Caibi Zhou‡
ab,
Liuhong Hu‡ab,
Ren Mua,
Xin Mei
*a,
Xingli Wua,
Chuanming Wangc and
Xiaolu Zhou
*ab
aCollege of Biological Science and Agriculture, Qiannan Normal University for Nationalities, 5 Jianjiang Avenue Middle Section, Duyun, Guizhou 558000, China. E-mail: xmeisci@yeah.net; arainbowl@163.com
bSchool of Crop Production Technology, Institute of Agricultural Technology, Suranaree University of Technology, Nakhon Ratchasima 30000, Thailand
cThe Second Affiliated Hospital of Guizhou University of Traditional Chinese Medicine, Guizhou 550000, China
First published on 26th August 2022
This work aims to study the effect of compound green tea (CGT) on liver lipid metabolism in mice based on metabolomics of liquid chromatography-mass spectrometry (LC-MS), and preliminarily identify potential biomarkers and pathways of action by using a metabonomic network database to explore the lipid-lowering effect of CGT. In this study, forty mice were randomly divided into four groups: compound tea treatment group (DH), high-fat model control group (NK), normal control group (CK) and positive drug group (YK). After a month of different interventions, the mice were weighed and the blood lipid indexes were detected. In addition, differential liver metabolites were monitored by using LC-MS. The results showed that CGT and positive drug treatment were able to decrease body weight, liver coefficient, TC, TG and LDL levels of obese mice, while increasing HDL levels. Among the 110 compounds obtained, 54 metabolites were significantly altered in the four comparisons. More importantly, 15 remarkably downregulated metabolites involved in Lysopc 16:1, Lysopc 18:1, and Lysopc 18:2 were found in the DH group when the mice were treated with CGT; meanwhile, the positive drug Xuezhikang was able to significantly downregulate 14 compounds, including (±)18-HEPE, and 6 keto-PGF1α, compared with the NK group. Besides, KEGG enrichment analysis also revealed the important metabolic pathways, such as linoleic acid metabolism, Biosynthesis of unsaturated fatty acids, and α-linolenic acid metabolism, were related to fatty acid metabolism. These results suggested that CGT could regulate the lipid metabolism in the liver of hyperlipidemia mice, and may regulate 54 potential biomarkers in mice through a related metabolic pathway to make them return to a normal state and improve the disorder of lipid metabolism.
Tea is the second most popular natural non-alcoholic beverage after water, and has been consumed all over the world for thousands of years. Studies on both human and animals have showed that tea consumption are associated with the blood lipid reduction and body weight loss.9–11 Recently, considerable functional components were identified from tea, including polyphenols,12 catechin,13 EGCG and caffeine,14 which are involved in promoting cholesterol reverse transport15 through regulating key transcription factors of lipid metabolism16 and activating lipid catabolism in liver.17 Some reports have found that caffeine in tea was able to promote lipolysis in adipocytes, and it worked with catechins to inhibit triglyceride accumulation and adipocyte proliferation.18,19 Compound green tea (CGT), a famous folk formula to reduce HLP, hypertension and hyperglycemia, consists of green tea (Camellia sinensis L.) and other five herbs (Lithocarpus polystachyus Rehd., Ilex latifolia Thunb., Mentha canadensis L., Nelumbo nucifera Gaertn., and Lonicera japonica Thunb.), which are consumed by the local people. CGT, in our previous report, proved to be able to regulate intestinal flora imbalance caused by obesity.20 Polyphenols extracted from Ilex latifolia Thunb. had the beneficial effect of antioxidant and anti-inflammatory by inhibiting MAPK and NF-kB activation.21 In addition, it has also been found that Nelumbo nucifera Gaertn. extracts were responsible for potential efficiency on hyperglycemia, HLP and inflammation through stimulating glucose consumption in HepG2 cells, as well as inhibiting the activities of α-glucosidase, pancreatic lipase and COX-2.22 Furthermore, Lonicera japonica Thunb. was able to improve the abnormalities caused by diabetes by resisting hyperglycemic activity and inhibiting the formation of AGEs.23
Metabolomics is normal used to explore potential biomarkers and establish the relative relationship between endogenous substances and physiological functions of diseases.24,25 This technology has been widely used in the research of HLP, which can provide valuable information for the diagnosis and treatment of HLP,26 and is of great significance to the research progress of HLP and the development of corresponding drugs.27 Therefore, in this study, we investigated the lipid-lowering mechanism of CGT, and studied the effect on lipid metabolism in liver of hyperlipidemic mice by ultra-performance liquid chromatography (UPLC) technology, which provides reference for development and utilization of CGT.
