Most drugs exhibit wide inter-individual variability in efficacy and toxicity, on account of genetic variants which encode drug-metabolizing enzymes and transporters [19]. However, pharmacogenomic data on the Jingpo population still remains scarce. Therefore, our research selected 57 VIP variants from 28 genes among 159 Jingpo participants and compared them with the other 26 populations. In conclusion, we found that only rs4291 (ACE) in the Jingpo population was significantly different from that in all other 26 populations. Rs20417 (PTGS2), rs1801280 (NAT2), rs1799929 (NAT2), rs2115819 (ALOX5) and rs1065852 (CYP2D6) in the Jingpo population significantly differed from those in most of 26 populations.

The ACE gene (chromosome 17q23) encodes Angiotensin 1-converting enzyme, and rs4291 variant is located in its promoter region. Previous South Korean research has found that compared to genotype AA, individuals with genotypes AT or TT at rs4291 had an increased risk of aspirin intolerance when asthmatics were treated with aspirin [20]. Irvin et al. have testified that compared with genotype TT, hypertensive patients with genotype AA or AT experienced reduced fasting glucose levels when treated with amlodipine, clothalidone, or lisinopril [21]. Furthermore, a recent study has confirmed that in patients receiving captopril for Alzheimer's disease, the genotype AA had a correlation with lowered severity of kidney failure in comparison to genotypes AT or TT [22]. In our research, the frequencies of AA, AT, and TT genotypes among the Jingpo participants were approximately 2.5%, 95.6%, and 1.9%, respectively. Overall, it is helpful for pharmacist to adjust drugs in accordance with the genotypes of the Jingpo individuals so that the efficiency and safety of drugs could be maximized.

Prostaglandin-endoperoxide synthase 2 (PTGS2) gene encode prostaglandin synthase cyclooxygenase-2 (COX-2) that a rate limiting enzyme in prostaglandin synthesis and, therefore, performs a unique role as a regulator of inflammation [23]. Rs20417 (− 765 G > C), located in the promoter region of PTGS2 gene, has been reported to have noticeable effects on the metabolism of NSAIDs. Aspirin is widely used as an antiplatelet drug for the treatment of stroke and myocardial infarction. However, a growing number of patients are experiencing aspirin resistance (AR), primarily due to genetic factors [24]. The research conducted by Vandana Sharma et al. has suggested that the carriers of C allele of PTGS2 rs20417 were more prone to developing AR than non-carriers [25]. Additionally, it has been reported that NSAID users with genotypes CG in rs20417 presented a prominently lowered cancer risk than non-NSAID users among US population [26]. In our study, the frequency of CG in the Jingpo population was about 0.6%, which was much lower than the other 26 populations. Therefore, the cancer risk caused by using NSAID among the Jingpo population should be considered.

N-acetyltransferase 2 (NAT2) gene, encodes the enzyme NAT2 that is supposed the main enzyme of xenobiotic acetylation [27]. It is involved in the biotransformation of various clinical drugs, containing antihypertensive, arylamine drugs and anti-tuberculosis [28]. Importantly, accumulating evidences have demonstrated that the variants of NAT2 rs1801280, and rs1799929 result in isoniazid and phenytoin poisoning with slow acetylation [29, 30]. Specifically, studies have manifested that the genotypes TT or CT at rs1799929 of NAT2 were correlated with increased likelihood of hepatotoxicity when treated with isoniazid for tuberculosis [31, 32]. Besides, Lawi et al. have demonstrated that patients with non-small cell lung carcinoma carrying rs1801280 CC genotype exhibit low acetylation rates of this enzyme, thereby worsening the cancer [33]. Of note, we observed that the frequency of genotypes CC at rs1801280 (0%), TT (0%) and CT (6.9%) at rs1799929 were lower among EAS in our study, suggesting that these drugs were relatively safe for the Jingpo people.

The ALOX5 gene is located on chromosome 10q11.21 and consists of 14 exons and 13 introns. It encodes 5-lipoxygenase enzyme which plays a pivotal role in the formation of leukotrienes. Leukotrienes are known to be performed a crucial role in inflammatory conditions. Lima et al. have come up with the idea that individuals with the GG genotype at rs2115819 of ALOX5 (A > G) in the white population exhibited a significantly greater FEV1 response when treated with montelukast for asthma compared to those with the AA or AG genotypes [34]. Encouraged by this research, Tantisira et al. have reported that homozygous GG individuals in the white population showed better the improvement in lung function of asthmatics treated with zileuton than homozygous AA [35], which was also in conformance with the research among Japanese conducted by H Kotani et al. [36]. In our study, the frequency of GG genotype in the Jingpo population was 76.1%, higher than the other 26 populations (1.8–64.8%). Overall, we hypothesize that Jingpo patients with asthma may experience improved therapeutic outcomes when treated with montelukast or zileuton.

Cytochrome P450 2D6 (CYP2D6), as a prominent drug gene, participated in the metabolism of commonly used drugs in diseases, including mental illness, pain management, tumors, and heart disease [37]. It has been reported that CYP2D6 is highly polymorphic, and the frequency of variation varies among populations [38]. CYP2D6*10 (rs1065852, Pro34Ser) was thought to be responsible for the CYP2D6 activity [39]. A relevant study has reported that early onset preeclampsia patients with the allele G at rs1065852 were prone to have no response to labetalol [40]. In addition, research on patients with ischemic stroke (IS) showed that the GG genotype at rs1065852 had a better effect on atorvastatin therapy. Hence, to minimize the side effects of atorvastatin, clinicians should consider to give lower dosage to patients with IS carrying GG genotype [41]. A study of breast cancer patients in Thailand have signaled that carriers with the A allele had higher recurrence rates and worse survival rate following tamoxifen treatment [42], which was consistent with the research conducted by Lu et al. in Asian [43]. According to our research, the frequencies of A allele in the Jingpo population were approximately 46.1%, much higher than SAS, EUR, AMR and AFR (3.5–25.6%), which may explain the negative consequences observed in tamoxifen treatment among Jingpo breast cancer patients.

However, our research still existed some deficiencies. First, the absence of detailed clinical characteristics of the participants hinders the comprehensive grasp of the clinical relevance associated with identified pharmacogenetic variations in Jingpo population. Additionally, our study is constrained by the lack of a comparative analysis with other databases. Future collaborations with these databases, employing suitable methods, could enhance our research by integrating more diverse genomic data, thereby augmenting the depth and scope of our analysis.