Carminic acid mitigates fructose-triggered hepatic steatosis by inhibition of oxidative stress and inflammatory reaction

Abstract Background Genistein was reported to adversely influence fetal development although this is yet to be fully understood as a mechanism. Methods In this study, pregnant rats were divided into control (Cont.) and genistein force-fed (2-mg/kg and 4-mg/kg) groups. Each group was divided further into five subgroups: GD-0, GD-6, GD-13, GD-18, and GD-20 based on the terminal gestational day (GD). On the respective terminal GD, the rats were sacrificed and blood samples and amniotic fluid were carefully collected and separated and placenta homogenates were prepared. These samples were evaluated for oxidative stress and inflammatory reaction. The weights of embryonic implant and placenta tissue were also recorded. Heat shock protein (Hsp) (60 and 90), corticosterone, and oxidative stress biomarkers were determined in all the samples. Results Fetal and placental weights in all genistein-exposed groups were significantly decreased. A fluctuation in the level of the Hsp was recorded with a significant decrease recorded in Hsp90 level in the placenta and amniotic fluid towards GD-20 along with a concomitant increase in the corticosterone level in the amniotic fluid in all genistein groups compared to control. Maternal serum at GD-18 and GD -20 recorded a significant increase in antioxidant level (SOD, GSH, CAT) in all genistein-exposed groups. However, these antioxidants were significantly reduced in the placenta and the amniotic fluid compared to control. Conclusions Genistein enhances the placenta function in attenuating the risk of oxidative stress in the amniotic fluid and deferentially suppressed inflammatory activities in the placenta during early gestation and towards late gestation period.

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II. Cytochrome P-450 enzymes and oxidative stress

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.2001.281.5.g1135 ◽

2001 ◽

Vol 281 (5) ◽

pp. G1135-G1139 ◽

Cited By ~ 215

Author(s):

Graham Robertson ◽

Isabelle Leclercq ◽

Geoffrey C. Farrell

Keyword(s):

Oxidative Stress ◽

Fatty Acid ◽

Molecular Oxygen ◽

Hepatic Steatosis ◽

Nonalcoholic Steatohepatitis ◽

Acid Oxidation ◽

Cellular Injury ◽

Second Hit ◽

Cytochrome P 450 ◽

And Oxidative Stress

Oxidative stress is present in the liver of humans with steatosis and nonalcoholic steatohepatitis (NASH) and is a plausible mediator of cellular injury, inflammatory recruitment, and fibrogenesis. CYPs 2E1 and 4A are the microsomal oxidases involved with fatty acid oxidation. Both enzymes can reduce molecular oxygen to produce prooxidant species, which, if not countered efficiently by antioxidants, create oxidative stress. In this theme article, we present the evidence that, in the context of hepatic steatosis, CYPs 2E1 and 4A could generate the “second hit” of cellular injury, particularly when antioxidant reserves are depleted, and propose ways in which this could contribute to the pathogenesis of NASH.

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Suppressing NLRP2 expression accelerates hepatic steatosis: A mechanism involving inflammation and oxidative stress

Biochemical and Biophysical Research Communications ◽

10.1016/j.bbrc.2018.10.132 ◽

2018 ◽

Vol 507 (1-4) ◽

pp. 22-29 ◽

Cited By ~ 1

Author(s):

Chen Li ◽

Qing Liu ◽

Liqun Xie

Keyword(s):

Oxidative Stress ◽

Hepatic Steatosis ◽

And Oxidative Stress

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Osteocalcin prevents insulin resistance, hepatic inflammation and autophagy associated with high-fat diet induced fatty liver hemorrhagic syndrome in aged laying hens

10.21203/rs.3.rs-18321/v1 ◽

2020 ◽

Author(s):

Xiaoling Wu ◽

Xinyu Zou ◽

Mi Zhang ◽

Haiqiang Hu ◽

Xueliang Wei ◽

...

