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. 2013:2013:540957.
doi: 10.1155/2013/540957. Epub 2013 Sep 12.

Metabolic Signatures of Kidney Yang Deficiency Syndrome and Protective Effects of Two Herbal Extracts in Rats Using GC/TOF MS

Linjing Zhao  1 , Hongbing Wu, Mingfeng Qiu, Wei Sun, Runmin Wei, Xiaojiao Zheng, Yiting Yang, Xue Xin, Haimiao Zou, Tianlu Chen, Jiajian Liu, Lina Lu, Jing Su, Chungwah Ma, Aihua Zhao, Wei Jia
Affiliations

Metabolic Signatures of Kidney Yang Deficiency Syndrome and Protective Effects of Two Herbal Extracts in Rats Using GC/TOF MS

Linjing Zhao et al. Evid Based Complement Alternat Med. 2013.

Abstract

Kidney Yang Deficiency Syndrome (KDS-Yang), a typical condition in Chinese medicine, shares similar clinical signs of the glucocorticoid withdrawal syndrome. To date, the underlying mechanism of KDS-Yang has been remained unclear, especially at the metabolic level. In this study, we report a metabolomic profiling study on a classical model of KDS-Yang in rats induced by hydrocortisone injection to characterize the metabolic transformation using gas chromatography/time-of-flight mass spectrometry. WKY1, a polysaccharide extract from Astragalus membranaceus and Lycium barbarum, and WKY2, an aqueous extract from a similar formula containing Astragalus membranaceus, Lycium barbarum, Morinda officinalis, Taraxacum mongolicum, and Cinnamomum cassia presl, were used separately for protective treatments of KDS-Yang. The changes of serum metabolic profiles indicated that significant alterations of key metabolic pathways in response to abrupt hydrocortisone perturbation, including decreased energy metabolism (lactic acid, acetylcarnitine), lipid metabolism (free fatty acids, 1-monolinoleoylglycerol, and cholesterol), gut microbiota metabolism (indole-3-propionic acid), biosynthesis of catecholamine (norepinephrine), and elevated alanine metabolism, were attenuated or normalized with different degrees by the pretreatment of WKY1 or WKY2, which is consistent with the observations in which the two herbal agents could ameliorate biochemical markers of serum cortisone, adrenocorticotropic (ACTH), and urine 17-hydroxycorticosteroids (17-OHCS).

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Figures

Figure 1
Figure 1
Visualization of biochemical effects of hydrocortisone-induced KDS-Yang in rats using a metabolic profiling approach. Typical GC/TOF MS spectra of serum samples from control group (a) and model group (b). (c) Metabolic profiles depicted by PLS-DA sores plot of GC/TOF MS spectral data from serum samples (n = 7, each dot denotes an individual rat).
Figure 2
Figure 2
Visualization of biochemical effects of hydrocortisone-induced KDS-Yang in rats pretreated with WKY1 (a) and WKY2 (b) using a metabolic profiling approach depicted by a 3D PLS-DA scores plot of GC/TOF MS spectral data from serum samples (n = 7; control group, red dot; model group, blank dot; WKY1 treatment group, dark green dots; and WKY2 treatment group, bright green dots; each dot denotes an individual rat).
Figure 3
Figure 3
The heatmap of model group; two prophylactic treatment groups (WKY1 and WKY2) compared with controls. Shades of red represent fold increase compared with control, green shades represent fold decrease compared with control, respectively.
Figure 4
Figure 4
Metabolomic pathways associated with KDS-Yang induced by hydrocortisone withdrawal. Green: down-regulated metabolites; Red: up-regulated metabolites.
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