Carbocisteine

Carbocisteine is an orally effective mucolytic agent. It inhibits the phosphorylation of NF-κB p65 and ERK1/2, regulates the crosstalk between Nrf2/HO-1 and NF-κB, and inhibits apoptosis, making it applicable in chronic obstructive pulmonary disease (COPD) research.

Methods: A549 cells and human alveolar epithelial cells were treated with 10–1000 μM Carbocisteine for 24 h; human airway epithelial cells were pretreated with 10 μM L-Carbocisteine for 3 days before infection; in addition, human airway epithelial cells were treated with 10 μM L-Carbocisteine for 72 h. The inflammation, viral infection and cell apoptosis were detected respectively.
Results:
1. Carbocisteine (10–1000 μM, 24 h) could alleviate hydrogen peroxide-induced inflammatory damage in A549 cells through the NF-κB and ERK1/2 MAPK pathways [4].
2. Pretreatment with Carbocisteine (10 μM) 3 days before infection could inhibit seasonal influenza A virus infection in human airway epithelial cells [5].
3. Carbocisteine (10 μM, 72 h) could inhibit oxidative stress-induced apoptosis in human airway epithelial cells [12].
4. Carbocisteine (10–1000 μM, 24 h) could reduce TNF-α-induced inflammatory response in human alveolar epithelial cells by inhibiting the NF-κB and ERK1/2 MAPK pathways in vitro [13].

Methods: Carbocisteine was administered to mice and rats via intragastric gavage or oral gavage in vivo. Different doses, frequencies and courses of treatment were used to intervene in animal models of cigarette smoke exposure, viral infection, emphysema, ulcerative colitis, COPD and SO₂ exposure respectively. Indicators such as pulmonary inflammation, phagocytic function, mucin expression, oxidative stress and steroid sensitivity were detected.
Results:
1. Carbocisteine (100 mg/kg, intragastric gavage, twice a day, from 1 day before cigarette smoke exposure to the end of the experiment) could alleviate virus-induced pulmonary inflammation in mice exposed to cigarette smoke [2].
2. Carbocisteine (100 mg/kg, oral administration) could promote the phagocytosis of apoptotic cells by alveolar macrophages in BALB/c mice [3].
3. Carbocisteine (125–250 mg/kg/d, intragastric gavage, once a week for 3 consecutive weeks) could prevent emphysema induced by cigarette smoke extract in rats [6].
4. Carbocisteine (500 mg/kg/d, oral administration, twice a day for 2 consecutive days) could inhibit oxidative stress, inflammatory response and cell apoptosis induced by acetic acid in rats with ulcerative colitis by regulating the interaction between Nrf2/HO-1 and NF-κB [7].
5. Carbocisteine (112.5–225 mg/kg/d, intragastric gavage for 12 weeks) could inhibit the expression of Muc5b in a mouse model of COPD [8].
6. Carbocisteine (300 mg/kg, oral administration, once a day for 6 consecutive weeks) could improve steroid resistance in a rat model of COPD [9].
7. Carbocisteine (250 mg/kg, twice a day, oral administration for 25 days) could inhibit the abnormal changes in the activities of fucosidase, sialidase, fucosyltransferase and sialyltransferase in the lung tissue of rats exposed to SO₂, and down-regulate the mRNA and protein expression of Muc5ac [10].
8. Carbocisteine (300 mg/kg, intragastric gavage, once a day, from week 6 to week 12 of smoking exposure) targeted histone deacetylase 2 in a thiol/GSH-dependent manner, restoring steroid sensitivity in rats [11].

H2O: 1.60 mg/mL (8.93 mM), Sonication is recommended.