Lauric acid ameliorates lipopolysaccharide (LPS)-induced liver inflammation by mediating TLR4/MyD88 pathway in Sprague Dawley (SD) rats

Khan, Hidayat Ullah; Aamir, Khurram; Jusuf, Patricia Regina; Sethi, Gautam; Sisinthy, Sreenivas Patro; Ghildyal, Reena; Arya, Aditya

doi:10.1016/j.lfs.2020.118750

Cited by 43 publications

(25 citation statements)

References 55 publications

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“…In this study, the activities of serum AST, ALT, and ALP in the LPS group were significantly higher than those in the CON group, which suggested that LPS induction caused liver damage in piglets. Our results are in line with those of Khan et al [ 39 ], who reported the serum levels of ALT and AST in Sprague Dawley rats; compared with the control group, the levels of AST and ALT in the LPS-treated group were higher. Xu et al [ 40 ] found that liver tissue was significantly damaged and serum ALT, AST, and ALP activities were significantly increased in LPS-treated mice.…”

Section: Discussionsupporting

confidence: 93%

Effects of Continuous LPS Induction on Oxidative Stress and Liver Injury in Weaned Piglets

Zhou

Zhong

et al. 2022

Veterinary Sciences

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Due to imperfections in their immune and digestive systems, weaned piglets are susceptible to invasions of the external environment and diseases, especially bacterial infections, which lead to slow growth, tissue damage, and even the death of piglets. Here, a model of weaned piglets induced by Escherichia coli lipopolysaccharide (LPS) was established to explore the effects of continuous low-dose LPS induction on the mechanism of liver injury. A total of forty-eight healthy 28-day-old weaned piglets (weight = 6.65 ± 1.19 kg) were randomly divided into two groups: the CON group and LPS group. During the experimental period of thirteen days, the LPS group was injected intraperitoneally with LPS (100 μg/kg) once per day, and the CON group was treated with the same volume of 0.9% NaCl solution. On the 1st, 5th, 9th, and 13th days, the serum and liver of the piglets were collected for the determination of serum biochemical indexes, an antioxidant capacity evaluation, and histopathological examinations. In addition, the mRNA expression levels of the TLR4 pathway and inflammatory cytokines were detected. The results showed that the activities of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP) in the serum increased after LPS induction. The activities of total antioxidant capacity (T-AOC) and glutathione peroxidase (GSH-Px) in the serum and liver homogenate of the LPS group were lower than those of the CON group, while the malondialdehyde (MDA) content in the serum and the activities of catalase (CAT) and superoxide dismutase (SOD) in the liver of the LPS group were higher than those in the CON group. At the same time, morphological impairment of the livers occurred, including hepatocyte caryolysis, hepatocyte vacuolization, karyopycnosis, and inflammatory cell infiltration, and the mRNA expression levels of TLR4, MyD88, NF-κB, TNF-α, IL-6, and IL-10 were upregulated in the livers after LPS induction. The above results were more obvious on the 1st and 5th days of LPS induction, while the trend during the later period was not significant. It was concluded that the oxidative stress and liver injury occurred at the early stage of LPS induction, while the liver damage weakened at the later stage. The weaned piglets probably gradually developed tolerance to the endotoxin after the continuous low-dose induction of LPS.

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Section: Discussionsupporting

confidence: 93%

Effects of Continuous LPS Induction on Oxidative Stress and Liver Injury in Weaned Piglets

Zhou

Zhong

et al. 2022

Veterinary Sciences

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“…Endotoxins, produced by ETEC, can cause intestinal inflammation through the TLR4/MyD88/NF-κB signaling pathway [ 45 ]. The anti-inflammatory effects of medium-chain triglycerides and lauric acid have been confirmed in previous studies [ 7 , 46 , 47 , 48 ]. It has been proven that formic acid and monolaurin pretreatment protected against the increase of plasma TNF-α, IL-6, and IL-1β and the mRNA expression of TNF-α, IL-1β, and IL-6 in the piglets after the ETEC challenge [ 24 ].…”

Section: Discussionsupporting

confidence: 75%

Zinc Laurate Protects against Intestinal Barrier Dysfunction and Inflammation Induced by ETEC in a Mice Model