100 mg of tea powder for chemical composition analysis was dissolved in 1.2 mL of 70% methanol extract and vortexed 30 s every 30 min for 6 times in total. Then, samples were placed at 4 °C overnight. Following centrifugation for 10 min at 12000×g, the supernatant was collected and filtered with a microporous membrane (SCAA-104, 0.22 μm pore size; ANPEL, Shanghai). Subsequently, the samples were analyzed using an UPLC-ESI-MS/MS system (UPLC, SHIMADZU Nexera X2; MS, Applied Biosystems 4500 Q TRAP). The analytical conditions were as follows, UPLC: column, Agilent SB-C18 (1.8 μm, 2.1 mm × 100 mm); the mobile phase was consisted of solvent A (pure water with 0.1% formic acid) and solvent B (acetonitrile with 0.1% formic acid). Sample measurements were performed with a gradient program that employed the starting conditions of 95% A, 5% B. Within 9 min, a linear gradient to 5% A, 95% B was programmed, and a composition of 5% A, 95% B was kept for 1 min. Subsequently, a composition of 95% A, 5.0% B was adjusted within 1.1 min and kept for 2.9 min. The flow velocity was set as 0.35 mL min; The column oven was set to 40 °C; The injection volume was 4 μL. LIT and triple quadrupole (QQQ) scans were acquired on a triple quadrupole-linear ion trap mass spectrometer (Q TRAP), QTRAP® 6500+ LC-MS/MS System, equipped with an ESI Turbo Ion-Spray interface, operating in positive and negative ion mode and controlled by Analyst 1.6.3 software (AB Sciex). The ESI source operation parameters were as follows: source temperature 500 °C; ion spray voltage (IS) 5500 V (positive), −4500 V (negative); ion source gas I (GSI), gas II (GSII), curtain gas (CUR) was set at 55, 60, and 25.0 psi, respectively; the collision gas (CAD) was high.
The sample extracts were analyzed using an LC-ESI-MS/MS system (UPLC, Shim-pack UFLC SHIMADZU CBM A system; MS, QTRAP® 6500+ System). The analytical conditions were as follows: Column, Waters ACQUITY UPLC HSS T3 C18 (1.8 μm, 2.1 mm × 100 mm), maintained at 40 °C. The mobile phase included phase A ultrapure water (0.04% acetic acid) and phase B acetonitrile (0.04% acetic acid). The gradient program was used: 95:
5 V/V at 0 min, 5
:
95 V/V at 11.0 min, 5
:
95 V/V at 12.0 min, 95
:
5 V/V at 12.1 min, 95
:
5 V/V at 14.0 min. The flow rate was 0.4 ml min−1 and the injection volume was 2 μL. The mass spectrum conditions were the same as those of tea extract analyzed by LC-MS/MS.
