Carbocisteine

Carbocisteine is an orally active mucolytic agent. Carbocisteine attenuates the phosphorylation of NF-κB p65 and ERK1/2. Carbocisteine modulates Nrf2/HO-1 and NFκB interplay. Carbocisteine inhibits Apoptosis. Carbocisteine is used in chronic obstructive pulmonary disease (COPD) research^{[1][2][3][4][5][6][7][8][9][10][11][12][13]}. In Vitro: Carbocisteine (10-1000 μM, 24 h) attenuates hydrogen peroxide-induced inflammatory injury in A549 cells via NF-κB and ERK1/2 MAPK pathways^[4].
Carbocisteine (L-Carbocisteine, 10 μM, from 3 days before infection) shows inhibitory effects on type A seasonal influenza virus infection in human airway epithelial cells^[5].
Carbocisteine (L-carbocisteine, 10 μM, 72 h) inhibits oxidant-induced apoptosis in cultured human airway epithelial cells^[12].
Carbocisteine (10-1000 μM, 24 h) attenuates TNF-α-induced inflammation in human alveolar epithelial cells in vitro through suppressing NF-κB and ERK1/2 MAPK signaling pathways^[13].
In Vivo: Carbocisteine (100 mg/kg, oral gavage, twice daily from 1 day before CS exposure until the end of the experiment) reduces virus-induced pulmonary inflammation in mice exposed to cigarette smoke^[2].
. Carbocisteine (100 mg/kg, p.o.) promotes phagocytosis of apoptotic cells by alveolar macrophages in BALB/c mice^[3].
. Carbocisteine (125-250 mg/kg/d, gavage, once a week for 3 weeks) protects against emphysema induced by cigarette smoke extract in rats^[6].
Carbocisteine (500 mg/kg/day, p.o., in two divided doses, 2 days) inhibits oxidative stress, inflammatory response, and apoptosis in acetic acid-induced UC by modulating the Nrf2/HO-1 and NFκB interplay in rats^[7].
Carbocisteine (112.5-225 mg/kg/d, gavage, 12 weeks) inhibits the expression of Muc5b in COPD mouse model^[8].
Carbocisteine (300 mg/kg, i.g., once every day for the last 6 weeks) ameliorates steroid resistance in rat COPD model^[9].
Carbocisteine (250 mg/kg ×2/day, p.o., 25 days) inhibits the changes in these enzyme (fucosidase, sialidase, fucosyltransferase and sialyltransferase) activities and the expressions of Muc5ac mRNA and protein in the lungin SO₂-exposed rats^[10].
Carbocysteine (300 mg/kg, p.o., every day both from week 6 to week 12 of smoke exposure) restores steroid sensitivity by targeting histone deacetylase 2 in a thiol/GSH-dependent manner in rats^[11].