Chen

Wang

et al. 2022

Nutrients

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Enterotoxigenic Escherichia coli (ETEC) infection is one of the most common bacterial causes of diarrhea in children and young farm animals. Medium-chain fatty acids (MCFAs) have been widely used for their antibacterial and immune functions. However, there is limited information regarding the role of MCFAs chelated with Zn in diarrhea induced by ETEC infection. Here, zinc laurate (ZnLa) was used to evaluate its protective effect in a mice diarrhea model induced by ETEC. A total of 45 ICR-weaned female mice were randomly assigned to marginal zinc deficiency (dZn), dZn, and ETEC infection groups (dZn+ETEC); ETEC infection was co-treated with a low, middle, or high dose of ZnLa (ZnLa LOW+ETEC, ZnLa MID+ETEC, and ZnLa HIGH+ETEC), respectively, to explore the effect and its mechanism of ZnLa on diarrhea and intestinal health of mice challenged with ETEC. To further compare the antibacterial efficiency of ZnLa and ZnSO4 in mice with ETEC infection, a total of 36 ICR-weaned female mice were randomly divided into ZnLa, ZnLa+ETEC, ZnSO4, and ZnSO4 and ETEC infection groups (ZnSO4+ETEC); moreover, the growth curve of ETEC also compared ZnLa and ZnSO4 in vitro. Mice pretreated with ZnLa were effectively guarded against body weight losses and increases in diarrhea scores induced by ETEC. ZnLa pretreatment also prevented intestinal barrier damage and ion transport in mice challenged with ETEC, as evidenced by the fact that the intestinal villus height and the ratio of villus height and crypt depth, tight junction protein, and Na+ absorption were higher, whereas intestinal permeability and anion secretion were lower in mice pretreated with ZnLa. In addition, ZnLa conferred effective protection against ETEC-induced intestinal inflammatory responses, as the increases in protein and mRNAs of proinflammatory cytokines were prevented in serum and jejunum, which was likely associated with the TLR4/MYD88/NF-κB signaling pathway. The increase in ETEC shedding and virulence-related gene expression was prevented in mice with ZnLa pretreatment. Finally, the growth of ETEC and virulence-related gene expression were lower in the ZnLa group than in ZnSO4 with an equal concentration of zinc. These findings suggest that ZnLa is a promising prevention strategy to remedy ETEC infection.

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“…Many studies have reported the weight-lowering effects of MCFAs [ 76 , 79 , 80 ] or PUFAs [ 28 , 81 ]. However, in the present study, although rats fed with HFD + KO and HFD + CO showed slightly, but significantly, lower daily food intake, we did not observe differences in BW and FER among the different groups in our experimental settings.…”

Section: Discussionmentioning

confidence: 99%

“…Studies have reported that LPS injection induces hyperlipidemia by significantly increasing total lipids, TC, TG, AST, and ALT activities [ 91 , 92 , 93 ]. A study by Khan et al [ 76 ] showed elevation in serum TC, non-HDL-C, LDL-C, and TG of LPS-treated male SD rats. Our findings were in accordance with previous studies showing that administration of LPS promoted hyperlipidemia, accompanied by elevated TG, TC, HDL-C, non-HDL-C, and CVD expectancy markers (i.e., AC and CRF) [ 93 , 94 ].…”

Section: Discussionmentioning

confidence: 99%

Partial Replacement of Dietary Fat with Krill Oil or Coconut Oil Alleviates Dyslipidemia by Partly Modulating Lipid Metabolism in Lipopolysaccharide-Injected Rats on a High-Fat Diet

Son

Kim

Lee

et al. 2022

IJERPH

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This study investigated the effects of partial replacement of dietary fat with krill oil (KO) or coconut oil (CO) on dyslipidemia and lipid metabolism in rats fed with a high-fat diet (HFD). Sprague Dawley rats were divided into three groups as follows: HFD, HFD + KO, and HFD + CO. The rats were fed each diet for 10 weeks and then intraperitoneally injected with phosphate-buffered saline (PBS) or lipopolysaccharide (LPS) (1 mg/kg). The KO- and CO-fed rats exhibited lower levels of serum lipids and aspartate aminotransferases than those of the HFD-fed rats. Rats fed with HFD + KO displayed significantly lower hepatic histological scores and hepatic triglyceride (TG) content than rats fed with HFD. The KO supplementation also downregulated the adipogenic gene expression in the liver. When treated with LPS, the HFD + KO and HFD + CO groups reduced the adipocyte size in the epididymal white adipose tissues (EAT) relative to the HFD group. These results suggest that KO and CO could improve lipid metabolism dysfunction.

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Lauric acid ameliorates lipopolysaccharide (LPS)-induced liver inflammation by mediating TLR4/MyD88 pathway in Sprague Dawley (SD) rats

Cited by 43 publications

References 55 publications

Effects of Continuous LPS Induction on Oxidative Stress and Liver Injury in Weaned Piglets

Effects of Continuous LPS Induction on Oxidative Stress and Liver Injury in Weaned Piglets

Zinc Laurate Protects against Intestinal Barrier Dysfunction and Inflammation Induced by ETEC in a Mice Model

Partial Replacement of Dietary Fat with Krill Oil or Coconut Oil Alleviates Dyslipidemia by Partly Modulating Lipid Metabolism in Lipopolysaccharide-Injected Rats on a High-Fat Diet

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