Catechins | Standard sample | Tea sample | mg ml−1 | Percent (%) | ||
---|---|---|---|---|---|---|
RT | Area | RT | Area | |||
GC | 4.728 | 8042.9 | 2.923 | 254.5 | 0.03 | 0.17% |
EGC | 7.001 | 4156.9 | 4.307 | 245.5 | 0.06 | 0.31% |
C | 8.839 | 1058.5 | 5.913 | 996.0 | 0.06 | 0.32% |
EC | 12.653 | 38![]() |
9.449 | 2373.8 | 0.06 | 0.33% |
EGCG | 12.985 | 45![]() |
10.567 | 18![]() |
0.40 | 2.12% |
GCG | 15.035 | 29![]() |
12.066 | 1869.6 | 0.06 | 0.34% |
ECG | 22.540 | 68![]() |
16.338 | 4139.1 | 0.06 | 0.32% |
CG | 23.814 | 14![]() |
17.906 | 709.3 | 0.05 | 0.26% |
Treatment | Initial body wt (g) | Final body wt (g) | TC/mmol L−1 | TG/mmol L−1 | LDL/mmol L−1 | HDL/mmol L−1 |
---|---|---|---|---|---|---|
a Values in capital letters are expressed as mean ± SD of 10 mice in each group, the values in lower case in the same column at p < 0.05. CK, normal control group; NK, high-fat model control group; YK, positive drug group; DH, compound tea treatment group. | ||||||
CK | 27.23 ± 1.29a | 43.75 ± 1.03bc | 2.81 ± 0.16c | 0.64 ± 0.02b | 0.55 ± 0.02b | 1.05 ± 0.07a |
NK | 28.01 ± 1.06a | 52.09 ± 1.56a | 3.69 ± 0.12a | 0.73 ± 0.09a | 0.69 ± 0.05a | 0.78 ± 0.03b |
YK | 27.71 ± 1.93a | 45.46 ± 1.28b | 2.97 ± 0.19bc | 0.56 ± 0.05bc | 0.53 ± 0.06b | 1.03 ± 0.04a |
DH | 27.08 ± 0.65a | 44.52 ± 1.16bc | 3.22 ± 0.06b | 0.47 ± 0.07c | 0.56 ± 0.03b | 1.04 ± 0.06a |
Metabolites | CK vs. NK | NK vs. DH | NK vs. YK | CK vs. DH | CK vs. YK | |||||
---|---|---|---|---|---|---|---|---|---|---|
VIP | log2![]() |
VIP | log2![]() |
VIP | log2![]() |
VIP | log2![]() |
VIP | log2![]() |
|
a The statistically selected metabolites with significant differences are shown in the annotations in the KEGG database. “↑” and “↓” indicate that metabolites are up-regulated and down-regulated, respectively. | ||||||||||
Lysopg 18:1 | 1.95 | 1.34 ↑ | ||||||||
Lysope 18:1 | 1.90 | 1.29 ↑ | ||||||||
Lysopa 18:0 | 1.29 | 1.79 ↑ | 1.37 | 1.34 ↑ | ||||||
Lysops 22:5 | 1.04 | −1.02 ↓ | 1.58 | 2.03 ↑ | ||||||
Lysope 14:0 | 1.05 | −1.26 ↓ | ||||||||
Lysopc 16:1 | 1.75 | −1.09 ↓ | 1.56 | −1.39 ↓ | ||||||
Lysopc 18:1 | 1.69 | −1.17 ↓ | ||||||||
Lysopc 18:2 | 1.74 | −1.02 ↓ | ||||||||
Lysopc 20:2 | 1.58 | −1.00 ↓ | 1.44 | 1.14 ↑ | ||||||
Lysopc 14:0 | 1.52 | −1.10 ↓ | ||||||||
Lysopc 15:0 | 1.63 | −1.22 ↓ | ||||||||
LysoPE (16:1(9Z)/0:0) | 1.17 | −1.23 ↓ | ||||||||
