Abstract
Tea tree oil (TTO) plays an important role in lipid metabolism, alleviating the inflammatory responses. Fatty liver is associated with lipid accumulation in hepatocytes, leading to inflammation. However, there is very limited information on the effects of TTO on lipid accumulation, and inflammation in bovine hepatocytes. This study aimed to evaluate whether TTO alleviates palmitic acid (PA)-induced lipid accumulation in bovine hepatocytes. Hepatocytes isolated from mid-lactating Holstein cows were pretreated with 100 μM PA for 72 h. Cells were either pretreated with PA alone (PA group) or with PA followed by 0.00625% TTO treatment for 12 h (PT group). Expression of fatty acid oxidant genes increased (P < 0.05) while fatty acid synthesis genes decreased (P < 0.05) in the PT group compared with the PA group. PA treatment resulted in increased (P < 0.05) expression of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6), but these increases were less in the PT group (P < 0.05). Compared to the PA group, expression of phosphorylated (p)-p65 and p-inhibitor κBα (p-IκBα) was suppressed (P < 0.05) by TTO treatment. TTO treatment limited (P < 0.05) the increase in intracellular reactive oxygen species (ROS) and prevented (P < 0.05) a reduction in mitochondrial membrane potential observed in response to PA treatment. Expression of endoplasmic reticulum (ER) stress genes was reduced (P < 0.05) in the PT group compared with the PA group. Our results suggest that TTO treatment attenuates the effects of PA in hepatocytes, leading to fatty acid oxidation, decreased fatty acid synthesis, suppressed inflammatory response, and reduced ER stress. Taken together, the results of this study suggest that TTO treatment may be a promising therapeutic approach to imbalanced lipid homeostasis, inflammation and ER stress in dairy cows shortly before and after calving.
Highlights
The transition period in dairy cattle, which spans from 3 weeks before to 3 weeks after calving, is a profoundly challenging time due to increases in energy requirements associated with gravidity and lactogenesis lead that to cattle entering a state of negative energy balance [1, 2]
We found that palmitic acid (PA) treatment gradually increased intracellular ATP, which was significantly higher in cells incubated with 100 and 200 μM PA for 3 days (Figure 1A)
Increased lipid mobilization leads to an increase in blood fatty acids, which are absorbed by the liver, leading to TG accumulation in liver and an enhanced inflammatory response accompanied by endoplasmic reticulum (ER) stress [34, 36]
Summary
The transition period in dairy cattle, which spans from 3 weeks before to 3 weeks after calving, is a profoundly challenging time due to increases in energy requirements associated with gravidity and lactogenesis lead that to cattle entering a state of negative energy balance [1, 2]. Cattle have to mobilize fat depots to release fatty acids as an energy source to compensate for reduced energy intake. PA is a common dietary long-chain free fatty acid; it is most abundant in liver triglycerides (TGs) in both normal cows and those with steatosis. Rukkwamsuk et al reported a significant increase in PA in dairy cows with fatty livers induced by high energy diets after parturition [5]. Bobe et al reported that accumulation of high levels of fat in the liver can lead to metabolic disorders such as ketosis and fatty liver [7]. Fatty liver is the most common form of chronic liver disease in high-yield dairy cows during the transition period [8,9,10]. Understanding the molecular mechanism of fatty liver and identification of effective therapeutic strategies is of the utmost importance
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