In vitroandin vivoantioxidative and hepatoprotective activity of aqueous extract of Cortex Dictamni

Abstract

AIMTo investigate the antioxidant and hepatoprotective effects of Cortex Dictamni aqueous extract (CDAE) in carbon tetrachloride (CCl4)-induced liver damage in rats.METHODSThe in vitro antioxidant effect of CDAE was investigated using α,α-diphenyl-β-picrylhydrazyl (DPPH), 2,2’-azino-bis (3-ethylbenzthiazoline-6-sulfonic acid) (ABTS), β-carotene bleaching, reducing power, and thiobarbituric acid reactive substance assays. A linoleic acid system, including ferric thiocyanate (FTC) and thiobarbituric acid (TBA) assays, was used to evaluate the inhibition of lipid peroxidation. The in vivo hepatoprotective and antioxidant effects of CDAE against CCl4-induced liver damage were evaluated in Sprague-Dawley rats. Silymarin was used as a positive control. Liver damage was assessed by determining hepatic histopathology and liver marker enzymes in serum. Enzyme and non-enzyme antioxidant levels and lipid peroxide content were measured in the liver. Cytochrome P450 2E1 (CYP2E1) protein expression was measured via immunohistochemical staining. Nuclear factor E2-related factor (Nrf2), heme oxygenase-1 (HO-1), NAD(P)H quinine oxidoreductase 1 (NQO1), and γ-glutamylcysteine synthetase catalytic subunit (γ-GCSc) protein expression was measured by Western blot.RESULTSOur results showed that CDAE exhibited a strong antioxidant activity in vitro. CDAE scavenged DPPH and ABTS radicals in a dose-dependent manner. CDAE inhibited lipid peroxidation with a lipid peroxide inhibition rate of 40.6% ± 5.2%. In the FTC and TBA assays, CDAE significantly inhibited lipid peroxidation (P < 0.01). In vivo histopathological studies indicated that CCl4-induced liver injury was alleviated following CDAE treatment in rats of both sexes. CDAE (160 and 320 mg/kg) significantly prevented CCl4-induced elevations of alkaline phosphatase, glutamate pyruvate transaminase, aspartate aminotransferase, and total bilirubin levels in rats of both sexes (P < 0.05, 0.01, or 0.001). Moreover, CDAE restored the decreased activities of hepatic antioxidant enzymes, including superoxide dismutase, catalase, and glutathione peroxidase, as well as non-enzyme antioxidant glutathione, which were induced by CCl4 treatment. CDAE significantly suppressed the up-regulation of CYP2E1 and promoted Nrf2, HO-1, NQO1, and γ-GCSc protein expression.CONCLUSIONCDAE exhibits good antioxidant performance in vitro, with marked radical-scavenging and anti-lipid peroxidation activities. CDAE is effective in preventing CCl4-induced hepatic damage in rats of both sexes. The hepatoprotective activity of CDAE may be attributable to its antioxidant activity, which may involve Keap1-Nrf2-mediated antioxidant regulation.

Phenolic Compounds from Water-Ethanol Extracts ofTetrapleura tetrapteraProduced in Cameroon, as Potential Protectors againstIn VivoCCl4-Induced Liver Injuries

“…Taken together, the results of the in vitro and in vivo antioxidant evaluation indicated that T. tetraptera showed good antioxidant activity, which may be attributable to its direct function in scavenging free radicals [32, 33]. The hepatoprotective properties of a diversity of plants have been previously reported, and these protective properties have been correlated with a high antioxidant potential [30]. Damage to the liver can be assessed through the determination the activity of enzymes such as alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP).…”

Lico A Causes ER Stress and Apoptosis via Up-Regulating miR-144-3p in Human Lung Cancer Cell Line H292

“…Furthermore, co-transfection with pre-miR-144 significantly suppressed luciferase activity of the reporter containing the wild-type 3′-UTR of the Nrf2 mRNA ( Figure 4C ), indicating that miR-144-3p down-regulated Nrf2 expression via directly binding to the putative binding site of Nrf2 mRNA. In this line of thinking, we tested the effect of lico A on Nuclear factor E2-related factor (Nrf2) expression, and the western blot results revealed lico A also decreased Nrf2 and its down-stream γ-glutamylcysteine synthetase catalytic subunit (γ-GCSc) protein levels ( Li et al, 2017 ) in H292 cell line ( Figure 4D ). To prove if lico A decreased Nrf2 expression via increasing miR-144-3p, first, co-transfection experiment of pre-miR-144 and lico A was conducted, and the results substantiated that lico A could enhance the decrease of Nrf2 protein level caused by miR-144-3p ( Figure 4E ).…”

Pre‑treatment with a combination of Shenmai and Danshen injection protects cardiomyocytes against hypoxia/reoxygenation‑ and H2O2‑induced injury by inhibiting mitochondrial permeability transition pore opening

“…I/R injury induces mitochondria to produce high level of ROS, including superoxide anion (O 2 -•), hydroxyl radical (OH -•) and hydrogen peroxide H 2 O 2 (39). Excessive amounts of ROS cause damage to mitochondria, inducing mPTP opening and mitochondrial depolarization (40). Furthermore, an increased concentration of cytosolic Ca 2+ activates a variety of cell death-associated processes following I/R.…”