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Effect of Liv.52 on reduced glutathione (GSH) and oxidized glutathione (GSSG) in t-BHP treated HepG2 cells 

Effect of Liv.52 on reduced glutathione (GSH) and oxidized glutathione (GSSG) in t-BHP treated HepG2 cells 

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Oxidative stress induced by toxicants is known to cause various complications in the liver. Herbal drug such as Liv.52 is found to have hepatoprotective effect. However, the biochemical mechanism involved in the Liv.52 mediated protection against toxicity is not well elucidated using suitable in vitro models. Hence, in the present study, the hepato...

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... The liver is specifically susceptible to oxidative damage and toxic because the portal vein transports blood directly to the liver after absorption by the intestine. Reactive oxygen species (ROS) play a crucial part in the progression and induction of liver diseases (Vidyashankar et al., 2010). Excessive ROS leads to oxidative stress and attacks cellular biomolecules, such as proteins, DNA, and lipids. ...
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Here, a novel decapeptide IVTNWDDMEK with Maillard reactivity derived from scallop Chlamys farreri mantle was identified. The structural characteristics and in vitro hepatoprotective effects of IVTNWDDMEK conjugated with ribose were further investigated. The changes in decapeptide structures were determined by ultraviolet–visible (UV–vis), Fourier transform infrared (FTIR), and atomic force microscopy (AFM), and the modification sites induced by Maillard reaction of IVTNWDDMEK and ribose were monitored by high performance liquid chromatography/tandem mass spectrometry (HPLC-MS/MS). Maillard reaction products (MRPs) of IVTNWDDMEK-ribose demonstrate hepatoprotective benefits through the suppression of DNA damage and apoptosis induced by oxidative stress in human HepG2 cells in addition to enhancing the antioxidant activities. Moreover, after treatment with decapeptide-ribose MRPs, the activities of cellular antioxidative enzymes, such as catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and glutathione reductase (GSH-Rx) were remarkably increased, while the content of malondialdehyde (MDA) was decreased compared with H2O2⁻treated group, thereby enhancing the intracellular antioxidant defenses. These findings demonstrate the potential utilization of decapeptide IVTNWDDMEK-ribose MRPs as food antioxidants to suppress oxidative damage. Practical Application In recent years, several food-derived bioactive peptides and their derivatives are regarded as good dietary antioxidants for reducing oxidative stress and improving liver function. Here, a novel Maillard reactive decapeptide IVTNWDDMEK, identified from scallop mantle hydrolysates by peptidomics in the previous study was synthesized. Then, the correlation between intercellular antioxidant activities and chemical structure changes of IVTNWDDMEK-ribose Maillard reaction conjugates was further studied. The preferable hepatoprotective activities of decapeptide IVTNWDDMEK-ribose MRPs indicated that these MRPs could be potentially utilized as food antioxidants or additives in the production of nutritional foods.
... Cancer, aging, coronary heart disease, neurodegenerative disorders (i.e., Alzheimer's disease), diabetes, and liver damage are all associated with an increased level of reactive oxygen species (ROS) formation. More selectively the mitochondrial electron transport chain is another main source of cellular ROS generator [2,3] . For the assessment of hepatoprotective activity in vitro model is more advantageous than in vivo [4] . ...
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Emerging data indicate that the mortality rate is rising due to liver disorders day-by-day in the developed countries. The present study was conducted to evaluate the potential of the Biofield Energy (The Trivedi Effect®) Treated test item (DMEM) in HepG2 cell-line. The test item was divided into two parts. One part of the test item received Consciousness Energy Healing Treatment by a renowned Biofield Energy Healer, Alice Branton and was labeled as the Biofield Energy Treated DMEM and the other part defined as untreated DMEM, where no Biofield Treatment was provided. Cell viability of the test items using MTT assay showed 113% and 129.9% viable cells in the untreated DMEM and Biofield Energy Treated DMEM groups, respectively suggested that the test items were nontoxic and safe in nature. The Biofield Energy Treated DMEM showed significant (p≤0.001) protection of cells by 15% against oxidative stress induced by t-BHP, while untreated DMEM group showed 0.4% protection. The level of IL-8 was significantly (p≤0.01) reduced by 32.15% in the Biofield Energy Treated DMEM group compared to the untreated DMEM group. Moreover, the level of ALT enzyme activity was significantly (p≤0.01) reduced by 53.2% in the Biofield Energy Treated DMEM group compared to the untreated DMEM group. Cholesterol level was significantly (p≤0.001) reduced by 37.35% in the Biofield Energy Treated DMEM group compared to the untreated DMEM group. Besides, the Biofield Energy Treated DMEM group showed 43.13% increased the level of albumin compared to the untreated DMEM group. Altogether, results suggested that Biofield Treatment significantly improved liver function. Thus, Consciousness Energy Healing (The Trivedi Effect®) Treatment could be utilized as a hepatoprotectant against several hepatic disorders such as Gilbert’s disease, cirrhosis, steatosis, alcohol abuse, hemochromatosis, Budd-Chiari syndrome, Wilson’s disease, cholangiocarcinoma, etc.
