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Tribulus terrestris L. is an annual herbaceous medicinal plant of Zygophyllaceae, which is cultivated commercially in China. Subrotund or irregular gray, sunken, necrotic spots ranging from 2 to 9 mm were observed on diseased leaves of T. terrestris landrace in Fushun County, Liaoning Province of northeast China in July 2021, with more than 32% of the plants being infected in a 18-ha field. The symptoms first appeared on older leaves and gradually spread to younger leaves. The lesions developed a white center gradually and became perforated; multiple lesions could coalesce (Fig. 1). Ten symptomatic leaves were collected and the diseased tissues were cut into small pieces, immersed in 1% NaOCl for 2 min, rinsed three times with sterile water, and placed on acidified potato dextrose agar (PDA) in Petri dishes at 25°C in darkness. Fifteen suspected Colletotrichum single-spore fungal isolates (JL1 to JL15) with consistent morphological characteristics were obtained, and isolate JL6 was selected for identification and pathogenicity testing. Colonies on PDA were flat with an entire margin, dense and white at first, then became dark gray with numerous black microsclerotia and formed a concentric circular pattern with aging. Conidia were single-celled, sickle-curved with a tapered tip and truncate base, ranging from 16.46 to 20.26 μm in length and 2.81 to 3.96 μm in width (n=100). Setae were dark brown, septate, straight with a slightly acute tip, 75.45 to 135.63×3.19 to 4.95 μm in size. Appressoria were dark brown, round or irregular, mostly in groups. All characteristics were consistent with the descriptions of C. truncatum (Damm et al. 2009). Further confirmation of the identification was determined according to methods described previously (Damm et al. 2009). The rDNA internal transcribed spacer region (OP364400, 585 bp), and actin (OP380867, 290 bp), beta-tubulin (OP380868, 498 bp), chitin synthase 1 (OP380869, 277 bp), glyceraldehyde-3-phosphate dehydrogenase (OP380870, 280 bp), and histone (OP380871, 411 bp) genes were amplified by PCR and sequenced (Carbone and Kohn 1999; Glass and& Donaldson 1995; Guerber et al. 2003; O'Donnell and Cigelnik 1997). BLAST results showed 98-100% similarity at 85-97% coverage compared to the corresponding sequences of the type strain CBS 151.35 (GU227862, GU227960, GU228156, GU228352, GU228254, and GU228058). Phylogenetic analysis combining all loci revealed that the isolate JL6 and the type strains of C. truncatum clustered in one group (Fig. 2). One-year-old healthy seedlings of T. terrestris (cultivar: landrace) were used for pathogenicity test. Suspension (1×105 conidia/mL) of isolate JL6 was sprayed on ten seedlings, and ten seedlings sprayed with sterilized distilled water were used as the control. Three replicates were performed on each treatment. All plants were kept at 28±1°C (12 h photoperiod), and were evaluated after 7 days. The inoculated plants showed lesions on the leaf surface, similar to those in the field, and the control remained symptomless. The pathogen was successfully reisolated and identified using the methods mentioned above. To our knowledge, this is the first report of C. truncatum causing anthracnose on T. terrestris, which will provide valuable information for designing strategies to manage anthracnose on T. terrestris.

