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Objectives: Pathophysiologic changes of frostbite have been postulated but rarely understood, especially the changes caused by chilly high altitude environment. Therefore, we investigated the pathophysiologic changes of high altitude frostbite (HAF) caused by cold and hypoxia.Methods: Forty Sprague-Dawley rats were randomly divided into 5 equal groups, namely, control, superficial HAF (S-HAF), partial-thickness HAF (PT-HAF), full-thickness HAF (FT-HAF), and partial-thickness normal frostbite (PT-NF) groups. The S-HAF, PT-HAF, and FT-HAF groups were fed under hypobaric hypoxic conditions simulating an altitude of 5000 m. Then, the PT-NF, S-HAF, PT-HAF, and FT-HAF models were constructed by controlling the duration of the direct freezing by liquid nitrogen. Animal vital signs were measured after the operation, and histopathologic changes were observed after routine hematoxylin and eosin staining. In addition, the microcirculation of frostbite tissues was monitored and compared by contrast ultrasonography during wound healing.Results: The S-HAF, PT-HAF, and FT-HAF groups showed significant differences in the microcirculatory and histopathologic changes in the various tissue layers (P < .05). In addition, combined cold and hypoxia caused more damage to frostbite tissue than pure cold. The circulation recovery of HAF models was significantly slower relative to NF models (P < .05).Conclusions: A safe and reproducible HAF model was proposed. More important, pathophysiologic determination of HAF provided the foundation and potential for developing novel and effective frostbite therapies. [ABSTRACT FROM AUTHOR]

Epigallocatechin-3-gallate (EGCG) is a major catechin in green tea with functions of antioxidant, anti-proliferative, anti-inflammatory and attenuating metabolic syndrome. In this study, rat model of benign prostatic hyperplasia (BPH) accompanied with metabolic syndrome was induced by fed on high-fat diet for 12 weeks combined with testosterone injection (10 mg/kg/d) from 9th to 12th weeks. EGCG was orally given from 9th to 12th weeks. Finally, the levels of glucose, total cholesterol, triglyceride, prostate weight, insulin-like growth factors (IGFs), inflammatory cytokines, antioxidant enzymes, and prostatic expression of IGF binding protein-3 (IGFBP-3) and peroxisome proliferator activated receptors (PPARs) were evaluated. It was found that EGCG significantly decreased the levels of glucose, total cholesterol, triglyceride, IGFs, and inflammatory cytokines, normalized the activities of antioxidant enzymes, as well as increased the prostatic expression of IGFBP-3 and PPARs. These results indicated that EGCG was able to exert anti-BPH activities in metabolic syndrome rats. [ABSTRACT FROM AUTHOR]

Cadmium (Cd) pollution is a serious environmental problem. Kidney is a main target organ of Cd toxicity. This study was undertaken to investigate the potential protective effects of epigallocatechin-3-gallate (EGCG) against chronic renal injury and fibrosis induced by CdCl 2 . Rat model was induced by exposing to 250 mg/L CdCl 2 through drinking water. The renal function was evaluated by detecting the levels of blood urea nitrogen (BUN) and serum creatinine (SCR). The oxidative stress was measured by detecting the levels of malondialdehyde (MDA), nitric oxide (NO), reduced glutathione/oxidized glutathione (GSH/GSSG) and renal enzymatic antioxidant status. Additionally, the renal levels of transforming growth factor-β1 (TGF-β1), Smad3, phosphorylation-Smad3 ( p p-Smad3), α-smooth muscle actin (α-SMA), vimentin and E-cadherin were measured by western blot assay. Renal levels of microRNA-21 (miR-21), miR-29a/b/c and miR-192 were measured by quantitative RT-PCR. It was found that EGCG ameliorated the CdCl 2 -induced renal injury, inhibited the level of oxidative stress, normalized renal enzymatic antioxidant status and E-cadherin level, as well as attenuated the over generation of TGF-β1, p p-Smad3, vimentin and α-SMA. EGCG also decreased the production of miR-21 and miR-192, and enhanced the levels of miR-29a/b/c. These results showed that EGCG could attenuate Cd induced chronic renal injury. [ABSTRACT FROM AUTHOR]

