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Metabolomic profiling identifies a novel mechanism for heat stroke ‑related acute kidney injury
Mol Med Rep. 2021 Apr;23(4):1. doi: 10.3892/mmr.2021.11880. Epub 2021 Jan 28.ABSTRACTHeat stroke can induce a systemic inflammatory response, which may lead to multi‑organ dysfunction including acute kidney injury (AKI) and electrolyte disturbances. To investigate the pathogenesis of heat stroke (HS)‑related AKI, a mouse model of HS was induced by increasing the animal's core temperature to 41˚C. Blood samples obtained from the tail vein were used to measure plasma glucose and creatinine levels. Micro‑positron emission tomography‑computed tomography (micro‑PET/CT), H&E staining and transmission electron ...
Source: Molecular Medicine Reports - March 3, 2021 Category: Molecular Biology Authors: Ling Xue Wenli Guo Li Li Santao Ou Tingting Zhu Liang Cai Wenfei Ding Weihua Wu Source Type: research

L-Arginine alleviates heat stress-induced intestinal epithelial barrier damage by promoting expression of tight junction proteins via the AMPK pathway.
This study tested the hypothesis that L-arginine regulates the TJ network by activating AMP-activated protein kinase (AMPK) signaling, which in turn improves intestinal barrier functions under HS. IEC-6 cells and rat small intestines were used as experiment models of heat stress. AICAR and dorsomorphin were used to activate and inhibit the AMPK pathway, respectively. Cell proliferation, apoptosis, differential gene expression and KEGG pathway analysis, intestinal paracellular permeability, intestinal morphology, and expression of HSP and TJ proteins, and p-AMPK were determined. L-Arginine promoted cell proliferation and re...
Source: Molecular Biology Reports - September 30, 2019 Category: Molecular Biology Authors: Xia Z, Huang L, Yin P, Liu F, Liu Y, Zhang Z, Lin J, Zou W, Li C Tags: Mol Biol Rep Source Type: research

JNK signaling is required for the MIP ‑1α‑associated regulation of Kupffer cells in the heat stroke response.
JNK signaling is required for the MIP‑1α‑associated regulation of Kupffer cells in the heat stroke response. Mol Med Rep. 2017 Jul 05;: Authors: Chen XJ, Tang ZZ, Zhu GG, Cheng Q, Zhang WK, Li HM, Fu W, Lu QP Abstract Severe heat stroke (HS) consists of extreme hyperthermia with thermoregulatory failure, leading to high morbidity and mortality. Liver injury is a complication of HS that is associated with inflammatory responses and Kupffer cells (KCs), which are resident macrophages in the liver that serve as a major source of inflammatory cytokines; however, the association and the underlying mech...
Source: Molecular Medicine Reports - July 6, 2017 Category: Molecular Biology Tags: Mol Med Rep Source Type: research

Oxidative stress regulates mitogen ‑activated protein kinases and c‑Jun activation involved in heat stress and lipopolysaccharide‑induced intestinal epithelial cell apoptosis.
In conclusion, these findings suggested a novel role of the ROS signaling pathway which involved activation of MAPKs and c‑Jun, following LPS combined with heat stress‑induced IEC‑6 cell apoptosis and impairment of the epithelial barrier. These results may facilitate understanding of pathological conditions involving ROS, such as heat stroke. PMID: 28656249 [PubMed - as supplied by publisher]
Source: Molecular Medicine Reports - June 29, 2017 Category: Molecular Biology Tags: Mol Med Rep Source Type: research

Sodium tanshinone IIA sulfonate improves inflammation, aortic endothelial cell apoptosis, disseminated intravascular coagulation and multiple organ damage in a rat heat stroke model.
Authors: Chen F, Li H, Zhu G, Chen X, Tang Z Abstract The aim of the present study was to investigate the effects of sodium tanshinone IIA sulfonate (STS) on inflammatory responses, aortic endothelial cell apoptosis, disseminated intravascular coagulation (DIC) and multiple organ damage in an animal model of classic heat stroke (CHS). The rats in the heat stroke (HS) and STS‑treated heat stroke (STS‑HS) groups were placed into a pre‑warmed animal temperature controller (ATC) at 35˚C. The moment at which the rectal temperature reached 43.5˚C was considered as the time of onset of HS. In the HS groups, the ra...
Source: Molecular Medicine Reports - May 13, 2017 Category: Molecular Biology Tags: Mol Med Rep Source Type: research