... Through reducing ROS production and calcium overload, BA may also prevent lysophosphatidylcholine-induced cardiac injury (38). Furthermore, t-BHP may induce hepatic oxidative damage by inducing cellular oxidative stress, including lipid peroxidation and glutathione levels (39). In the present study, treatment with t-BHP increased the production of ROS compared with untreated controls, whereas pretreatment with BA greatly decreased ROS levels, indicating that the protective effect of BA was attributed to reducing intracellular ROS levels caused by t-BHP. ...
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... HepG2 also preserves the activity of several phase I, phase II, and antioxidant enzymes (Vidyashankar et al., 2010). Besides, HepG2 cells have the advantage of ready availability and assurance in reproducibility of experiments (Hewitt and Hewitt, 2004). ...
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... Treatment with AAPH decreased GSH by 58.1% ( Figure 4A) which was eliminated by pre-treatment of cells with all four peptides at 50 µM, while at 100 µM, P2 and P6 further increased (p < 0.05) GSH concentrations above that of normal cells. It has been found that in HepG2 cells, reduced glutathione (GSH) is approximately 30-fold higher than its oxidized form GSSG [36]. In the present study, the concentration of GSSG was below the detection limit. ...
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... As reported previously, t-BHP is a representative ROS producer during the redox process and can stably induce cytotoxicity and apoptosis in different cell types, which is primarily due to increased production of intracellular ROS and free radicals [29,30]. Our results showed that establishing the oxidative stress model by exposing hUCBDSCs to t-BHP resulted in a significant decrease of cell viability, whereas G-Rg1 treatment markedly abrogated the cytotoxic effect of t-BHP and promoted cell survival. ...
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Human umbilical cord blood-derived stromal cells (hUCBDSCs) possess strong capability of supporting hematopoiesis and immune regulation, whereas some stress conditions cause reactive oxygen species (ROS) accumulation and then lead to oxidative injury and cell apoptosis. Ginsenoside Rg1 (G-Rg1) has been demonstrated to exert antioxidative and prosurvival effects in many cell types. In this study, the tert-Butyl hydroperoxide (t-BHP), an analog of hydroperoxide, was utilized to mimic the oxidative damage to hUCBDSCs. We aimed to investigate the effects of Ginsenoside Rg1 on protecting hUCBDSCs from t-BHP-induced oxidative injury and apoptosis, as well as the possible signaling pathway involved. It was shown that the treatment of hUCBDSCs with G-Rg1 markedly restored the t-BHP-induced cell viability loss, promoted the CFU-F formation, and inhibited cell apoptosis. G-Rg1 also caused a reduced production of LDH and MDA while significantly enhancing the activity of SOD. Mechanistically, G-Rg1 promoted the phosphorylation of Akt and FoxO3a and led to the cytoplasmic translocation of FoxO3a, which in turn suppressed FoxO3a-modulated expression of proapoptotic Bim and elevated the ratio of Bcl-2 to Bax. All these results suggest that G-Rg1 enhances the survival of t-BHP-induced hUCBDSCs and protects them against apoptosis at least partially through Akt–FoxO3a–Bim signaling pathway.
... 31 By preventing intracellular glutathione depletion and lipid peroxidation, it also reportedly inhibits hepatic cell death evoked by tertiary-butyl hydroperoxide. 32 There are other reports that indicate the usefulness of plantbased antioxidants in the management of NASH. Genistein is a strong antioxidant agent that is capable of decreasing the plasma TNF-a level and attenuating the incidence of NASH 33 . ...
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The objective of the present study is to evaluate the effect of the extract of a well-known hepatospecific polyherbal formulation, Liv.52, in an experimental model of high-fat diet (HFD)-induced nonalcoholic steatohepatitis (NASH) in rats. Feeding a HFD for 15 weeks resulted in significant impairment of the lipid profile, elevation of hepatic enzyme markers, and insulin resistance in rats. The histological examination of the liver furthermore indicated fibrotic changes and fat deposition in hepatic tissues. The treatment with Liv.52 extract [125 mg/kg body weight per os (b.wt. p.o.)], which was administered from week 9 onward, reversed the HFD-induced changes to a statistically significant extent, compared to the untreated positive control animals. The effect observed with Liv.52 extract was comparable to that of pioglitazone (4 mg/kg b.wt.), a standard drug that is useful in the management of NASH. The treatment with Liv.52 extract significantly reduced steatosis, collagen deposition, and necrosis in hepatic tissues, which indicates its antifibrotic and antinecrotic properties. The results obtained in the present set of experiments indicate that Liv.52 extract effectively reverses metabolic and histological changes associated with HFD-induced NASH.
