Rumex aquaticus.   Water dock   Family: Polygonaceae
PART USED: Root
TASTE: Astrngent and sweetish   ODORLESS
ACTIONS
1. Alterative.[1]
2. Deobstruent.[1]
3. Detergent.[1]
PREPARATIONS: Infusion taken internally.[1] Powdered root has been used as a dentrifice.[1]
Liquid extract 4-8 ml.[1]
HABITAT: By rivers and ditches.
ORIGIN: Northern Europe and Great Britain.
DESCRIPTION: Leaves; triangular, around three times as long a wide, alternate, with a sheath round the stem at the base of the leaves. Root; blackish or dark brown outer surface, the remains of a few branches, and transverse rings of rootlet scars.
References
Inner Path can not take any responsibility for any adverse effects from the use of plants. Always seek advice from a professional before using a plant medicinally.
Constituents
Antraquinones, about 0.6%.[1] Tannins, about 20%.[1]
References
[1] Drogenkunde, 8th Ed. Heinz, A., Hoppe. Pub. W. de Gruyter (1975) Berlin
Research

The cytoprotective effect of Rumex Aquaticus Herba extract against hydrogen peroxide-induced oxidative stress in AGS cells
Eun Jeong Cho, Seung In Um, Jeong Hoon Han, Byeonghee Kim, Sang Beom Han, Ji Hoon Jeong, Hak Rim Kim, Inkyeom Kim, Wan Kyun Whang, Eunhwa Lee, Uy Dong Sohn
Abstract
The Rumex Aquaticus Herba extract containing quercetin-3-ß-D-glucuronopyranoside (ECQ) has been reported to exhibit various pharmacological activities, including anti-inflammatory and anti-oxidative effects. This plant has been traditionally used for the treatment of diarrhea, disinfestation, edema and jaundice, and as an antipyretic drug. The aim of the present study was to investigate the ability of ECQ to protect against oxidative damage and to determine its signaling mechanism in AGS cells. The protein expressions of heme oxygenase-1 (HO-1) and nuclear factor-erythroid 2 related factor 2 (Nrf2) were measured by Western blots. Cell viability was measured by MTT assay. Intracellular reactive oxygen species (ROS) levels were measured using 2',7'-dichlorofluorescein diacetate. Glutathione peroxidase levels were measured using kits. The protein expressions of HO-1 and its upstream mediator, Nrf2, increased after ECQ treatment. The HO-1 inhibitor, ZnPP, repressed the protective effect of ECQ on H2O2-induced cell damage. We found that LY294002, a specific PI3 K/Akt inhibitor, suppressed ECQ-induced HO-1 expression. ECQ significantly attenuated H2O2-induced cytotoxicity and ROS generation. Also, ECQ enhanced the antioxidant enzyme activities of glutathione peroxidase. These results suggest that ECQ exerts a cytoprotective effect against H2O2-induced oxidative stress by upregulation of Nrf2/HO-1 via the PI3 K/Akt pathway.
Arch Pharm Res 2016 Dec;39(12):1739-1747. doi: 10.1007/s12272-016-0863-0. Epub 2016 Nov 24. PMID: 27885462 pubmed.ncbi.nlm.nih.gov

Protective effect of extract from Rumex aquaticus herba on ethanol-induced gastric damage in rats
Hyun Soo Kwak 1, Sun Young Park, Thao Thanh Nguyen, Chung Hyo Kim, Jong Mi Lee, Jung Sook Suh, Wan Kyunn Whang, Uy Dong Sohn
Abstract
Background/aims: In this study, we investigated the gastroprotective effect of extract including quercetin-3-O-ß-D-glucuronopyranoside (EIQ) from Rumex aquaticus herba against the ethanol-induced gastric damage in rats.
Methods: The rats were divided into eight groups composed of a non-ethanol group, only EIQ (10 mg/kg) group, groups with absolute ethanol after pretreatment with various doses of EIQ (1, 3 and 10 mg/kg), rebamipide (10 mg/kg), stillen (40 mg/kg) and a control receiving only absolute ethanol. Ethanol-induced gastric lesions, lipid peroxidation, neutrophil infiltration and glutathione level were measured. Superoxide dismutase (SOD) and catalase activity were assessed by an assay kit. Protein expression of SOD, catalase or hemoxygenase-1 (HO-1) was assessed by western blotting analysis.
Results and conclusion: In the absolute ethanol treated group, gastric lesion and malondialdehyde levels were significantly increased with enhanced myeloperoxidase activity. Administration of EIQ 1 h prior to ethanol treatment significantly inhibited the formation of gastric lesions and the elevation of the malondialdehyde levels with myeloperoxidase activity. In addition, pretreatment with EIQ significantly increased the level of glutathione, and elevated the activity and protein expression of radical scavenging enzymes, such as SOD, catalase and HO-1. EIQ may exert anti-inflammatory and anti-oxidative effects against ethanol-induced gastric injury through the reduction of lipid peroxidation, myeloperoxidase activity and free radicals.
Pharmacology 2012;90(5-6):288-97. doi: 10.1159/000342767. Epub 2012 Oct 1. PMID: 23037147 pubmed.ncbi.nlm.nih.gov

Flavonoids isolated from Rumex aquaticus exhibit neuroprotective and neurorestorative properties by enhancing neurite outgrowth and synaptophysin
Orsolya Orbán-Gyapai, Aparna Raghavan, Andrea Vasas, Peter Forgo, Judit Hohmann, Zahoor A Shah 1
Abstract
There is heightened interest in the field of stroke recovery as there is need for agents that would prevent the debilitating effects of the disorder, thereby tremendously reducing the societal and economic costs associated with it. In this study, the isolation of two flavonoids--quercetin-3-O-galactoside (1) and quercetin-3-O-arabinoside (2)--from Rumex aquaticus (western dock) and their neuroprotective effects were reported in the oxygen-glucose deprivation (OGD) model of in vitro ischemia using rat pheochromocytoma (PC12) cell line. Bioassay-guided fractionation of the ethyl-acetate extract of Rumex aquaticus L. afforded the isolation of compounds 1 and 2. The structures of compounds were established on the basis of spectroscopic analyses (UV, mass spectrometry (MS) and nuclear magnetic resonance spectroscopy (NMR). Both compounds were isolated for the first time from this species. In the course of the pharmacological experiments it was detected that these flavonoids at 10 µM concentration significantly improved cell survival in the oxygen-glucose deprivation model of ischemia. Moreover, they also increased neurite outgrowth in differentiated PC12 cells subjected to ischemic insult. Investigations on the cellular mechanism for the observed effect revealed that compound 1 (10 µM) enhances the expression of synaptophysin - a marker of synapses, and an indicator of synaptic plasticity. Rapid restoration of neurological function following injury is paramount to the prevention of debilitating consequences of ischemic stroke. This combination of neuroprotection and neuritogenic potential could be particularly useful in the recovery phase of stroke.
CNS Neurol Disord Drug Targets . 2014;13(8):1458-64. doi: 10.2174/1871527313666141023154446. PMID: 25345505 pubmed.ncbi.nlm.nih.gov