Keyword(s):

Oxidative Stress ◽

Insulin Resistance ◽

Inflammatory Reaction ◽

High Fat Diet ◽

Laying Hens ◽

Density Lipoprotein ◽

Inflammatory Factors ◽

Pathological Changes ◽

High Fat ◽

Tnf Α

Abstract Background: Osteocalcin (OCN), as an energy-regulating hormone, involves in preventing nonalcoholic steatohepatitis. Laying hens have been used as an animal model for investigating liver function and related metabolic disordersas that the synthesis of fat in laying hens is much faster than in mammals with limited adipose tissue. The aim of this study was to investigate the effects of OCN on fatty liver hemorrhagic syndrome (FLHS) in aged laying hens. Methods: Thirty 68-week-old White Plymouth laying hens were randomly assigned into conventional single-bird cages, and the cages were randomly allocated into one of three treatments: normal diet (ND + vehicle , ND+V), high-fat diet (HFD + vehicle, HFD+V), and HFD + OCN (3 μg/bird, 1 time/2 days, i.m.) for 40 days. At experimental day 30, oral glucose tolerance tests (OGTT) and insulin tolerance tests (ITT) were performed. At the end of experiment, the hens were euthanized followed blood collection. The plasma aspartate transaminase (AST), alkaline phosphatase (ALP), total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C) were measured using an automatic biochemistry analyzer. Pathological changes in the liver were examined under both light and transmission electron microscopes. The plasma inflammatory factors including interleukin-1 (IL-1), IL-6, and tumor Necrosis Factor-alpha (TNF-α) were analyzed by ELISA, and the gene expressions of these inflammatory factors in the liver were analyzed by Real-time PCR. And oxidative stress was evaluated using Malondialdehyde (MDA) and Glutathione peroxidase (GSH-Px) assay kits. Results: The results showed HFD hens had more severe liver haemorrhage and fibrosis than ND hens. The ultra-microstructural examination showed that hepatocytes of HFD hens appeared necrotic pyknosis associated with great intracellular electron, mitochondrial swelling, shrunk nucleus and absence of autolysosomes. OCN mitigated these pathological changes by improved HFD hens’ insulin resistance via alleviating the glucose intolerence and improving insulin sensitivity; inhibited HFD-induced oxidative stress as evidenced by decreased liver concentrations of MDA but increased GSH-Px; and reduced the inflammatory reaction with reducing blood IL-6 and TNF-α concentrations and mRNA expressions. Conclusion: These results suggest a high-fat diet promotes the FLHS development in aged hens, while OCN prevents the FLHS process through inhibiting insulin resistance, inflammatory reaction, oxidative stress and fibrosis, and acting autophagy.

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Açaí (Euterpe oleracea Mart.) seed extract protects against hepatic steatosis and fibrosis in high-fat diet-fed mice: Role of local renin-angiotensin system, oxidative stress and inflammation

Journal of Functional Foods ◽

10.1016/j.jff.2019.103726 ◽

2020 ◽

Vol 65 ◽

pp. 103726 ◽

Cited By ~ 4

Author(s):

Matheus Henrique Romão ◽

Graziele Freitas de Bem ◽

Izabelle Barcellos Santos ◽

Ricardo de Andrade Soares ◽

Dayane Teixeira Ognibene ◽

...

Keyword(s):

Oxidative Stress ◽

Hepatic Steatosis ◽

High Fat Diet ◽

Renin Angiotensin System ◽

Seed Extract ◽

Euterpe Oleracea ◽

High Fat ◽

Angiotensin System ◽

Euterpe Oleracea Mart

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Four Novel Dammarane-Type Triterpenoids from Pearl Knots of Panax ginseng Meyer cv. Silvatica

Molecules ◽

10.3390/molecules24061159 ◽

2019 ◽

Vol 24 (6) ◽

pp. 1159 ◽

Cited By ~ 1

Author(s):

Zeng Qi ◽

Zhuo Li ◽

Xuewa Guan ◽

Cuizhu Wang ◽

Fang Wang ◽

...

Keyword(s):

Oxidative Stress ◽

Inflammatory Response ◽

Oxidative Damage ◽

Cigarette Smoke ◽

Panax Ginseng ◽

Inflammatory Reaction ◽

A549 Cells ◽

Protective Effects

Panax ginseng Meyer cv. Silvatica (PGS), which is also known as “Lin-Xia-Shan-Shen” or “Zi-Hai” in China, is grown in forests and mountains by broadcasting the seeds of ginseng and is harvested at the cultivation age of 15–20 years. In this study, four new dammarane-type triterpenoids, ginsengenin-S1 (1), ginsengenin-S2 (2), ginsenoside-S3 (3), ginsenoside-S4 (4), along with one known compound were isolated from pearl knots of PGS. Ginsengenin-S2 significantly alleviated oxidative damage when A549 cells were exposed to cigarette smoke (CS) extract. In addition, ginsengenin-S2 could inhibit the CS-induced inflammatory reaction in A549 cells. Protective effects of ginsengenin-S2 against CS-mediated oxidative stress and the inflammatory response in A549 cells may involve the Nrf2 and HDAC2 pathways.

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