ABSTRACT
Objective: To explore whether Antrodia cinnamomea can prolong the survival time of stroke-prone spontaneously hypertensive rats, and to investigate the underlying mechanisms from the proteomics perspective. Methods: A total of 80 male stroke-prone spontaneously hypertensive rats were randomly divided into two groups (control group and Antrodia cinnamomea treated group, n= 40). The animals were intragastrically given Antrodia cinnamomea (150 mg/kg). Then the death of the animals in the two groups was observed. Another 6 stroke-prone spontaneously hypertensive rats were randomly divided into drug treatment group and control group, with the drug treatment group intragastrically given Antrodia cinnamomea (150 mg/kg), and the brain proteomics were compared between the two groups 90 days later, with WKY rats used as normal controls. The differentially expressed proteins before and after drug treatment were subjected to mass spectrometry analysis, and the results of mass spectrometry analysis were further confirmed by Western blotting analysis. Results: Antrodia cinnamomea significantly prolonged the survival time of stroke-prone spontaneously hypertensive rats (P < 0.05), and proteomics results showed that Antrodia cinnamomea increased the expression of glutathione S-transferase (GST) and superoxide dismutase (SOD), which were also confirmed by Western blotting analysis. Further study revealed that the total anti-oxidative capability (T-AOC) of the animals was increased (T-AOC; [66.48 ± 16.17] U/g vs [124.75 ± 28.43] U/g, P< 0.05), which was manifested by the increased activity of GST and SOD (GST: [40.33 ± 5.24] U/mg vs [70.50 ± 6.24] U/ mg, P<0.05; SOD; [109.25 ± 23.61] U/mg vs [192.60 ± 23.95] U/mg, P<0.05), and decreased levei of malondialdehyde ([3.96 ± 0.45] nmol/mg vs [2.04 ± 0.31] nmol/mg, P<0.05). Conclusion: Long-term treatment with Antrodia cinnamomea can prolong the lifespan of stroke-prone spontaneously hypertensive rats, which might be related to the increased activity of anti-oxidative enzymes and the decreased oxidative damage.
ABSTRACT
Arginine vasopressin (AVP) is a neuropeptide with vasoconstrictive, antidiuretic, cardiovascular regulative and hepatic glycogenolysis effects, that also affects other behaviors including modulating learning. A number of studies on AVP regulation have been conducted in various metabolic diseases (disorders). In this study, the immunoreactivities of AVP in the paraventricular nucleus (PVN) and supraoptic nucleus (SON) and mRNA expressions in the hypothalamus were investigated by immunohistochemistry and quantitative real-time PCR (RT-qPCR) in stroke-prone spontaneously hypertensive rats at different ages (i.e., at postnatal months [PM] 1, 8, and 12). Blood glucose levels in the PM 8 group were higher than in the other groups. However, cresyl violet positive neurons were detected in the PVN and SON of all animals, and numbers of cresyl violet positive neurons were similar in all aged groups. In addition, AVP immunoreactivity was detected in the PVN and SON of all age groups, and AVP immunoreactivity and mRNA expression levels were found to be increased in proportion to age by immunohistochemistry and RT-qPCR. These results suggest that the diabetic condition is temporally generated after hypertension has developed. Furthermore, our findings suggest that increased AVP expressions in the hypothalamic PVN and SON are associated with hypertension by age.
Subject(s)
Aged , Animals , Humans , Arginine , Arginine Vasopressin , Benzoxazines , Blood Glucose , Glycogenolysis , Hypertension , Hypothalamus , Immunohistochemistry , Learning , Metabolic Diseases , Molybdenum , Neurons , Neuropeptides , Oxides , Paraventricular Hypothalamic Nucleus , Rats, Inbred SHR , Real-Time Polymerase Chain Reaction , RNA, Messenger , Supraoptic Nucleus , ViolaABSTRACT
Aim To investigate the effects of an angiotensin Ⅱ receptor blocker,candesartan, on aorta oxidative stress-LOX-1 pathway in salt-loaded stroke-prone spontaneously hypertensive rats (SHRSP).Methods 12-week-old salt-loaded SHRSP were treated with candesartan(1.0 mg?kg-1?d-1)or a diuretic, trichlormethiazide(TCM,1.6 mg?kg-1?d-1) or no treatment(n=6) in each for 2 weeks. Age-matched salt-loaded WKY rats were served as control(n=6).Systolic blood pressure(SBP)was measured weekly throughout the 2-week period by means of the tail-cuff method.Thoracic aortas were extracted and 24 h urine was collected.NAD(P)H oxidase subunits(p22 phox, p47 phox and gp91 phox)mRNA expression in aorta were assayed by real-time PCR. LOX-1 and type Ⅳ collogen mRNA expression were examined by RT-PCR. gp91 phox and LOX-1 protein expression in aorta were assayed by immunohistochemistry.Urinary albumin excretion was examined by ELISA.Results At the end of the 2nd week, SBP was significantly higher in salt-loaded SHRSP than that in salt-loaded WKY rats. Treatment with candesartan and TCM significantly decreased SBP in salt-loaded SHRSP at similar levels.NAD(P)H oxidase subunits (p47 phox and gp91 phox)and LOX-1 mRNA expression in aorta were markedly higher in salt-loaded SHRSP than those in salt-loaded WKY rats.Candesartan and TCM had the effect of reducing the systolic blood pressure at similar levels. Candesartan significantly down-regulated aorta p22 phox, gp91 phox,LOX-1 and type Ⅳ collogen mRNA expression and decreased urine albumin excretion in salt-loaded SHRSP(P