Abstract
Oxidative stress plays a role in regulating a variety of physiological functions in living organisms and in the pathogenesis of articular cartilage diseases. Piper kadsura Ohwi is a traditional Chinese medicine that is used as a treatment for rheumatic pain, and the extracts have anti-inflammatory and antioxidant effects. However, there is still no study related to cell protection by P. kadsura. The P. kadsura extracts (PKE) were obtained by microwave-assisted extraction, liquid-liquid extraction, and column chromatography separation. The extracts could effectively scavenge free radicals in the antioxidant test, the EC50 of extracts is approximately the same as vitamin C. PKE decreased the apoptosis of SW1353 cells treated with H2O2 and could upregulate the gene expression of antioxidant enzymes (SOD-2, GPx, and CAT) and the Bcl-2/Bax ratio, as well as regulate PARP, thus conferring resistance to H2O2 attack. PKE protects cells against apoptosis caused by free radicals through the three pathways of JNK, MEK/ERK, and p38 by treatment with MAPK inhibitor. The identified components of PKE were bicyclo [2.2.1] heptan-2-ol-1,7,7-trimethyl-,(1S-endo)-, alpha-humulene, and hydroxychavicol by gas chromatography–mass spectrometry.
Highlights
Osteoarthritis (OA) is a progressive degenerative joint disease that affects cartilage, synovium, synovial joints, and muscles around the joints [1,2]
Cellular apoptosis in SW1353 cells treated with P. kadsura extracts (PKE) (60 μg/mL), PKE (60 μg/mL) with 3.6 mM added H2O2, and 3.6 mM H2O2 for 24 h was determined according to cellular vitality
Using SW1353 cells as test subjects, we investigated the protective effects of extracts from P. kadsura on its cytotoxicity and oxidative damage
Summary
Osteoarthritis (OA) is a progressive degenerative joint disease that affects cartilage, synovium, synovial joints, and muscles around the joints [1,2]. Inflammation of the synovial membrane results in asymmetrical stenosis of the joint cavity, joint pain, stiffness, and dysfunction It is caused by extracellular matrix (ECM) degradation and dysregulation of some inflammatory factors [3]. H2O2 is the major source of endogenous ROS; it has been extensively used to induce oxidative stress in in vitro models and to induce apoptosis in several types of cells, instate of the cell and damages the cell’s proteins, lipids, and DNA [5]. When ROS exceeds the ability of cells to load, th internal antioxidant capacity and oxidative capacity of the cells are unbala2nofc2e3d This called oxidative stress, and this result can destroy the normal structure of the mitochon dria in the cell and its function, leading to death or apoptosis [7,8]. This technique ca conMveirctroewleacvtreo-amssaigstneedtiecxternacetrigoyn i(nMtAo Eh)ehaat saat cahisepveecdifriecmfraerqkuabelnecryesaunltds tinemthpeearraetausre to rap oifdclhyemheicaatl tshyentrheeascist,iobinommeadtiecriniael,sa.nMd AneEwc-manatearcihaliemvaenhuifgachtuyrienlgd. sT,hsieslteeccthivniqtyu,eacnand reactio croantveesr,taenledcttrhomisamgneetthicoednceragnyuinsteolheesastsaotlavsepnetc,icfiocnfrseuqmueenlceysasnednteermgpye, raantudreptroordaupcidelyless wast htehaatnthdeoretaractdioitniomnaatlehrieaalst.inMgAsyEnctahneascehsi[e1v7e].high yields, selectivity, and reaction rates, attrotpnahdrtdoohitsottShieesWoSicsenWot1miaofv3lf1et5eh3htt3hhe5eeaoce3fetdafaiclenrlrcesctgtailtisclncssshuuyuoosllnasahwfterrhoPilcenwce.hshgseioksonsoansngxd[od1dislrdo7vuro]axeor.ctinaycidtvyt,eaeetcxtseositsvotnrraefsoeucOsfstmstAOr(ieenPA[sldK6esu]s[E.is6cn)eT]ed.dnhfuoTeebrrchygaeeoiydHm,xaa2ibidnoOmydfa2Httpopihvrf2oioOsestdhss2suetiptusscrosedessypsltessurseiosdstsposywteopracitissrenitoeletvlsposetsehsiiortanmitnngviiealedOsatsoersAtiigm-raeitlleaartteht thsyemprpottoecmtivseaenfdfecctesllouflPa.rkaadpsoupratoesxitsr.act (PKE) for oxidative stress to cells on OA-related symptoms and cellular apoptosis
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