... Each tablet of Liv.52 contains extracts of the following medicinal plants in definite proportions in powder form: Himsra (Capparis spinosa) 65 mg, Kasani (Cichorium intybus) 65 mg, Mandur bhasma 33 mg, Kakamachi (Solanum nigrum) 32 mg, Arjuna (Terminalia arjuna) 32 mg, Kasamarda (Cassia occidentalis) 16 mg, Biranjasipha (Achillea millefolium) 16 mg, and Jhavuka (Tamarix gallica) 16 mg. It is rich in phenolic compounds particularly polyphenols and is used since a long time to combat liver disorders and plays a pivotal role in detoxification of xenobiotics from liver [10][11][12] both in human and animal models. Few studies, however, have been reported to address the hepatoprotective effects of Liv.52 in rat to establish the correlation between the hepatoprotective potency and biological activity [10][11][12]. ...
... It is rich in phenolic compounds particularly polyphenols and is used since a long time to combat liver disorders and plays a pivotal role in detoxification of xenobiotics from liver [10][11][12] both in human and animal models. Few studies, however, have been reported to address the hepatoprotective effects of Liv.52 in rat to establish the correlation between the hepatoprotective potency and biological activity [10][11][12]. ...
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Metabolic enzymes such as alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) were evaluated in Indian teleostean fishes, namely, Anabas testudineus (Bloch) and Heteropneustes fossilis (Bloch), for an exposure to 30 days of Excel Mera 71 (17.2 mg/L), a glyphosate formulation, and subsequent depuration under Liv.52, a plant extract at a dose of 187.5 mg/d/250 L for the same period in the same tissues under laboratory condition. ALT activity was significantly increased (P < 0.05) in all the tissues and raised up to 229.19% in liver of A. testudineus (229.19%) and 128.61% in liver of H. fossilis. AST also increased significantly (P < 0.05) and was maximum in liver of H. fossilis (526.19%) and minimum in gill of A. testudineus (124.38%). ALP activity was also raised highly in intestine of H. fossilis (490.61%) but was less in kidney of H. fossilis (149.48%). The results indicated that Excel Mera 71 caused alterations in the metabolic enzymatic activities in fish tissues and AST showed the highest alteration in both the fishes, while lowest in ALP and ALT in A. testudineus and H. fossilis, respectively. During depuration under Liv.52, all the enzyme activities came down towards the control condition which indicated the compensatory response by the fish against this herbicidal stress and it was in the following order: AST > ALT > ALP, in A. testudineus, while H. fossilis showed the following trend: ALT > AST > ALP. Therefore, these parameters could be used as indicators of herbicidal pollution in aquatic organisms and were recommended for environmental monitoring for investigating the mechanism involved in the recovery pattern.
... Several in vivo and in vitro model ( Hep G2 cell line for tert-butyl hydroperoxide induced toxicity) on liv-52 demonstrate that it play significant role in detoxification of drug and other xenobiotics.[219,220] . Plant that use in formulation of liv-52 medicine are Achillea millefolium, Capparis spinosa, Cassia occidentalis Cinchorium intybus Solanum nigrum Tamarix gallica Terminalia arjuna Eclipta alba, Phyllanthus niruri Boerhavia diffusa, Phyllanthus embilica Fumaria officinalis Terminalia chebula Tinospora cordifolia Andrographis paniculatamain which is rich of phenol component mainly polyphenols that serve protective role in damaged hepatic cells via free radical salvage[216,221]. ...
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Hepatic disorder is leading cause for withdrawals of drugs from market. Resent research on hepatotoxicity suggest that reactive secondary metabolites of drug, xenobiotics, excessive alcohol consumption and some disease conditions are responsible for liver injury. These compounds directly affect mitochondrial permeability transitional pore, mitochondrial respiratory chain, cytochromes P-450, and glutathione S-acyltransferases etc. Synthetic drugs for treatment of liver injury can further cause liver damage, so herbal medication is the only way to cure hepatic injury. Various plant extracts and ployherbal medications have been clinically approved for their potent hepatoprotective activity. These review papers focus on cause hepatotoxicity by various toxic compounds and their cure by herbal medication. This review summarizes mechanism of hepatotoxicity by various toxins and also provides data on hepatoprotective plants with their phytoconstituents which can be further useful for isolation of novel phytochemical constituents form plants for the treatment of liver injury.
... Nevertheless, t-BHP represents a useful model not only for investigating the mechanism of oxidative cell injury, but also for the study of protective effects of different natural compounds. Protective effects against t-BHP were confirmed for flavonoids [21,30,31]; berberine [32]; anthocyanins [25]; baicalin [33]; phenolic compounds [34,35]; olive oil [36]; macelignan obtained from perennial herb Myristica fragrans Houtt [37]; caffeic acid phenethyl ester [38]; the herbal drug Liv 52 [39]; chestnut [40]; and a novel antioxidant protein molecule isolated from the herb Phyllanthus niruri [11]. ...
... H 2 O 2 does not regulate the mRNA of the antioxidant enzyme, probably because of a higher degree of decomposition or lower stability in aqueous solution. An increased level of SOD in t-BHP-treated HepG2 cells was observed by Vidyashankar et al. [39] as well. In our study we also found out that H 2 O 2 and t-BHP influenced the level of antioxidant enzymes differently. ...