(±)17-HETE [(±)17-hydroxy-5Z,8Z,11Z,14Z-eicosatetraenoic acid] | 1.77 | −8.23 ↓ | 1.40 | 8.61 ↑ | 1.59 | −8.23 ↓ | ||||
13-HOTrE [13S-hydroxy-9Z,11E,15Z-octadecatrienoic acid] | 1.33 | −4.89 ↓ | 1.30 | −6.38 ↓ | 1.60 | −5.31 ↓ | ||||
cis-11,14-Eicosadienoic acid (C20:2) | 1.70 | 1.20 ↑ | 1.27 | 1.14 ↑ | ||||||
9-HOTrE [9S-hydroxy-10E,12Z,15Z-octadecatrienoic acid] | 1.64 | −1.41 ↓ | 1.68 | −1.34 ↓ | ||||||
Tetradecanedioic acid | 1.07 | −1.30 ↓ | 1.64 | −1.96 ↓ | ||||||
PE (18:1(9Z)/0:0) | 1.90 | 1.37 ↑ | 1.40 | 1.41 ↑ | ||||||
(±)5-HEPE [(±)-5-hydroxy-6E,8Z,11Z,14Z,17Z-eicosapentaenoic acid] | 2.15 | −1.69 ↓ | ||||||||
(±)7-HDHA [(±)7-hydroxy-4Z,8E,10Z,13Z,16Z,19Z-docosahexaenoic acid] | 1.26 | −1.14 ↓ | 1.10 | −1.10 ↓ | ||||||
13-oxo-ODE [13-oxo-9Z,11E-octadecadienoic acid] | 1.07 | −1.17 ↓ | 1.44 | −1.43 ↓ | ||||||
Stearidonic acid | 1.19 | −1.56 ↓ | 2.17 | 1.71 ↑ | 1.64 | −2.04 ↓ | ||||
p-Mentha-1,3,8-triene | 1.07 | −1.05 ↓ | 2.12 | 1.63 ↑ | 1.59 | −1.26 ↓ | ||||
(±)12-HEPE [(±)-12-hydroxy-5Z,8Z,10E,14Z,17Z-eicosapentaenoic acid] | 1.17 | −2.28 ↓ | 1.28 | −5.55 ↓ | 1.24 | −4.98 ↓ | ||||
(±)12-HETE [(±)12-hydroxy-5Z,8Z,10E,14Z-eicosatetraenoic acid] | 1.33 | −2.12 ↓ | 1.74 | −2.31 ↓ | 1.32 | −6.64 ↓ | 1.44 | −6.83 ↓ | ||
(±)15-HEPE [(±)-15-hydroxy-5Z,8Z,11Z,13E,17Z-eicosapentaenoic acid] | 1.31 | −7.09 ↓ | 1.36 | −7.09 ↓ | 1.72 | −12.40 ↓ | 1.63 | −12.40 ↓ | ||
(±)17-HDHA [(±)17-hydroxy-4Z,7Z,10Z,13Z,15E,19Z-docosahexaenoic acid] | 1.93 | −7.99 ↓ | 2.36 | −7.99 ↓ | 1.39 | −12.24 ↓ | 1.48 | −12.24 ↓ | ||
12,13-EpOME [(±)12(13)-epoxy-9Z-octadecenoic acid] | 1.08 | −1.48 ↓ | ||||||||
14(S)-HDHA [14S-hydroxy-4Z,7Z,10Z,12E,16Z,19Z-docosahexaenoic acid] | 1.15 | −1.93 ↓ | 1.19 | −2.04 ↓ | 1.31 | −6.71 ↓ | 1.38 | −6.82 ↓ | ||
(±)18-HEPE [(±)-18-hydroxy-5Z,8Z,11Z,14Z,16E-eicosapentaenoic acid] | 1.28 | −7.45 ↓ | 1.39 | −12.01 ↓ | 1.48 | −12.01 ↓ | ||||
(±)18-HETE [(±)18-hydroxy-5Z,8Z,11Z,14Z-eicosatetraenoic acid] | 1.36 | −1.65 ↓ | 1.43 | −2.56 ↓ | ||||||
(±)9-HETE [(±)-9-hydroxy-5Z,7E,11Z,14Z-eicosatetraenoic acid] | 1.28 | −6.09 ↓ | 1.38 | −11.66 ↓ | 1.48 | −11.66 ↓ | ||||
11(S)-HETE [11S-hydroxy-5Z,8Z,12E,14Z-eicosatetraenoic acid] | 1.55 | −1.71 ↓ | 1.27 | −1.94 ↓ | ||||||
11,12-EET [(±)11,(12)-epoxy-5Z,8Z,14Z-eicosatrienoic acid] | 1.51 | −1.71 ↓ | 1.23 | −1.92 ↓ | ||||||
14,15-EET [(±)14(15)-epoxy-5Z,8Z,11Z-eicosatrienoic acid] | 1.46 | −1.63 ↓ | ||||||||
Cuminaldehyde | 1.14 | −1.34 ↓ | 1.39 | −1.71 ↓ | ||||||
