Gastroprotective Effects of Lion’s Mane Mushroom Hericium erinaceus

Hericium erinaceus is a famous tonic in oriental medicine. The gastroprotective effects of aqueous extract of H. erinaceus against ethanol-induced ulcers in Sprague Dawley rats were investigated. The possible involvements of lipid peroxidation, superoxide dismutase, and catalase were also investigated. Acute toxicity study was performed. The effects of aqueous extract of H. erinaceus on the ulcer areas, ulcer inhibition, gastric wall mucus, gross and histological gastric lesions, antioxidant levels, and malondialdehyde (MDA) contents were evaluated in ethanol-induced ulcer in vivo. In acute toxicity study, a high dose of 5 g/kg did not manifest any toxicological signs in rats. The extract promoted ulcer protection as ascertained by a significant reduction of the ulcer area. Furthermore, it exhibited a significant protection activity against gastric mucosal injury by preventing the depletion of antioxidant enzymes. The level of MDA was also limited in rat stomach tissues when compared with the ulcer control group. Immunohistochemistry showed upregulation of HSP70 protein and downregulation of BAX protein in rats pretreated with the extract. The aqueous extract of H. erinaceus protected gastric mucosa in our in vivo model. It is speculated that the bioactive compounds present in the extract may play a major role in gastroprotective activity

Effects of Schiff base derived metal complexes on experimentally induced gastric ulcer and excision wound in rats / Shahram Golbabapour

Schiff base metal complexes have shown various bioactivities in a number of diseases. This work was conducted to evaluate bioactivity of three Schiff base metal derivatives [Cu(II), Co(II) and Zn(II) complexes] on gastric tissue for their gastroprotective properties, and on excision wound in accelerating the wound repair process in vivo. The toxicity of the complexes were examined in both acute and subchronic levels. In the gastroprotection experiment, male rats were divided into 6 groups [normal control, ulcer control, standard control, Cu complex, Co complex and Zn complex) and received 5 mL/kg of the vehicle (Tween-20 (5%)], omeprazole (20 mg/kg) or any of the complexes (20 mg/kg) dissolved in the vehicle, respectively. Then all of the groups but the normal control group received 5 mL/kg ethanol (95%). The animals euthanized and their stomachs were dissected for gross evaluation, microscopic observations, immunohistology assessments and endogenous bioassays. In the wound healing experiment, under sedation condition, a circle of ~314.16 mm2 of the anterior dorsal side of the nape was excised from each rat (male). Rats were divided into 5 groups (wound control, standard control, Cu complex, Co complex and Zn complex) and received a topical application of 0.2 mL (two time per day) of either the vehicle [Tween-20 (5% v/v) and CMC (2% v/v)], Intrasite gel or any of the complexes (20 mg/kg) dissolved in the vehicle, respectively. After 15 days, the rats were euthanized and the skin area was excised for gross evaluation, microscopic observations, immunohistology assessments, endogenous bioassays and apoptosis array. The laboratory results showed no histopathological and biochemical signs of toxicity. Gastroprotection rate for the pretreatment with either Co or Zn complexes showing less gastric lesions (~86% protection) against oral administration of ethanol. Histological assessment confirmed the protective features of these complexes. Endogenous bioassays appeared comparable with omeprazole (especially for Co and Zn complexes). The lipid peroxidation activity was remarkably low among these three complexes. The expression of HSP70 and BAX appeared comparable according to the protection rates, where the higher protection rate showed higher expression of HSP70 and lower expression of BAX as confirmed by western blot assay. Wound repair rate was measured 90%, 88% and 82% for Cu, Co and Zn complexes respectively, as compared with the standard control group (93%) where that of the wound control group was 78%. Bioactivity of tissue homogenates showed comparable results among the standard control group and the three complexes [especially Cu(II) and Co(II) complexes]. Microscopic structure of wound and immunohistochemistry against TGFβ1, Ki67 and α-smooth muscle actin showed mild histological differences among the groups. Apoptotic protein array revealed that the treatment with Cu(II) complex caused similar protein profile except for IGFBP-1 to IGFBP-4. Co(II) complex also appeared different in the expression profile of IGFBP-4 and IGFBP-5 with reference to the standard control group. Out of these three complexes, Zn(II) complex showed similar protein profile for the studied proteins

