Streptomycin is an effective antibiotic against Mycobacterium tuberculosis and is used in the study of tuberculosis (TB)[1]. Streptomycin acts as a protein synthesis inhibitor, binding irreversibly to the small 16S rRNA of the 30S ribosomal subunit, interfering with protein synthesis [2]. Streptomycin originally had broad Gram-negative and Gram-positive coverage, but its spectrum of activity has been significantly narrowed due to antibiotic resistance [3]. Streptomycin is an aminoglycoside antibacterial drug with poor oral absorption and can be administered intramuscularly or intravenously [4].
In vitro, treatment of guinea pig ventricular myocytes with streptomycin (40 μM) for 2 min significantly inhibited the stretch-induced increase in Ca2+. The decrease in Ca2+ occurred 18 seconds after the application of streptomycin (n=13 cells). In all cells, the decrease in Ca2+ occurred in less than 60 seconds, indicating that streptomycin has a calcium homeostatic effect on cardiomyocytes [5]. Streptomycin (5, 50μg/ml) can effectively inhibit the survival and proliferation of Mycobacterium tuberculosis in human macrophages infected with Mycobacterium tuberculosis[6].
In vivo, Streptomycin (50-100 mg/kg) was used to treat mice infected with Mycobacterium avium complex (MAC) by intramuscular injection for 4 weeks, which significantly reduced the MAC bacterial load in the spleen and liver, and showed partial protection in histopathological examination, but did not completely eliminate the infection. The liposome encapsulation effect of Streptomycin was better than that of the free form[7].
References:
[1] Cohen K A, Stott K E, Munsamy V, et al. Evidence for expanding the role of streptomycin in the management of drug-resistant Mycobacterium tuberculosis[J]. Antimicrobial agents and chemotherapy, 2020, 64(9): 10.1128/aac. 00860-20.
[2] Weisblum B, Davies J. Antibiotic inhibitors of the bacterial ribosome[J]. Bacteriological reviews, 1968, 32(4_pt_2): 493-528.
[3] Guardabassi L, Courvalin P. Modes of antimicrobial action and mechanisms of bacterial resistance[J]. Antimicrobial resistance in bacteria of animal origin, 2005: 1-18.
[4] EDSON R S, TERRELL C L. The aminoglycosides: streptomycin, kanamycin, gentamicin, tobramycin, amikacin, netilmicin, and sisomicin[C]//Mayo Clinic Proceedings. Elsevier, 1987, 62(10): 916-920.
[5] Gannier F, White E, Lacampagne A, et al. Streptomycin reverses a large stretch induced increase in [Ca2+] i in isolated guinea pig ventricular myocytes[J]. Cardiovascular research, 1994, 28(8): 1193-1198.
[6] Crowle A J, Sbarbaro J A, Judson F N, et al. Inhibition by streptomycin of tubercle bacilli within cultured human macrophages[J]. American Review of Respiratory Disease, 1984, 130(5): 839-844.
[7] Gangadharam P R J, Ashtekar D A, Ghori N, et al. Chemotherapeutic potential of free and liposome encapsulated streptomycin against experimental Mycobacterium avium complex infections in beige mice[J]. Journal of Antimicrobial Chemotherapy, 1991, 28(3): 425-435.
链霉素（Streptomycin）是一种有效的抗结核分枝杆菌的抗生素，用于结核病 （TB）的研究[1]。Streptomycin起到蛋白质合成抑制剂的作用，不可逆地与30S 核糖体亚基的小16S rRNA结合，干扰蛋白质合成[2]。Streptomycin最初具有广泛的革兰氏阴性和革兰氏阳性覆盖率，但由于抗生素耐药性，其活性谱已显著缩小[3]。Streptomycin是一种氨基糖苷类抗菌药物，口服吸收差，可以通过肌肉或静脉注射给药[4]。
在体外，Streptomycin（40μM）处理豚鼠心室肌细胞2min，显著抑制了拉伸诱导的Ca2+增加，Ca2+的下降发生在应用链霉素18秒后（n=13个细胞），在所有细胞中，Ca2+在不到60秒的时间内下降，表明Streptomycin对心肌细胞具有钙稳态调节作用[5]。Streptomycin（5、50μg/ml）处理感染结核杆菌的人类巨噬细胞，能够有效抑制细胞内的结核分枝杆菌的存活和增殖[6]。
在体内，Streptomycin（50-100mg/kg）通过肌肉注射治疗感染鸟分枝杆菌复合体（MAC）的小鼠4周，显著降低了脾脏和肝脏中的MAC菌负荷，且在组织病理学检查中显示出部分保护作用，但未完全清除感染，Streptomycin脂质体包封效果优于游离形式[7]。