Synergistic topical application of salt-processed Phellodendron amurense and Sanguisorba officinalis Linne alleviates atopic dermatitis symptoms by reducing levels of immunoglobulin E and pro-inflammatory cytokines in NC/Nga mice.

Atopic dermatitis is a chronic inflammatory skin disease, and salt-processed Phellodendron amurense (CPE) and Sanguisorba officinalis Linne (SOE) are widely used as anti-inflammatory agents in Asia. Therefore, the present study investigated the efficacy of CPE, SOE, and CPE+SOE in the treatment of atopic dermatitis-like symptoms in mice. Following topical application of 1,3­butylen glycol (control), 30% CPE, 30% SOE, 15% CPE+15% SOE or 0.1% hydrocortisone (HC) on the atopic dermatitis­like skin lesions of 2,4-dinitrochlorobenzene­treated NC/Nga mice for 5 weeks, the severity of clinical atopic dermatitis, mast cell infiltration, serum expression levels of immunoglobulin (Ig)E, IgG1, interleukin (IL)-4 and interferon (IFN)-γ, and cytokine expression in the dorsal skin were measured. Compared with the control group, treatment with CPE alleviated the clinical severity of the AD symptoms, with decreased numbers of mast cells, decreased expression levels of serum tumor necrosis factor (TNF)­α, IL­4 and IFN­Î³, and decreased expression levels of inflammatory cytokines in the dorsal lesions. Treatment with SOE did not reduce these expression levels, however, the serum expression levels of IgE and IgG1 were suppressed to similar levels as those in the CPE group. Furthermore, synergistic treatment with CPE and SOE relieved the clinical severity of atopic dermatitis, reduced the serum expression levels of IgE, IgG1, TNF­α, IL­4 and IFN­Î³, and suppressed the mRNA expression levels of TNF­α, IL­4, IL­13, and IFN­Î³ in the dorsal skin lesions. Treatment with CPE+SOE was superior to treatment with HC alone for reducing dermal thickness and suppressing the production of several cytokines. Therefore, combined treatment with CPE and SOE may be an effective alternative intervention for the management of atopic dermatitis.

The supplementation of Korean mistletoe water extracts reduces hot flushes, dyslipidemia, hepatic steatosis, and muscle loss in ovariectomized rats.

Since Korean mistletoe (Viscum album) has been used for alleviating metabolic diseases, it may also prevent the impairment of energy, glucose, lipid, and bone metabolisms in an estrogen-deficient animal model. We determined that long-term consumption of Korean mistletoe water extract (KME) can alleviate menopausal symptoms such as hot flush, increased abdominal fat mass, dyslipidemia, hyperglycemia, and decreased bone mineral density in ovariectomized (OVX) rats fed a high-fat diet, and explored the mechanisms of the effects. OVX rats were divided into four groups and fed high-fat diets supplemented with either 0.6% dextrin (control), 0.2% lyophilized KME + 0.4% dextrin (KME-L), or 0.6% lyophilized KME (KME-H). Sham rats were fed with the high-fat diets with 0.6% dextrin as a normal-control without estrogen deficiency. After eight weeks, OVX rats exhibited impaired energy, glucose and lipid metabolism, and decreased uterine and bone masses. KME-L did not alleviate energy dysfunction. However, KME-H lowered serum levels of total-, LDL-cholesterol, and triglycerides and elevated serum HDL-cholesterol levels in OVX rats with dyslipidemia, to similar levels as normal-control rats. Furthermore, KME-H improved HOMA-IR, an indicator of insulin resistance, in OVX rats. Surprisingly, KME-H fed rats had greater lean mass in the abdomen and leg without differences in fat mass but neither dosage of KME altered bone mineral density in the lumbar spine and femur. The increased lean mass was related to greater phosphorylation of mTOR and eukaryotic translation initiation factor 4E-binding protein 1 (4E-BP1) in the quadriceps muscles. Hepatic triglyceride contents were lowered with KME-H in OVX rats by increasing carnitine palmitoyltransferase-1 (CPT-1) expression and decreasing fatty acid synthase (FAS) and sterol regulatory element-binding protein-1c (SREBP-1c) expression. In conclusion, KME may be useful for preventing some menopausal symptoms such as hot flushes, dyslipidemia, hepatic steatosis, and loss of muscle mass in post-menopausal women.