2-Methylbutyroylcarnitine | 1.23 | −2.08 ↓ | 1.02 | −2.15 ↓ | ||||||
6 keto-PGF1α [6-oxo-9α,11α,15S-trihydroxy-prost-13E-en-1-oic acid] | 1.08 | −1.54 ↓ | 1.19 | −2.03 ↓ | 1.09 | −3.87 ↓ | ||||
PGF1α | 1.39 | 1.52 ↑ | ||||||||
PGF2α | 1.10 | −2.11 ↓ | ||||||||
PGD2 | 1.17 | −3.20 ↓ | ||||||||
TXB2 | 1.28 | −2.58 ↓ | ||||||||
Punicic acid | 1.05 | −2.22 ↓ | 1.40 | −2.42 ↓ | 1.38 | −2.61 ↓ | ||||
12-Hete | 1.16 | −2.86 ↓ | 1.33 | −3.09 ↓ | ||||||
γ-Linolenic acid (C18:3N6) | 1.02 | −1.05 ↓ | ||||||||
Palmitoleic acid (C16:1) | 1.04 | −1.10 ↓ | ||||||||
EPA [5Z,8Z,11Z,14Z,17Z-eicosapentaenoic acid] | 1.00 | −1.31 ↓ | ||||||||
8,15-Dihete | 1.09 | −1.08 ↓ | ||||||||
3-Methylglutaric acid | 1.06 | −1.34 ↓ | 1.38 | −1.38 ↓ | ||||||
cis-7-Hexadecenoic acid | 1.01 | −1.04 ↓ | ||||||||
2,2-Dimethyl succinic acid | 1.07 | −1.33 ↓ | 1.29 | −1.31 ↓ | ||||||
9-oxo-ODE [9-oxo-10E,12Z-octadecadienoic acid] | 1.36 | −1.25 ↓ |
The expression of metabolites was found to be altered significantly in the NK group when the mice were fed with high-fat diet. Among them, 6 metabolites, Lysopg 18:1, Lysope 18:1, Lysopa 18:0, cis-11,14-eicosadienoic acid (C20:2), PE (18:1(9Z)/0:0), and PGF1α, were significantly upregulated in NK group, of which PE (18:1(9Z)/0:0) had the highest content in NK group with log2FC > 1.37, and Lysopa 18:0 increased most with log2
FC > 1.79; Lysopc 18:0 and 18:1 were also increased but were not screened as significant substances; PGF1α was not significantly different in the comparison between other groups; ten metabolites were significantly downregulated in NK group compared to that in the CK group, of which (±)17-HETE had the lowest content with log2
FC < −8.23.
When evaluated the substance level, it was found that 16 metabolites were screened in the comparison of NK vs. DH, among which 15 significantly downregulated metabolites, with the example of 6 keto-PGF1α, Lysopc 16:1, Lysopc 18:1, and Lysopc 18:2, were observed in the DH group with the exception of (±)17-HETE (log2FC > 8.61).
In addition, the positive drug XZK (the YK group) was applied to estimate the efficacy of lowering blood lipids. It was shown that 14 compounds were significantly downregulated compared with the NK group, with the example of (±)18-HEPE, 6 keto-PGF1α, and (±)12-HETE, while 2 compounds were upregulated in YK group, which were stearidonic acid, and p-mentha-1,3,8-triene.
