The Effect of Hibiscus Sabdariffa on Lipid Profile, Creatinine, and Serum Electrolytes: A Randomized Clinical Trial

Background. Hibiscus Sabdariffa L. (HS), a member of malvaceae family, is a medicinal plant with a worldwide fame. Its effect on reducing serum lipids is mentioned in several studies. The purpose of this study was to assess the efficacy of this plant in reducing the serum's lipids in hypertensive patients. Materials and Methods. Ninety hypertensive patients were randomly assigned to receive Hibiscus Sabdariffa (HS) tea or black tea for 15 days. The patients were asked to drink the tea within 20 minutes following its preparation. This process had to be repeated two times, daily. Patient's FBS and lipid profile were collected at the first visit day (day 0) and on the day 30. Results. There was no significant differences between pre and post experiment values within the two groups. An upward trend in total cholesterol, HDL, and LDL cholesterol was evident in both groups. The increase in total and HDL cholesterol in both groups relative to their initial values were significant. Conclusion. Hibiscus Sabdariffa is probably a safe medicinal plant. No significant harmful changes in cholesterol, triglyceride, BUN, serum creatinine, Na and K levels were observed within 15 days after the discontinuation of the medication

Melatonin inhibits endothelin-1 and induces endothelial nitric oxide synthase genes expression throughout hepatic ischemia/reperfusion in rats

The production of reactive oxygen species (ROS) and dysfunction of vasculature play a central role in the pathophysiology of hepatic ischemia/reperfusion (I/R) injury. The aim of this study was to evaluate the beneficial effects of melatonin on reducing liver I/R injury in rats. Four study groups were formed: (1) saline - administered, control group (Control), (2) melatonin-administered group (MEL), (3) saline -administered I/R group (I/R) and (4) melatonin-administered I/R group (MEL+ I/R). Melatonin was injected intraperitoneally (15 mg/kg) 20 min before ischemia and immediately after reperfusion. After reperfusion, blood and ischemic liver tissues were collected. The group subjected to ischemia showed a significant increase in the serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels, as well as an increase in hepatic malondialdehyde (MDA) concentration. These increases were significantly inhibited by melatonin. Although, I/R augmented the endothelin-1 (ET-1) gene expression and the level of big endothelin-1 (big ET-1) in liver tissue, melatonin attenuated these increases. Conversely, non-significant decrease in endothelial nitric oxide synthase (eNOS) mRNA expression in I/R group was significantly elevated by melatonin in MEL+ I/R group. Melatonin exerts beneficial effects on ischemia/reperfusion liver injury through its anti-oxidative function as well as regulation of hepatic microcirculation.Key words: Melatonin, oxidative stress, ischemia/reperfusion injury, endothelin and nitric oxide synthase

Co-Exposure Effects of LPS with Various Aflatoxin B1 Doses in Isolated Perfused Rat Liver Model

Background: Activation of inflammatory cells can cause more chemicals induced-hepatotoxicity. Aflatoxin B1 (AFB1) is a fungal toxin that induces acute hepatotoxicity in humans and animals. This study was conducted to examine the effect of co-exposure LPS and various aflatoxin B1 doses on the damage hepatic parameters in isolated perfused rat liver. Methods: Thirty-two male wistar rats (250-300g) were divided to eight groups including Control and LPS; three groups with various doses of AFB1 (0.01, 0.1 and 1 ppm) and three groups with various doses of AFB1 and Lipopolysaccharide (LPS) (300 ppm). Activity of Aspartate transaminase (AST) and Alanine transaminase (ALT) were determined in perfusate. Thiobarbituric acid reactive substances (TBARS) and Glutathione (GSH) concentrations were measured in homogenate liver. Results: At two groups of AFB 1 (with LPS and without LPS) at AFB1 concentrations of 0.1 and 1 ppm, elevation of AST and ALT enzymes activity were indicated. Values of GSH in both of groups (AFB 1 with LPS and without LPS) had reduced at concentration of 1 ppm. TBARS concentrations were enhanced in AFB1 concentration of 1 ppm in both of groups (with LPS and without LPS), however in comparison between groups (with LPS and without LPS) in similar concentrations significant different did not observe (P<0.05). Conclusion: Non-injurious dose of LPS did not enhance liver susceptibility to various doses of AFB1 in perfused rat liver. This may be in part of due to extrahepatic factors, which contribute, in more liver damage