Mitochondrial dysfunction in proximal tubular epithelial cells is a key event in acute kidney injury (AKI), which is a risk factor for the development of chronic kidney disease (CKD). Apelin is a bioactive peptide that protects against AKI by alleviating inflammation, inhibiting apoptosis, and preventing lipid oxidation, but its role in protecting against mitochondrial damage remains unknown. Herein, we examined the protective effects of apelin on mitochondria in cisplatin-stimulated human renal proximal tubular epithelial cells and evaluated its therapeutic efficacy in cisplatin-induced AKI mice. In vitro, apelin inhibited the cisplatin-induced mitochondrial fission factor (MFF) upregulation and the fusion-promoting protein optic atrophy 1 (OPA1) downregulation. Apelin co-treatment reversed the decreased levels of the deacetylase, Sirt3, and the increased levels of protein acetylation in mitochondria of cisplatin-stimulated cells. Overall, apelin improved the mitochondrial morphology and membrane potential in vitro. In the AKI model, apelin administration significantly attenuated mitochondrial damage, as evidenced by longer mitochondrial profiles and increased ATP levels in the renal cortex. Suppression of MFF expression, and maintenance of Sirt3 and OPA1 expression in apelin-treated AKI mice was also observed. Finally, exogenous administration of apelin normalized the serum level of creatinine and urea nitrogen and the urine levels of NGAL and Kim-1. We also confirmed a regulatory pathway that drives mitochondrial homeostasis including PGC-1α, ERRα and Sirt3. In conclusion, we demonstrated that apelin ameliorates renal functions by protecting tubular mitochondria through Sirt3 upregulation, which is a novel protective mechanism of apelin in AKI. These results suggest that apelin has potential renoprotective effects and may be an effective agent for AKI treatment to significantly retard CKD progression.

With rapid progress in cancer diagnosis and treatment in the last two decades, outcomes in oncological patients have improved significantly. However, the incidence of acute kidney injury (AKI) in this population has also increased significantly. AKI complicates many aspects of patients' care and adversely affects their prognoses; thus, accurately diagnosing the risk factors for AKI ensures appropriate management. AKI may be caused by pre-renal, intrinsic renal, and post-renal reasons, as well as for combined reasons. This review summarizes the potential etiologies of AKI according to the three classifications. For each underlying cause of AKI, the cancer itself and/or cancer treatment may contribute to a patient developing AKI. Therefore, we present disease- and treatment-related factors for each cause category, with special focus on immune checkpoint inhibitors, which are being used increasingly more often. It is important for nephrology services to be knowledgeable to provide the best level of care.

The utility of traditional methods for detecting seed-borne fungi is limited by the fact some fungi are unculturable or difficult to isolate. The seed-borne pathogens affecting Panax ginseng cultivation have not been fully characterized. Seed-borne fungi can be identified based on the high-throughput sequencing of internal transcribed spacer (ITS) amplicons. A hierarchical clustering tree diagram analysis based on operational taxonomic units revealed a relationship between the seed-borne fungi and the region from which the seeds were collected. This study analyzed the fungal diversity on 30 ginseng seed samples from the main ginseng-producing areas of China. The 50 most abundant genera were identified including those responsible for ginseng diseases, Fusarium, Alternaria, Nectria, Coniothyrium, Verticillium, Phoma, and Rhizoctonia. Fusarium species, which are the primary causes of root rot, were detected in all seed samples. The results of a phylogenetic analysis indicated that the seed-borne fungal species originating from the same region were closely related. Fungi on ginseng seeds from eight different regions were divided into eight clades, suggesting they were correlated with the local storage medium. A total of 518 Fusarium isolates were obtained and 10 species identified, all of which can be detrimental to ginseng production. Pathogenicity tests proved that seed-borne Fusarium species can infect ginseng seedlings and 2-year-old ginseng root, with potentially adverse effects on ginseng yield and quality.

