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Medicine-food homology is a long-standing concept in traditional Chinese medicine. YiNianKangBao (YNKB) tea is a medicine-food formulation based on Sichuan dark tea (Ya’an Tibetan tea), which is traditionally used for its lipid-lowering properties. In this study, we evaluated the effects of YNKB on dyslipidemia and investigated the mechanism underlying its correlation with gut microbiota and serum metabolite regulation. Wild-type mice were fed a normal diet as a control. Male ApoE-/- mice were randomly divided into three high-fat diet (HFD) groups, a model group, and two treated groups (100, 400 mg/kg/d for low, high-dose), and fed by gavage for 12 weeks. Serum lipid levels, composition of gut microbiota, and serum metabolites were then analyzed before treatment with YNKB. We extracted the ingredients of YNKB in boiled water for one hour. YNKB supplementation at a high dose of 400 mg/kg/day reduced bodyweight gains (relative epididymal fat pad and liver weight), and markedly attenuated serum lipid profiles and atherosclerosis index, with no significant differences present between the low-dose treatment and HFD groups. Gut microbiota and serum metabolic analysis indicated that significant differences were observed between normal, HFD, and YNKB treatment groups. These differences in gut microbiota exhibited strong correlations with dyslipidemia-related indexes and serum metabolite levels. Oral administration of high-dose YNKB also showed significant lipid-lowering activity against hyperlipidemia in apoE-deficient mice, which might be associated with composition alterations of the gut microbiota and changes in serum metabolite abundances. These findings highlight that YNKB as a medicine-food formulation derived from Sichuan dark tea could prevent dyslipidemia and improve the understanding of its mechanisms and the pharmacological rationale for preventive use. [ABSTRACT FROM AUTHOR]

Recent studies have demonstrated that adiponectin (APN) attenuates cerebral ischemic/reperfusion via globular adiponectin (gAD). However, the therapeutic role of gAD in cerebral ischemic injury in type 1 diabetes mellitus (T1DM) remains unclear. Our results showed that gAD improved neurological scores and reduced the infarct volumes in the 8-week T1DM (T1DM-8W) mice, but not in the 2-week T1DM (T1DM-2W) mice. Moreover, the ischemic penumbra APN levels increased and peaked in T1DM-2W mice, and reduced to normal in T1DM-8W mice, while the APN receptor 1 (AdipoR1) expression change was the opposite. Administration of rosiglitazone in T1DM-2W mice up-regulated the expression of AdipoR1 and restored the neuroprotection of gAD, while intracerebroventricular injection of AdipoR1 small interfering RNA (siRNA) in T1DM-8W mice reversed it. Furthermore, the expression of p-PERK, p-IRE1 and GRP78 were increased whereas the expressions of CHOP and cleaved caspase-12 as well as the number of apoptotic neurons were decreased after gAD treatment in T1DM-8W mice. These beneficial effects of gAD were reversed by pretreatment with AdipoR1 siRNA. These results demonstrated a dynamic dysfunction of APN/AdipoR1 accompanying T1DM progression. Interventions bolstering AdipoR1 expression during early stages and gAD supplementation during advanced stages may potentially reduce the cerebral ischemic injury in diabetic patients. [ABSTRACT FROM AUTHOR]

Introduction Understanding the neural basis underlying major depressive disorder ( MDD) is essential for the diagnosis and treatment of this mental disorder. Aberrant activation and functional connectivity of the default mode network ( DMN) have been consistently found in patients with MDD. It is not known whether effective connectivity within the DMN is altered in MDD. Objects The primary object of this study is to investigate the effective connectivity within the DMN during resting state in MDD patients before and after eight weeks of antidepressant treatment. Methods We defined four regions of the DMN (medial frontal cortex, posterior cingulate cortex, left parietal cortex, and right parietal cortex) for each participant using a group independent component analysis. The coupling parameters reflecting the causal interactions among the DMN regions were estimated using spectral dynamic causal modeling ( DCM). Results Twenty-seven MDD patients and 27 healthy controls were included in the statistical analysis. Our results showed declined influences from the left parietal cortex to other DMN regions in the pre-treatment patients as compared with healthy controls. After eight weeks of treatment, the influence from the right parietal cortex to the posterior cingulate cortex significantly decreased. Conclusion These findings suggest that the reduced excitatory causal influence of the left parietal cortex is the key alteration of the DMN in patients with MDD, and the disrupted causal influences that parietal cortex exerts on the posterior cingulate cortex is responsive to antidepressant treatment. [ABSTRACT FROM AUTHOR]