosed with JM (300 mg/kg) for 7 days before I/R. I/R injury was induced by clamping the renal hilums for 45 min and then reperfusing the kidneys for 15 h. Blood samples were taken to evaluate the levels of alanine aminotransferase (ALT), blood urea nitrogen, creatinine, superoxide dismutase (SOD), malondialdehyde (MDA), interleukin 1β (IL-1β), IL-6, and tumor necrosis factor α (TNF-α). The levels of creatinine, ALT, MDA, IL-1β, IL-6, and TNF-α were lower in JM + I/R than in I/R rats, whereas SOD level only was higher in JM + I/R than in Sham rats. No biochemical or histological damage was observed in JM rats compared with Sham rats; however, less histological damage was observed in JM + I/R rats compared with I/R rats. To our knowledge, this is the first report of nephroprotective activity of J. mollis against damage induced by I/R. This activity may be related to decreased levels of proinflammatory cytokines (IL-1β, IL-6, and TNF-α) and modulation of oxidative stress markers (SOD and MDA) observed in the present study.

Background : Various hepatoprotective herbal products from plants are available in Mexico, where up to 85% of patients with liver disease use some form of complementary and alternative medicine. However, only few studies have reported on the biological evaluation of these products. Objective : Using a model of carbon tetrachloride (CCl₄ )-induced hepatotoxicity in rats, we evaluated the effects of commercial herbal extracts used most commonly in the metropolitan area of Monterrey, Mexico. Materials and Methods : The commercial products were identified through surveys in public areas. The effect of these products given with or without CCl₄ in rats was evaluated by measuring the serum concentrations of aspartate amino transferase (AST) and alanine amino transferase (ALT), and histopathological analysis. Legalon^® was used as the standard drug. Results : The most commonly used herbal products were Hepatisan^® capsules, Boldo capsules, Hepavida^® capsules, Boldo infusion, and milk thistle herbal supplement (80% silymarin). None of the products tested was hepatotoxic according to transaminase and histological analyses. AST and ALT activities were significantly lower in the Hepavida+CCl₄ -treated group as compared with the CCl₄ -only group. AST and ALT activities in the silymarin, Hepatisan, and Boldo tea groups were similar to those in the CCl₄ group. The CCl₄ group displayed submassive confluent necrosis and mixed inflammatory infiltration. Both the Hepatisan+CCl₄ and Boldo tea+CCl₄ groups exhibited ballooning degeneration, inflammatory infiltration, and lytic necrosis. The silymarin+CCl₄ group exhibited microvesicular steatosis. The Hepavida+CCl₄ - and Legalon+CCL₄ -treated groups had lower percentages of necrotic cells as compared with the CCl₄ -treated group; this treatment was hepatoprotective against necrosis. Conclusion : Only Hepavida had a hepatoprotective effect.

Introduction. Ischemia/reperfusion (IR) injury, often associated with liver surgery, is an unresolved problem in the clinical practice. Spironolactone is an antagonist of aldosterone that has shown benefits over IR injury in several tissues, but its effects in hepatic IR are unknown. Objective. To evaluate the effect of spironolactone on IR‐induced damage in liver. Materials and Methods. Total hepatic ischemia was induced in rats for 20 min followed by 60 min of reperfusion. Spironolactone was administered and hepatic injury, cytokine production, and oxidative stress were assessed. Results. After IR, increased transaminases levels and widespread acute inflammatory infiltrate, disorganization of hepatic hemorrhage trabeculae, and presence of apoptotic bodies were observed. Administration of SPI reduced biochemical and histological parameters of liver injury. SPI treatment increased IL‐6 levels when compared with IR group but did not modify either IL‐1β or TNF‐α with respect to IR group. Regarding oxidative stress, increased levels of catalase activity were recorded in IR + SPI group in comparison with group without treatment, whereas MDA levels were similar in IR + SPI and IR groups. Conclusions. Spironolactone reduced the liver damage induced by IR, and this was associated with an increase in IL‐6 production and catalase activity.

Diabetes mellitus presents a great diversity of treatments that cause adverse effects; therefore, plants are a source of compounds that may have fewer adverse effects; Cinnamomum cassia (C. cassia) has compounds with potential antidiabetic activity. The objective was to evaluate the antidiabetic effect of C. cassia oil (CCO) and its impact on oxidative stress in Wistar rats. Five groups were evaluated: (1) sham (SH), (2) 300 mg/kg CCO (CCO), (3) diabetic (D) induced with alloxan, (4) D + 300 mg/kg of CCO (D + CCO), and (5) D + 500 mg/kg of metformin (D + MET); all were treated for 5 days. CCO did not show alteration in aspartate aminotransferase (AST) and alanine aminotransferase (ALT) vs. SH. D + CCO vs. D significantly reduced glucose (333 ± 109 vs. 458 ± 81 mg/dL), ALT (66 ± 15 vs. 160 ± 54 U/L), AST (119 ± 26 vs. 243 ± 104 U/L), and blood urea nitrogen (18.8 ± 2.3 vs. 29.2 ± 6.9 mg/dL). No significant changes were observed in D + CCO vs. D in malondialdehyde (MDA), reduced glutathione (GSH), and superoxide dismutase (SOD), whereas a significant reduction in MDA and GSH was achieved in D + MET, with an increase in SOD. There was a reduction in Rela and Gpx in D + CCO and D + MET vs. D. CCO has antidiabetic and anti-inflammatory effects and reduces ALT, AST, and BUN levels.

Plant extracts with antioxidant activities have shown nephroprotection against IR injury. Jatropha dioica (Jd) possesses antioxidant activity. Our aim was to evaluate the effects of a hydroalcoholic Jd extract against IR injury in Wistar rats. Rats were divided into groups (n = 6): sham (SH); no toxicity (JdTox; 300 mg/kg/day of extract for 7 days); IR (on day 7 [I: 45 min/R: 24 h]); and Jd+IR (same treatment as JdTox; same surgical procedure as IR). AST and LDH were significantly lower in the JdTox. IR exhibited significantly higher CrS, BUN, and MDA compared with SH; Jd+IR showed reductions in these markers. GSH and SOD levels were significantly lower in IR compared with SH; an increase in these markers was observed in the Jd+IR. Histologically, IR showed significant increases in medullary tubular necrosis, medullary protein casts, and medullary vascular congestion compared with SH and JdTox. In Jd+IR, a significant decrease was observed only in medullary tubular necrosis. Therefore, the evaluated hydroalcoholic Jd extract dose showed no nephrotoxicity and hepatotoxicity. Jd extract pretreatment attenuated IR-induced renal injury, as evidenced by the improved serum markers of renal damage and oxidative stress.