American ginseng (

American ginseng (Panax quinquefolium) is a valuable medicinal plant that is commercially cultivated in China. In May 2020, Sclerotinia root rot of American ginseng was observed on 4-year-old plants in Fusong County in northeastern China, which is the most important part of the country for American ginseng cultivation. The pathogen only infected the tuberous ginseng roots, with sclerotia tightly attached to the root surface. Infected roots, which were brownish and had a watery soft rotted appearance (Fig. 1), eventually became hollow and filled with sclerotia. There were no significant changes to the aboveground plant parts during the initial infection stage, but as the disease progressed, the foliage became discolored and wilted because of the damaged roots. More than 31% of the plants in a 30-ha field were infected. Symptomatic roots were collected and sclerotia were removed from the diseased tissue, immersed in 1% NaClO for 1 min, rinsed three times with sterile water, and placed on acidified potato dextrose agar (PDA) in Petri dishes. After an incubation in darkness at 20 °C for 2-3 days, 21 suspected Sclerotinia isolates were obtained. Isolates JH1 and JH2 were randomly selected for identification. On PDA, colonies produced sparse, white, and cottony aerial mycelia (i.e., wool-like appearance), with septate, branched, and hyaline hyphae. Within 4 days of incubation, the PDA surface was covered with white hyphae. Small and white sclerotial primordia formed 3 days later and were irregularly distributed in the middle and along the edge of the Petri dish. After maturing, the hardened and black sclerotia had an irregular shape and size, ranging from 1.4 × 1.5 to 4.1 × 7.5 mm (n = 50). Most of the sclerotia developed separately, with approximately 15-25 per plate (Fig. 2). On the basis of their morphology, the isolates were initially identified as Sclerotinia sp. (Mordue and Holliday 1976; Kohn 1979). Using the JH1 and JH2 rDNA internal transcribed spacer (ITS) region (GenBank accession no. MZ031405 and MZ031406) and the aspartyl protease gene specific to S. sclerotiorum (MZ292709 and MZ292710) in GenBank as queries, BLAST searches revealed that the sequences were respectively 99%-100% similar to S. sclerotiorum sequences KF859933 and AF271387. The primer pairs for amplifying the ITS region and the aspartyl protease gene were respectively ITS4/ITS5 (White et al. 1990) and SSaspr F/SSaspr R (Abd-Elmagid et al. 2013). The pathogenicity of JH1 and JH2 was evaluated using healthy plants. The roots of 4-year-old ginseng plants were washed, wiped with 75% alcohol, and transferred to flower pots containing sterile sand and sorghum grain (10:1 v/v) infested with 10-day-old isolates. For both isolates, 12 plants were inoculated, with four plants per pot. Control plants were transferred to flower pots containing sorghum grain lacking fungus. The inoculated samples were incubated in a greenhouse (12 h photoperiod and 25 °C) for 25 days before they were examined. The test was repeated twice. The inoculated roots exhibited the same symptoms as those observed in the field, whereas the controls remained symptomless. The same fungus was reisolated from all infected roots and resequencing results confirmed its identity. To the best of our knowledge, this is the first report of S. sclerotiorum causing Sclerotinia root rot on American ginseng in China. Because this disease is detrimental to the production of American ginseng, effective management strategies will need to be developed.

Siberian ginseng (

Asian ginseng (Panax ginseng) is a valuable medicinal plant that is commercially cultivated in China. A long postharvest storage period is required before ginseng is processed. From October 2019 to May 2020, snow rot was observed on the roots of 4- and 5-year-old fresh ginseng stored in three cold storage facilities located in Tonghua and Changbai cities in northeastern China, which are the most important regions for Asian ginseng production. We sampled 1,000 ginseng roots from the three cold storage facilities, and the average disease incidence was 21%. Initially, sparse hyphae and microsclerotia appeared on the root epidermis. Lesions gradually softened and the epidermis detached easily. Multiple infected sites slowly converged, resulting in the formation of a dense complex of multiple sclerotia and thick hyphae on the surface of the ginseng root as well as internal decay. The infection eventually spread to the adjacent ginseng roots (Fig. 1). Sixteen diseased ginseng roots were collected and then sclerotia were removed from the root surface, immersed in 1% NaClO for 2 min, rinsed three times with sterile water, and placed on potato dextrose agar (PDA) containing streptomycin (40 μg/mL) in Petri dishes. After a 3-day incubation at 20 °C in darkness, 22 suspected Sclerotinia isolates were obtained. Isolates SN1 and SN2 were randomly selected for identification. On PDA, fast-growing colonies produced white, sparse, powdery, and cotton-like aerial mycelia, and the reverse side showed the same color (Fig. 2). Small and white sclerotial primordia formed 3 days later and a ring of sclerotia was detected at the plate periphery. At 7 to 10 days after incubation, the mature sclerotia were black, spherical-to-subspherical, and elongated or fused to form irregular shapes. Each Petri dish produced 55-65 sclerotia, measuring 1.1 × 1.2 to 3.2 × 3.9 mm (n = 100). The sclerotia were firmly attached to the agar surface. The isolates were initially identified as Sclerotinia sp. (Saito 1997). After sequencing the nuclear ribosomal internal transcribed spacer region (MW927134 and MW927135) and the β-tubulin gene (MW929179 and MW929180) (White et al. 1990; Glass and Donaldson 1995), BLAST searches revealed 100% homology with JX262268 and JX296007 of the published S. nivalis strain KGC-S0601, respectively. The pathogenicity of the two isolates was tested using detached ginseng roots. Briefly, healthy roots were washed, surface-disinfested with 75% alcohol, and rinsed with sterile water. Mycelial plugs (5 mm diameter) removed from the margin of actively growing colonies on PDA were placed on the ginseng roots. For each isolate, four roots were inoculated, with two plugs per root. Additionally, PDA plugs without mycelia were used as the negative control. The roots were placed in a fresh-keeping box at 20 °C in darkness and evaluated after 7 days. The pathogenicity test was repeated twice. The symptoms on the inoculated roots were the same as those observed on the roots during cold storage, whereas the control roots remained symptomless. The same fungus was reisolated consistently from all infected roots and its identity was confirmed by resequencing, thereby fulfilling Koch's postulates. To the best of our knowledge, this is the first report of S. nivalis causing postharvest snow rot on Asian ginseng in China. The occurrence of this disease threatens the postharvest storage of Asian ginseng. Hence, effective management strategies must be developed.