Ethnopharmacology relevance Calculus Bovis , also known as Niuhuang, is a rare traditional Chinese medicine that has been widely used in China for 2000 years in pharmacology for sedation, anti-spasm, relieving fever, diminishing inflammation and recovering gallbladder functions. Aim of the study This study aimed to investigate the choleretic potential and molecular responses in rats to Calculus Bovis (CB) administration after 17α-ethynylestradiol (EE)-induced cholestasis. Material and methods CB (50 and 100 mg/kg per day) was intragastrically (i. g.) given to experimental rats for five consecutive days in coadministration with EE (5 mg/kg daily for five days, s.c.). The levels of serum biomarkers were determined biochemically. The histopathology of the liver tissue was evaluated. Expression of bile salt export pump (BSEP) and multidrug resistance-associated protein 2 (MRP2) were studied by western blot and immunohistochemical assay. The expression of Akt and phospho-Akt (pAkt) were also measured by western blot. Results In response to EE, CB treatment significantly prevented an increase in serum levels of alanine aminotransferase (ALT), alkaline phosphatase (ALP), gamma glutamyltransferase (GGT) and total bilirubin (TBIL). CB treatment also repaired tissue lesions caused by EE. Western blots showed that EE significantly decreased the protein expression of BSEP and MRP2. EE also dramatically increased levels of pAkt and decreased levels of Akt. Compared to the EE group, CB treatment increased levels of hepatic BSEP and MRP2 while pAkt levels decreased and Akt levels increased. Immunohistochemistry also indicated that EE decreased the expression of BSEP and MRP2. LY294002 is a selective PI3K inhibitor and showed similar beneficial effects as CB. Decreased expression of BSEP and MRP2 caused by EE were also prevented by LY294002 treatment. Conclusion Calculus Bovis administration can alleviate liver injury and up-regulate the expression of BSEP and MRP2 in 17α-ethynylestradiol-induced cholestasis by a mechanism that may involve inhibiting the activated PI3K/Akt signaling pathway. [ABSTRACT FROM AUTHOR]

Green tea ( Camellia sinensis ) is an extremely popular beverage worldwide. Epigallocatechin-3-gallate (EGCG) is one of the major catechins isolated from green tea and contributes to its beneficial therapeutic functions including antioxidant, anti-inflammatory and anti-cancer effects. However, the effect of EGCG on mastitis is not yet known. This study was to investigate the protective potential of EGCG against mastitis in rats. The rat mastitis model was induced by injecting lipopolysaccharide (LPS) into the duct of mammary gland. The mammary gland was collected after the experimental period. The levels of mammary oxidative stress and inflammatory responses were assessed by measuring the local activities of antioxidant enzymes and the levels of inflammatory cytokines. The mammary expressions of mitogen-activated protein kinases (MAPKs), nuclear factor κB-p65 (NFκB-p65) and hypoxia-inducible factor-1α (HIF-1α) were evaluated by western blot analysis. It was found that EGCG obviously normalized LPS-induced low activities of antioxidant enzymes as well as decreased the high levels of inflammatory cytokines. Additionally, EGCG inhibited the mammary over-expression of MAPKs, NFκB-p65 and HIF-1α. These results indicated that EGCG was able to attenuate LPS-induced mastitis in rats by suppressing MAPK related oxidative stress and inflammatory responses. [ABSTRACT FROM AUTHOR]

Rosa rugosa (Thunb.) is used in Chinese traditional medicine with the functions of promoting blood circulation, relieving the depressed liver and attenuating breast disorders. This study was to investigate the anti-hyperplasia effects of the polyphenols-rich fraction from R. rugosa (FRR) in rat. Rat model of hyperplasia of mammary gland (HMG) was induced by intramuscularly injected with estrogen (0.5 mg/kg/d) for 25 days, and followed with progestogen (5 mg/kg/d) for another 5 days. Meanwhile, FRR was orally given for 30 days. Then, the levels of estradiol and oxidative stress were assessed. The mammary expressions of AKT and JNK were evaluated by Western blot analysis. The expressions of NFκB-p65, COX-2 and VEGF were measured by immunohistochemical analysis. The whole results indicated that FRR could exert anti-hyperplasia effects in rat via modulating the mammary expression of JNK and AKT, as well as alleviating the NFκB related oxidative stress and inflammatory responses. [ABSTRACT FROM AUTHOR]