Danggui Buxue decoction alleviates cyclophosphamide-induced myelosuppression by regulating β-hydroxybutyric acid metabolism and suppressing oxidative stress

Autor: Yiqiao Gao, Yixin Zhang, Wei Liu, Nan Zhang, Qinghe Gao, Jingfang Shangguan, Na Li, Ying Zhao, Yanlong Jia
Jazyk: angličtina
Rok vydání: 2023
Předmět:
Zdroj: Pharmaceutical Biology, Vol 61, Iss 1, Pp 710-721 (2023)
Druh dokumentu: article
ISSN: 13880209
1744-5116
1388-0209
DOI: 10.1080/13880209.2023.2201606
Popis: AbstractContext Danggui Buxue Decoction (DBD) is an effective complementary medicine in alleviating myelosuppression after chemotherapy (MAC). However, its mechanism of action is elusive.Objective To illustrate that regulating β-hydroxybutyric acid (β-OHB) metabolism and suppressing oxidative stress could be a potential mechanism of action for DBD in alleviating MAC.Materials and methods After HPLC quantification and dose testing (3, 6 and 10 g/kg, gavage) of DBD, Sprague-Dawley rats were divided into control, cyclophosphamide (CTX) (30 mg/kg CTX for 5 days, intraperitoneal administration) and CTX + DBD groups (6 g/kg DBD for 14 days, gavage). Blood cell counts, thigh bone histological examination, β-OHB levels, oxidative stress indices and HDAC1 activity were tested. The biological function of β-OHB was verified in vitro (hBMSC cells were incubated in culture mediums that contained 40 μM CTX and β-OHB in 0, 1, 2.5, 5, 10 mM) and in vivo (MAC rat model, 3 g/kg β-OHB for 14 days, gavage).Results Rats in the CTX + DBD group showed upregulated blood cell counts (118–243%), β-OHB levels (495 nmol/mL in blood, 122 nmol/mg in marrow supernatant) and downregulated HDAC1 activity (59%), and oxidative stress indices (60–85%). In vitro, 5 mM β-OHB improved hBMSC cell migration (123%) and proliferation (131%). In vivo, rats treated with 3 g/kg β-OHB showed upregulated blood cell counts (121–182%) and downregulated HDAC1 activity (64%) and oxidative stress indices (65–83%).Discussion and conclusions DBD, a traditional Chinese medicine, alleviates MAC by intervening in β-OHB metabolism and oxidative stress.
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