Mitochondrial dysfunction in proximal tubular epithelial cells is a key event in acute kidney injury (AKI), which is a risk factor for the development of chronic kidney disease (CKD). Apelin is a bioactive peptide that protects against AKI by alleviating inflammation, inhibiting apoptosis, and preventing lipid oxidation, but its role in protecting against mitochondrial damage remains unknown. Herein, we examined the protective effects of apelin on mitochondria in cisplatin-stimulated human renal proximal tubular epithelial cells and evaluated its therapeutic efficacy in cisplatin-induced AKI mice. In vitro, apelin inhibited the cisplatin-induced mitochondrial fission factor (MFF) upregulation and the fusion-promoting protein optic atrophy 1 (OPA1) downregulation. Apelin co-treatment reversed the decreased levels of the deacetylase, Sirt3, and the increased levels of protein acetylation in mitochondria of cisplatin-stimulated cells. Overall, apelin improved the mitochondrial morphology and membrane potential in vitro. In the AKI model, apelin administration significantly attenuated mitochondrial damage, as evidenced by longer mitochondrial profiles and increased ATP levels in the renal cortex. Suppression of MFF expression, and maintenance of Sirt3 and OPA1 expression in apelin-treated AKI mice was also observed. Finally, exogenous administration of apelin normalized the serum level of creatinine and urea nitrogen and the urine levels of NGAL and Kim-1. We also confirmed a regulatory pathway that drives mitochondrial homeostasis including PGC-1α, ERRα and Sirt3. In conclusion, we demonstrated that apelin ameliorates renal functions by protecting tubular mitochondria through Sirt3 upregulation, which is a novel protective mechanism of apelin in AKI. These results suggest that apelin has potential renoprotective effects and may be an effective agent for AKI treatment to significantly retard CKD progression.

The utility of traditional methods for detecting seed-borne fungi is limited by the fact some fungi are unculturable or difficult to isolate. The seed-borne pathogens affecting