Subsequently, we compared the blood lipids in CGT or XZK group with the normal diet group. The contents of all 27 differential metabolites showed a downward trend when mice were fed with CGT, of which (±)15-HEPE had the largest reduction with log2FC < −12.40, follow by (±)17-HDHA (log2
FC < −12.24), and (±)18-HEPE (log2
FC < −11.66), and GLA and EPA were slightly reduced with log2
FC < 1.05 and 1.31, respectively; Lysopcs (16:1, 14:0, 15:0) also significantly decreased; in addition to the three abovementioned compounds in CK group, another 19 metabolites were found downregulated in the YK group, including 6 keto-PGF1α, (±)9-HETE, tetradecanedioic acid, (±)17-HETE, etc. However, Lysopc 20:2 was higher in the YK group than that in the CK group.
Clinically, TG, TC, LDL-C and HDL-C indicators are often used to diagnose HLP.32 Study indicated that the increased serum TC and LDL-C levels are major hazard factors for the occurrence of atherosclerosis. In this study, CGT successfully regulated the serum levels of TG, TC, LDL-C and HDL-C in HLP mice induced by high-fat diet. Firstly, the results showed that the final body weight, TC, TG and LDL-C levels of mice fed with high-fat diet were significantly increased, while HDL-C was notably decreased. Contrary to NK group, the final body weight, the serum levels of TC, TG, LDL-C and HDL-C of mice in DH group and YK group were reversed after one month of CGT treatment, and there was no significant difference from CK group. These results clearly suggested that CGT and positive drug XZK treatment may well regulate the serum lipid levels of HLP mice, and have preventive and therapeutic effects on HLP. CGT may also have an inhibitory effect on atherosclerosis, mainly due to the up-regulation of free radical scavenging enzymes and the reduction of risk factors for lipoprotein (a) and plasma oxidized LDL.
Lipid is an important component of cytomembrane, mainly composed of polyunsaturated fatty acids (PUFAs). Common PUFAs include GLA, diphenylmethyl-GLA (DGLA), EPA, docosahexaenoic acid (DHA) and arachidonic acid (AA), etc.33 They are derived from LA and ALA in the diet through the action of desaturase, and their activity decrease with age.34,35 LA, an essential PUFAs for the human body, is the precursor of prostaglandins (PGs), a class of lipid mediators produced by enzymatic metabolism of AA, and leucine trienes through the AA pathway. AA is converted into intermediate metabolites of PGs via the action of prostaglandin H synthase (PGH) catalyzed by phospholipase A2 (PLA2) under various physiological and pathological stimuli. In our study, the intake of a high-fat diet led to an increase in the content of PGF1α in mice, suggesting that PGF1α participated in the pathological process of diseases such as inflammation and lipid disorders. Moreover, the decreased content of 6-keto PGF1α could be explained by the fact that both CGT and positive drug XZK treatment may reverse the damage of high-fat diet to mice.
PUFAs, such as ALA, oleic acid (OA), and LA with the ability of inducing endoplasmic reticulum stress, regulating lipid production and lipolysis,36 and inhibiting hepatic steatosis, which are considered to have excellent potential in the treatment of various diseases.37 GLA, belongs to the n-6 series of PUFAs, was mainly involved in the metabolism of LA, which may regulate dyslipidemia through inhibiting the synthesis of serum TC, and eliminating the accumulation of serum TG.38 Furthermore, EPA consumption is thought to be associated with the formation of eicosanic acid, lipoxins and analytical proteins, as well as the regulation of dyslipidemia and the decrease of blood lipids.39 A report claimed that conjugated linoleic acid (CLA), the main PUFA in the organism, can reduce the oxidized form of glutathione, increase the activity of glutathione-dependent antioxidant enzymes, and prevent HLP dyslipidemia, ectopic lipid deposition, insulin resistance and the adverse consequences of metabolic syndrome. Furthermore, the slight reduced the levels of GLA and EPA were observed in DH group compared to CK group, which probably attributed to an increased LA and ALA metabolisms caused by CGT treatment, which resulted in alleviation of dyslipidemia in mice (Fig. 3).