A Concise Review on Epigenetic Regulation: Insight into Molecular Mechanisms

Epigenetic mechanisms are responsible for the regulation of transcription of imprinted genes and those that induce a totipotent state. Starting just after fertilization, DNA methylation pattern undergoes establishment, reestablishment and maintenance. These modifications are important for normal embryo and placental developments. Throughout life and passing to the next generation, epigenetic events establish, maintain, erase and reestablish. In the context of differentiated cell reprogramming, demethylation and activation of genes whose expressions contribute to the pluripotent state is the crux of the matter. In this review, firstly, regulatory epigenetic mechanisms related to somatic cell nuclear transfer (SCNT) reprogramming are discussed, followed by embryonic development, and placental epigenetic issues

Autoimmune Hepatitis and Stellate Cells: An Insight into the Role of Autophagy

Autoimmune hepatitis is a necroinflammatory process of liver, featuring interface hepatitis by T cells, macrophages and plasma cells that invade to periportal parenchyma. In this process, a variety of cytokines are secreted and liver tissues undergo fibrogenesis, resulting in the apoptosis of hepatocytes. Autophagy is a complementary mechanism for restraining intracellular pathogens to which the innate immune system does not provide efficient endocytosis. Hepatocytes with their particular regenerative features are normally in a quiescent state, and, autophagy controls the accumulation of excess products, therefore the liver serves as a basic model for the study of autophagy. Impairment of autophagy in the liver causes the accumulation of damaged organelles, misfolded proteins and exceeded lipids in hepatocytes as seen in metabolic diseases. In this review, we introduce autoimmune hepatitis in association with autophagy signaling. We also discuss some genes and proteins of autophagy, their regulatory roles in the activation of hepatic stellate cells and the importance of lipophagy and tyrosine kinase in hepatic fibrogenesis. In order to provide a comprehensive overview of the regulatory role of autophagy in autoimmune hepatitis, the pathway analysis of autophagy in autoimmune hepatitis is also included in this article. </jats:sec

Ferulago angulata activates intrinsic pathway of apoptosis in MCF-7 cells associated with G(1) cell cycle arrest via involvement of p21/p27

Ferulago angulata is a medicinal plant that is traditionally known for its anti-inflammatory and antiulcer properties. The present study was aimed to evaluate its anticancer activity and the possible mechanism of action using MCF-7 as an in vitro model. F. angulata leaf extracts were prepared using solvents in the order of increasing polarity. As determined by MTT assay, F. angulata leaves hexane extract (FALHE) revealed the strongest cytotoxicity against MCF-7 cells with the half maximal inhibitory concentration (IC50) value of 5.3 ± 0.82 μg/mL. The acute toxicity study of FALHE provided evidence of the safety of the plant extract. Microscopic and flow cytometric analysis using annexin-V probe showed an induction of apoptosis in MCF-7 by FALHE. Treatment of MCF-7 cells with FALHE encouraged the intrinsic pathway of apoptosis, with cell death transducing signals that reduced the mitochondrial membrane potential with cytochrome c release from mitochondria to cytosol. The released cytochrome c triggered the activation of caspase-9. Meanwhile, the overexpression of caspase-8 suggested the involvement of an extrinsic pathway in the induced apoptosis at the late stage of treatment. Moreover, flow cytometric analysis showed that FALHE treatment significantly arrested MCF-7 cells in the G1 phase, which was associated with upregulation of p21 and p27 assessed by quantitative polymerase chain reaction. Immunofluorescence and the quantitative polymerase chain reaction analysis of MCF-7 cells after treatment with FALHE revealed an upregulation of Bax and a downregulation of Bcl-2 proteins. These findings proposed that FALHE suppressed the proliferation of MCF-7 cells via cell cycle arrest and the induction of apoptosis through intrinsic pathway