Siberian ginseng (Eleutherococcus sessiliflorus (Rupr. & Maxim.) S. Y. Hu, Araliaceae), is a perennial medicinal plant that is widely cultivated in China. Leaf spot was observed in 2- and 3-year-old Siberian ginseng in Zuojia County (126°05'23.2″E, 44°03'09.5″N), northeast China, in August 2019. Polygonal or irregular black spots ranging from 2 to 9 mm in diameter were found on infected leaves, and each leaf had dozens of spots. The green color around the lesions gradually faded. As the disease progressed, the spots withered and multiple lesions merged into large disease spots, causing leaf wilting (Fig. 1). More than 38% of plants in one 25-ha field were infected in 2019. Fifteen diseased leaves were collected from those plants and cut into 5-mm pieces. The pieces were surface-disinfected by immersion in 1% NaOCl for 2 min and then rinsing twice with sterile distilled water. The leaf pieces were placed on acidified potato dextrose agar (PDA, pH 4.7) in Petri plates, and incubated in the dark at 25°C. Nineteen isolates were obtained and all were purified from a single spore in water agar. Isolate CWJ7 was randomly selected for identification and pathogenicity testing. The colonies on PDA were olivaceous gray to olivaceous black, velvet, with dense hyphae and a scalloped or irregular margin. The reverse side was gray-black and surrounded by tawny halos. The conidia were aseptate and variable in shape and dimension: piriform, columnar, drop-shaped, dumbbell-shaped or oval, measuring 4.90 (7.03) 9.50 × 2.10 (2.78) 3.40 µm (n=100), and chlamydospores were absent. Black pycnidia (132.2-241.5 µm in diameter) appeared after 7 days. The pathogen was initially identified as Phoma or Phoma-like (Boerema et al. 2004). Further confirmation was also determined by sequencing the nuclear ribosomal internal transcribed spacer region (GenBank accession no. MT912950), 28S ribosomal RNA gene (MT912968), and genes encoding β-tubulin (MT920618), the second largest subunit of RNA polymerase II (MT920619) and translation elongation factor (MT946526) (de Hoog and Gerrits van den Ende 1998; Rehner & Samuels 1994; Liu et al. 1999; Vilgalys & Hester 1990), and Blast searches showed 90%-100% homology with GU237754, GU237938, KT389780, KT389575, and KY484705, respectively. In a phylogenetic analysis combining all loci, CWJ7 and the type strains of Boeremia linicola clustered in one group (Fig. 2). Based on its morphological characteristics and phylogenetic analysis, isolate CWJ7 was identified as B. linicola as revised in 2019 (Jayawardena et al. 2019). Healthy 2-year-old plants were used for pathogenicity testing. The leaves of nine potted plants (one plant per pot, three plants per replicate) were spray-inoculated with a suspension of conidia (1×105 spores/ml) from colonies on PDA for 7 days and cultured for 48 h under continuous black light. Nine plants were sprayed with sterile water as the control. This experiment was repeated twice. All plants were cultured in a greenhouse (25°C, 12-h photoperiod, 78% relative humidity). Clear plastic bags were used to maintain high humidity. After 7 days, the inoculated plants showed lesions on the leaves, similar to those observed in the field. The control plants remained symptomless. The pathogen was reisolated and identified by sequencing. This is the first report of B.linicola causing Siberian ginseng leaf spot, and a new record of this species in China. This disease poses a threat to production and management strategies should be developed.