Fermenting soybeans with Bacillus licheniformis potentiates their capacity to improve cognitive function and glucose homeostaisis in diabetic rats with experimental Alzheimer's type dementia.

PURPOSE: Brain insulin resistance is related to both diabetes and Alzheimer's disease. We investigated whether both chungkookjangs, soybeans fermented in a traditional method (TFC) and with Bacillus lichenifomis (SFC), can protect against cognitive dysfunction and glucose dysregulation in rats with Alzheimer's disease and type 2 diabetes. METHODS: Partial pancreatectomy (Px) and ICV ß-amyloid (25-35) infusion into the CA1 region were fed either control diet (AD-CON), 10% cooked soybeans (CSB), 10% TFC, or 10% SFC in a high fat diet for 8 weeks. Px rats infused ß-amyloid (35-25) as a normal-control group (Non-AD-CON). RESULTS: SFC increased isoflavonoid aglycones, DDMP soyasaponin ßg, E soyasaponin Be and lysoposphatidylcholines in comparison to CSB. SFC markedly decreased its accumulation in ß-amyloid deposition in AD rats and improved hippocampal insulin signaling (pAkt → pGSK → pTau) that exacerbated in AD-CON rats. AD rats markedly impaired cognitive function than Non-AD-CON rats as measured by a water maze and passive avoidance tests while the disturbance was prevented in an ascending order of CON < CSB and TFC < SFC. In comparison to Non-AD rats, AD-CON rats lowered whole body glucose infusion rates and increased hepatic glucose output at hyperinsulinemic state during euglycemic hyperinsulinemic clamp which SFC normalized in AD rats. Interestingly, insulin secretion, especially at the second phase during hyperglycemic clamp, was higher in AD-CON rats, compared to Non-AD rats while CSB, TFC, SFC lowered it in AD-rats. However, SFC restored ß-cell mass in AD rats that reduced ß-cell mass by increased ß-cell apoptosis. CONCLUSIONS: ß-Amyloid accumulation in the hippocampus exacerbated insulin resistance and decreased ß-cell mass and SFC prevented their exacerbation in AD diabetic rats.

Chronic activation of central AMPK attenuates glucose-stimulated insulin secretion and exacerbates hepatic insulin resistance in diabetic rats.

We investigated the effects of chronic AMP-activated kinase (AMPK) activation in the hypothalamus on energy and glucose metabolism in 90% pancreatectomized diabetic rats. Diabetic rats fed a high fat diet were divided into 3 groups and intracerebroventricular (ICV) administered with one of the following: 5-amino-1-ß-D-ribofuranosyl-imidazole-4-carboxamide (AICAR, AMPK activator; 80 µg/day), AICAR+compound C (AMPK inhibitor; 6.2 µg/day), or an artificial cerebrospinal fluid (control) by means of osmotic pumps for 4 weeks. In the hypothalamus, central AICAR activated the phosphorylation of AMPK whereas adding compound C suppressed the activation. AICAR increased body weight and epididymal and retroperitoneal fat mass by increasing energy intake for the first 2 weeks and decreasing energy expenditure, whereas compound C reversed the AICAR effect on energy metabolism. Indirect calorimetry revealed that ICV-AICAR decreased carbohydrate oxidation, but not fat oxidation, compared to the control. During euglycemic hyperinsulinemic clamp, central AICAR increased hepatic glucose output at hyperinsulinemic states. ICV-AICAR increased expressions of hepatic genes involved in fatty acid synthesis and decreased expression of hepatic genes related to thermogenesis whereas compound C nullified the AICAR effect. Insulin secretion in the first and second phases decreased in AICAR-treated rats at hyperglycemic clamp, but compound C nullified the decrease. However, central AICAR did not alter ß-cell mass via its proliferation or apoptosis. In conclusion, chronic hypothalamic AMPK activation impaired energy metabolism and glucose homeostasis by increasing food intake, increasing hepatic glucose output and decreasing insulin secretion in diabetic rats. The impairment of energy and glucose homeostasis by AMPK activation was nullified by an AMPK inhibitor.