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Lipid Mediators of Acute Allergic and Inflammatory Reactions
Published in William S. Lynn, Inflammatory Cells and Lung Disease, 2019
Non-steroidal anti-inflammatory agents generally directly block cyclooxygenase and lipoxygenase.20, 164, 304–307 Examples include aspirin, indomethacin, sulfinpyrazone, ibuprofen, and anisodamine. Certain of these agents block PMN, PL, and smooth muscle responses to the meditors discussed here.20, 86–88, 101, 104, 108, 109, 129, 131, 132, 135, 151, 164, 165, 304–307 In vivo indomethacin and ibuprofen ameliorate endotoxin shock,308, 309 sulfinpyrazon blocks C5a-induced pulmonary dysfunction, and various AA antimetabolites block arachidonate-induced toxicity. 193, 194 Many of these drugs also block edema formation and the localization of leukocytes into inflammatory sites.97, 98, 280, 310–312 The use of these agents in inflammation is well known. Their use in more generalized syndromes must await clinical trials. Reports from the People’s Republic of China indicate that anisodamine may ameliorate septic shock and ARDS in humans.307
Protecting Pancreatic β-cells from Metabolic Insults
Published in Christophe Wiart, Medicinal Plants in Asia for Metabolic Syndrome, 2017
Anisodamine (Figure 2.24) from Anisodus tanguticus (Maxim.) Pascher at a concentration 1 mg/mL reduced by 40% the production of malondialdehyde by hamster pancreatic islet beta HIT cells challenged with alloxan.371 This tropane alkaloid at a concentration of 1 mmol/L enhanced glucose-induced insulin secretion from beta HIT from 4262 µunits/mg protein increased to 6412 µunits/mg.372 Anisodamine is a nonselective muscarinic antagonist for M1 and M2 receptors.373 In rodent β-cell lines, M1 activation stimulate insulin secretion.128
The Use of Chemical Warfare Agents during the Syrian Civil War
Published in Brian J. Lukey, James A. Romano, Salem Harry, Chemical Warfare Agents, 2019
Arik Eisenkraft, Avshalom Falk
Atropine, the primary antidote in CWNA/OP poisoning, has several limitations: it is not effective alone, and additional drugs, currently oximes, are required for effectiveness; repeated/escalating doses are required until a clinical response is obtained; furthermore, atropinization, the indicator of clinical response, is reached slowly and may not always occur (Eisenkraft and Falk, 2016a; McDonough and Shih, 2007). In the case of a shortage of atropine and autoinjectors, several substitutes may be considered, such as scopolamine (Dolgin, 2013; Koplovitz and Schulz, 2010; Markel et al., 2008). Another atropine substitute or adjunct is the atropine-like anticholinergic alkaloid anisodamine, which is somewhat less potent but also less toxic, has additional beneficial pharmacological activities, and was shown to be effective in some case reports on OP-poisoned patients who were slow responders to atropine (Eisenkraft and Falk, 2016a; Kaur et al., 2014). Another supportive therapy suggested by us is infusion of Intralipid® emulsion (ILE), which is used today in resuscitation of patients severely poisoned by an overdose of lipophilic drugs (Eisenkraft and Falk, 2016b). As in the case of anisodamine, systemic studies on its role in CWNA poisoning have not been done, but favorable results from its use in some cases of severe OP poisoning and a sound pharmacological rationale make it a possible supportive adjunct in severe CWNA poisoning (Eisenkraft and Falk, 2016b). The need to administer more than one antidote simultaneously in the case of CWNA/OP poisoning was addressed by the use of autoinjectors with a combination of atropine and oxime or with an additional central component (an anticonvulsant or benactyzine). An alternative approach is to explore antidotes with more than one pharmacological activity. The antitussive drug Caramiphen, which has both anticholinergic and antiglutamatergic activities, was shown to be neuroprotective in animal models of OP poisoning and thus a candidate for development as an OP antidote (Apland et al., 2018; Raveh et al., 2014; Schultz et al., 2014). Novel strategies such as bioscavengers, novel reactivators, and neuroprotectants, which are promising in drug discovery and early pre-clinical research, are options for the more distant future (Dolgin, 2013).
Anisodamine alleviates lipopolysaccharide-induced pancreatic acinar cell injury through NLRP3 inflammasome and NF-κB signaling pathway
Published in Journal of Receptors and Signal Transduction, 2020
Zheng Li, Chunyang Xu, Yuanzhuo Tao, Yuji Liang, Qixian Liang, Junbao Li, Renwen Li, Hongwei Ye
Anisodamine (An), which is a cholinergic receptor antagonist, is mainly extracted from Anisodamine of the nightshade family. Previous studies proved that An can effectively improve cell tolerance to hypoxia and ischemia, reduce the adhesion of inflammatory factors and white blood cells, thereby alleviating inflammatory response [7,8]. In cellular research, You et al. [9] reported that An inhibits the levels of inflammatory cytokines in rat pulmonary microvascular endothelial cells (PMVECs), thereby relieving LPS-induced acute lung injury. In animal experiment, An pretreatment can reduce glycerine-induced oxidative stress, inflammatory response, and cell apoptosis in renal tissues, thereby improving renal dysfunction in rat models of renal injury [10]. Thus, these previous findings suggested that An has a promising value in ameliorating inflammatory response. In recent years, An has been applied not only for the treatment of general diseases, but also for the treatment of many severe acute diseases and patients after cardiac surgery [11,12]. Nonetheless, studies on An in the treatment of acute pancreatitis are less reported.