![]() | ||
Fig. 3 Lipid metabolism in liver of high fat mice treated with CGT. Red characters represent an increase in content, and green characters represent a decrease in content. |
Lysopcs, one of phospholipids, have a variety of physiological functions and are closely related to metabolic diseases such as diabetes, atherosclerosis, dyslipidemia, and cardiovascular diseases.40,41 Several reports have demonstrated that Lysopcs may change in certain diseases in vivo. For instance, Lysopcs have the ability to regulate the metabolism of LDL-C, and are involved in atherosclerosis caused by sterol, as well as may also damage endothelial cells by inducing lipid peroxidation of cytomembrane.42 In this study, the elevated levels of Lysopc 18:0 and Lysopc 18:1 in the hepatic tissue of hyperlipidemic mice was observed, suggesting that the intake of high-fat diet destroyed the balance of lipid metabolism and caused dyslipidemia in mice. By contrast, there were a significant decreased levels of Lysopc 16:1, Lysopc 18:1, and Lysopc 18:2 in DH group, which indicated that CGT consumption might be of therapeutic potential to treat dyslipidemia and reducing inflammation in patients with abnormal lipid metabolism. The fecal metabolites of 17 patients with liver cirrhosis and 24 healthy people were clinically detected, which was found that the concentrations of Lysopc 16:0, Lysopc 18:0, Lysopc 18:1 and Lysopc 18:2 in their metabolites were significantly increased, while the concentrations of bile acids and bile pigments were decreased, indicating that the metabolic homeostasis of fatty acids and lipids were also disturbed in patients with liver cirrhosis as liver function damage.43 Furthermore, numerous relevant studies have reported that the level of Lysopcs in serum appeared to increase in animals fed with high-fat diet.44,45 Thus, these findings were consistent with the results in this study, suggesting that Lysopcs level can be served as a specific metabolic marker to evaluate HLP induced by high-fat diet, however CGT treatment was able to alleviate metabolic disorders.
CGT | Compound green tea |
LC-MS | Liquid chromatography-mass spectrometry |
DH | Compound tea treatment group |
NK | High-fat model control group |
CK | Normal control group |
YK | Positive drug group |
XZK | Xuezhikang |
HLP | Hyperlipidemia |
HDL-C | High-density lipoprotein |
TC | Total cholesterol |
LDL-C | Low density lipoprotein |
TG | Triglyceride |
MRM | Multiple reaction monitoring |
PUFAs | Polyunsaturated fatty acids |
DGLA | Diphenylmethyl-GLA |
EPA | Eicosapentaenoic acid |
GLA | Gamma-linolenic acid |
DHA | Docosahexaenoic acid |
AA | Arachidonic acid |
LA | Linoleic acid |
ALA | α-Linolenic acid |
PGH | Prostaglandin H synthase |
PLA2 | Phospholipase A2 |
PGF1α | Prostaglandin F1α |
OA | Oleic acid |
CLA | Conjugated linoleic acid |
Lysopg | Lysophosphatidylglycerol |
Lysope | Lysophosphatidylethanolamine |
Lysopa | Lysophosphatidic acid |
Lysops | Lysophosphatidylserine |
Lysopc | Lysophosphatidylcholine |
PGD2 | Prostaglandin D2 |
TXB2 | Thromboxane B2 |
Footnotes |
† Electronic supplementary information (ESI) available. See https://doi.org/10.1039/d2ra02831j |
‡ C. B. Zhou and L. H. Hu are first authors and contribute to this work. |
This journal is © The Royal Society of Chemistry 2022 |