Quercetin protects against heat stroke-induced myocardial injury in male rats: Antioxidative and antiinflammatory mechanisms.
Abstract Heat stroke is characterilized by hyperthermia, systemic inflammation, and multiple organ failure including arterial hypotension. This definition can be fulfilled by a rat model of heat stroke used in the present study. Anesthetized animals were exposed to heat exposure (43 °C for 70 min) and then returned to room temperature (26 °C) for recovery. One hour before heat exposure, an intraperitoneal dose of quercetin (30 mg/kg) or vehicle (normal saline 1 ml/kg) was administered to the experimental groups of rats. Additional injection was administered immediately after the onset of heat stroke. Immedi...
Source: Chemico-Biological Interactions - January 15, 2017 Category: Molecular Biology Authors: Lin X, Lin CH, Zhao T, Zuo D, Ye Z, Liu L, Lin MT Tags: Chem Biol Interact Source Type: research

Heat shock protein 70 and AMP‐activated protein kinase contribute to 17‐DMAG‐dependent protection against heat stroke
Abstract Heat shock protein 70 (Hsp70) preconditioning induces thermotolerance, and adenosine monophosphate (AMP)‐activated protein kinase (AMPK) plays a role in the process of autophagy. Here, we investigated whether 17‐dimethylaminoethylamino‐17‐demethoxy‐geldanamycin (17‐DMAG) protected against heat stroke (HS) in rats by up‐regulation of Hsp70 and phosphorylated AMPK (pAMPK). To produce HS, male Sprague–Dawley rats were placed in a chamber with an ambient temperature of 42°C. Physiological function (mean arterial pressure, heart rate and core temperature), hepatic and intestinal injury, inflammatory me...
Source: Journal of Cellular and Molecular Medicine - May 30, 2016 Category: Molecular Biology Authors: Yung‐Chieh Tsai, Kwok‐Keung Lam, Yi‐Jen Peng, Yen‐Mei Lee, Chung‐Yu Yang, Yi‐Ju Tsai, Mao‐Hsiung Yen, Pao‐Yun Cheng Tags: Original Article Source Type: research

Heat shock protein 70 and AMP ‐activated protein kinase contribute to 17‐DMAG‐dependent protection against heat stroke
Abstract Heat shock protein 70 (Hsp70) preconditioning induces thermotolerance, and adenosine monophosphate (AMP)‐activated protein kinase (AMPK) plays a role in the process of autophagy. Here, we investigated whether 17‐dimethylaminoethylamino‐17‐demethoxy‐geldanamycin (17‐DMAG) protected against heat stroke (HS) in rats by up‐regulation of Hsp70 and phosphorylated AMPK (pAMPK). To produce HS, male Sprague–Dawley rats were placed in a chamber with an ambient temperature of 42°C. Physiological function (mean arterial pressure, heart rate and core temperature), hepatic and intestinal injury, inflammatory me...
Source: Journal of Cellular and Molecular Medicine - May 30, 2016 Category: Molecular Biology Authors: Yung ‐Chieh Tsai, Kwok‐Keung Lam, Yi‐Jen Peng, Yen‐Mei Lee, Chung‐Yu Yang, Yi‐Ju Tsai, Mao‐Hsiung Yen, Pao‐Yun Cheng Tags: Original Article Source Type: research

Heat shock protein 70 and AMP-activated protein kinase contribute to 17-DMAG-dependent protection against heat stroke.
Abstract Heat shock protein 70 (Hsp70) preconditioning induces thermotolerance, and adenosine monophosphate (AMP)-activated protein kinase (AMPK) plays a role in the process of autophagy. Here, we investigated whether 17-dimethylaminoethylamino-17-demethoxy-geldanamycin (17-DMAG) protected against heat stroke (HS) in rats by up-regulation of Hsp70 and phosphorylated AMPK (pAMPK). To produce HS, male Sprague-Dawley rats were placed in a chamber with an ambient temperature of 42°C. Physiological function (mean arterial pressure, heart rate and core temperature), hepatic and intestinal injury, inflammatory mediators...
Source: J Cell Mol Med - May 30, 2016 Category: Molecular Biology Authors: Tsai YC, Lam KK, Peng YJ, Lee YM, Yang CY, Tsai YJ, Yen MH, Cheng PY Tags: J Cell Mol Med Source Type: research

Decreasing or increasing heat shock protein 72 exacerbates or attenuates heat-induced cell death, respectively, in rat hypothalamic cells
In this study, we found that increasing HSP72 levels with mild heat preconditioning or decreasing HSP72 levels with pSUPER plasmid expressing HSP72 small interfering RNA significantly attenuated or exacerbated heat-induced cell death in cultured primary hypothalamic cells, respectively. Our findings suggest that HSP72 plays a pivotal role in heat-induced cell death and may be associated with heat tolerance.
Source: FEBS Open Bio - September 4, 2015 Category: Molecular Biology Source Type: research

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