Emerging medical therapies in crush syndrome – progress report from basic sciences and potential future avenues
Published in Renal Failure, 2020
Ning Li, Xinyue Wang, Pengtao Wang, Haojun Fan, Shike Hou, Yanhua Gong
Anisodamine is a belladonna alkaloid, which is isolated from the traditional Chinese medicinal herb Salvia miltiorrhiza belonging to the Solanaceae family [50,51]. It is mainly used to relieve circulatory diseases in clinical conditions such as disseminated intravascular coagulation (DIC) and skeptic shock [52,53]. The research of Yu et al. [54] showed that anisodamine activated α 7 nicotinic acetylcholine receptor (α7nAChR) to increase the level of serum estradiol. This further enhanced insulin sensitivity in reducing serum potassium, which in turn helped to reduce the on-site mortality of the CS mouse model. These findings also encourage further research on anisodamine for the treatment of CS at the disaster site. Fan et al. [55] found that anisodamine treatment inhibited the increase of high mobility group box 1 protein (HMGB1) in CS rat and mouse models. However, the effect of anisodamine on proinflammatory cytokines in CS and its relationship with mortality needs further study [56].
Hemolysis associated with Russula subnigricans ingestion in a patient with glucose-6-phosphate dehydrogenase deficiency
Published in Clinical Toxicology, 2023
Yuting Pu, Feichi Wang, Hongliang Zhang, Xiangping Chai, Bing Xiao
Five patients (patient 1–5) were admitted to our hospital for suspected mushroom poisoning. Patient 1 was a 60-year-old male who had picked some mushrooms from the mountain near his house and sun-dried them. He claimed that all the mushrooms were collected from one location and were all the same species, with no miscellaneous mushrooms collected. Patient 2 was a 58-year-old female, who was the wife of patient 1 and cooked the sun-dried mushrooms for dinner. Patients 3–5 were three granddaughters of patients 1 and 2. About 1 h after they ingested the mushrooms, they all began to have nausea, stomach aches, and vomiting. They denied other symptoms such as convulsions, muscle soreness, or darkened urine. They received gastric lavage 3 h after ingestion of the mushrooms in the local facility before they were transferred to our hospital. The remainder of the mushrooms were sent to the laboratory to be identified. Morphological assessment by an experienced mycologist and patented software (software patent number 7395548) identified the mushrooms to be Russula subnigricans. This was further confirmed by molecular biological tests using a loop-mediated isothermal amplification assay [3], which reported 99.84% of homology to Russula subnigricans. Acute Russula subnigricans poisoning was diagnosed, and given the unfavorable prognosis, the patients were treated with hemoperfusion though their initial blood tests were unremarkable. Other medications included anisodamine to relieve abdominal pain and vomiting, and acetylcysteine (8 grams per day, intravenously) to scavange reactive oxygen species. Symptoms of patient 1–5 resolved rapidly, and the blood and urine tests of patient 1, 3, 4, and 5 remained unremarkable during their hospital stays, with no evidence of myoglobinuria, or elevated serum concentrations of creatine kinase or myoglobin. However, although the serum creatine kinase activity and myoglobin concentration were within normal range for patient 2 (except for a transient mild elevation in serum myoglobin on day 2), the hemoglobin concentration began to drop on the second day of hospitalization, while the bilirubin concentrations (mainly unconjugated bilirubin) began to rise (Figure 1). Hemolysis in patient 2 was suspected and then confirmed by peripheral blood smear. This unexpected anomaly prompted us to investigate the underlying etiology of hemolysis. A thorough autoimmune antibody screening revealed no positive results, and a hemoglobin electrophoresis assay excluded the possibility of hemoglobinopathy. Interestingly, the glucose-6-phosphate dehydrogenase (G6PD) activity of patient 2 was notably decreased, while that of all the other four patients were within the normal range. Sequencing of the G6PD gene in patient 2 revealed a heterozygous missense mutation in Exon 2, in which an adenosine was replaced by a guanosine (c. 185 A > G), leading to a substitution of histidine by arginine (p. His62Arg). This was a previously reported mutation which could cause World Health Organization (WHO) Class III G6PD deficiency [6]. Patients 1, 3, 4, and 5 were discharged on the third day of hospitalization, while patient 2 was hospitalized for 10 days until her bilirubin concentrations decreased to within normal range.