The Role of TNF-α in Aflatoxin B-1 Induced Hepatic Toxicity in Isolated Perfused Rat Liver Model

Aflatoxin B-1 (AFB1) is one of the major mycotoxins causing food contamination. Previous studies have shown that AFB1 can induce carcinogenicity and toxic effects in the isolated perfused rat liver and these effects are associated with its metabolites and peroxidation activity. Here we surveyed whether these pathogenic effects of AFB1 are associated with TNF-α as an inflammatory cytokine in general liver damages. In this study, we used twenty male Wistar rats (250-300 g). Rats were divided into four groups. Control group was pre-treated with LPS and then perfused with KHBB. The second group was pretreated with PTX and LPS and then perfused with KHB. The third group was pre-treated with LPS and then perfused with AFB-1 and KHB. The last group was pretreated with LPS and PTX and then perfused with AFB1 and KHB. Results revealed that aflatoxin B1 significantly increased the enzyme activity of aminotransferase and levels of lipid peroxidation. Also, the levels of Glutathione decreased in the aflatoxin group significantly. TNF-α released in perfusate and increased in aflatoxin B1 group significantly and decreased in AFB-1+PTX. Exposure to Aflatoxin B1 may induce reactive oxygen species, so these species may induce overproduction of proinflammatory cytokines such as TNF-α and may cause more damage to hepatic cells

The aqueous extract of Artemisia Absinthium L. stimulates HO-1/MT-1/Cyp450 signaling pathway via oxidative stress regulation induced by aluminium oxide nanoparticles (α and γ) animal model

Abstract Background This research aimed to evaluate the protective effects of Artemisia Absinthium L. (Abs) against liver damage induced by aluminium oxide nanoparticles (Al2O3 NPs) in rats, including both structural and functional changes associated with hepatotoxicity. Methods Thirty-six rats were randomly divided into six groups (n = 6). The first group received no treatment. The second group was orally administered Abs at a dose of 200 mg/kg/b.w. The third and fifth groups were injected intraperitoneally with γ-Al2O3 NPs and α-Al2O3 NPs, respectively, at a dose of 30 mg/kg/b.w. The fourth and sixth groups were pre-treated with oral Abs at a dose of 200 mg/kg/b.w. along with intraperitoneal injection of γ-Al2O3 NPs and α-Al2O3 NPs, respectively, at a dose of 30 mg/kg/b.w. Results Treatment with γ-Al2O3 NPs resulted in a significant decrease (P < 0.05) in total body weight gain, relative liver weight to body weight, and liver weight in rats. However, co-administration of γ-Al2O3 NPs with Abs significantly increased body weight gain (P < 0.05). Rats treated with Al2O3 NPs (γ and α) exhibited elevated levels of malondialdehyde (MDA), inducible nitric oxide synthase (iNOS), alanine transaminase (ALT), and aspartate aminotransferase (AST). Conversely, treatment significantly reduced glutathione peroxidase (GPx), catalase (CAT), total superoxide dismutase (T-SOD), and total antioxidant capacity (TAC) levels compared to the control group. Furthermore, the expression of heme oxygenase-1 (HO-1) and metallothionein-1 (MT-1) mRNAs, cytochrome P450 (CYP P450) protein, and histopathological changes were significantly up-regulated in rats injected with Al2O3 NPs. Pre-treatment with Abs significantly reduced MDA, AST, HO-1, and CYP P450 levels in the liver, while increasing GPx and T-SOD levels compared to rats treated with Al2O3 NPs. Conclusion The results indicate that Abs has potential protective effects against oxidative stress, up-regulation of oxidative-related genes and proteins, and histopathological alterations induced by Al2O3 NPs. Notably, γ-Al2O3 NPs exhibited greater hepatotoxicity than α-Al2O3 NPs