Astragalus membranaceus Bunge (Fabaceae) is a perennial medicinal herb widely cultivated in China. In June 2018, root rot was observed on two-year-old A. membranaceus plants in Chaoyangshan town (northeastern China). In a 40-ha field, over 40% of the plants exhibited root rot and the infected area ranged from 10 to 70% of the roots. The roots first exhibited circular or irregular brown, sunken and necrotic lesions, and finally multiple lesions coalesced. The infected root surface was destroyed, showing rusty and dry rot (Fig. 1). Symptoms were concentrated in the main roots (Carlucci et al. 2017). The aboveground parts of infected plants did not initially show symptoms but gradually wilted; 7.6% of the plants died when root decay became severe. Infected roots were not used for processing and were not marketable. Ten infected roots were collected from May to October 2018 from the above location. The diseased root tissue was cut into 25 mm3 pieces, immersed in 1% NaOCl for 2 minutes, rinsed three times with sterile water and placed on water agar in Petri plates. After 15 days of incubation at 20°C, 11 single-spore isolates were obtained. Isolates HQ1 and HQ2 were randomly selected for morphological and molecular identification. Colonies grown for 10 days produced yellow, cottony to felty aerial mycelium on potato dextrose agar. Conidiophores originating laterally or terminally from the mycelium were solitary to loosely aggregated and unbranched or sparsely branched. Macroconidia predominated and were cylindrical, with a tendency to gradually widen towards the tip; 1- to 3-septate; and 20.2 to 31.0 × 3.0 to 6.7 µm (n=100). Microconidia had mostly 0¬- to 1-septate and 8.6 to 16.7 × 1.9 to 5.1 µm (n=100) (Fig. 1). Chlamydospores were rare, but occasional chlamydospore chains were observed. The isolates were tentatively identified as Dactylonectria torresensis (Cabral et al. 2012a). Further confirmation of the two isolates was conducted by DNA sequencing of the internal transcribed spacer (ITS, GenBank accession no. MN558983 and MN558984), β-tubulin (TUB, MN561692 and MN561693), histone 3 (HIS3, MN561694 and MN561695), and translation elongation factor (TEF, MN561696 and MN561697) genes (Cabral et al. 2012b). These sequences had 99 to 100% match with D. torresensis (JF735362 for ITS, JF735492 for TUB, JF735681 for HIS3 and JF735870 for TEF). Phylogenetic trees based on analyses of a concatenated alignment of all loci grouped these isolates into the D. torresensis clade (Fig. 2). The same two isolates were tested for pathogenicity. Healthy two-year-old plants were taken from the field, and their roots were disinfected with 75% alcohol for 3 minutes, rinsed with sterile water three times, immersed in a 1×105/ml spore suspension or sterile water (control) for 10 minutes, transferred to a tray filled with sterile sand and placed in a greenhouse (12 h photoperiod, 25°C). Twelve plants grown in three pots were used for each isolate, and the same number of plants were inoculated as a control. This experiment was repeated three times. After one month, inoculated plant roots showed the same symptoms as those observed in the field, while the controls remained symptomless and no pathogen was recovered. The same fungus was reisolated from all the infected plants and confirmed by sequencing all of the above genes. This is the first report of D. torresensis causing root rot in A. membranaceus in China. The occurrence of this disease poses a threat, and management strategies need to be developed.

Ginseng (Panax ginseng) is a perennial herbaceous plant and a precious traditional Chinese medicine. P. ginseng is widely cultivated in Asia, particularly the Changbai Mountain area in China (Wang et al. 2019). Alternaria species can grow under a wide range of temperatures that occur worldwide (Konstantinova et al. 2002). Alternaria panax was reported as the main cause of Alternaria leaf spot of ginseng (Deng et al. 2013); however, a small-spored Alternaria species was isolated from leaf spot symptoms during recent surveys. In our study, leaf spot disease of P. ginseng was observed during 2017 in the Fusong district, Jilin, China. The disease was widespread, with 20 to 30% of the fields affected. Leaves of the affected plants showed brown to black necrotic spots. The fungus was isolated from symptomatic leaves on potato dextrose agar and characterized morphologically under the microscope. Colonies of pure cultures were initially dark brown and then turned black after 7 days. Strains (TCS 15013001 and TCS 15013002) were grown on water agar embedded with surface-sterilized ginseng spot tissues under a 12/12-h light/dark cycle at room temperature. Conidia observed on the lesions were dark brown or olive-brown, ovoid or ellipsoid, short beaked, with three to seven transverse and zero to five longitudinal septa, and 14.9 to 36.5 μm (average 25.8 μm) × 5.8 to 17.9 μm (average 12.5 μm). Based on its morphological characteristics, the pathogen was identified as Alternaria sp. (Simmons 2007). Single-spore cultures were obtained, and their genomic DNA was extracted. The rDNA internal transcribed spacer (ITS, GenBank accession nos. MN394879 and MN394880), endopolygalacturonase (endoPG, MN410909 and MN410910), Alternaria major allergen (Alta1, MN410911 and MN410912), and the portion of the histone 3 (H3, MN410913 and MN410914), elongation factor 1-alpha (EF1-α, MN410915 and MN410916), the RNA polymerase II 2nd largest subunit (RPB2, MN410917 and MN410918), and glyceraldehyde 3-phosphate dehydrogenase (gpd, MN410919 and MN410920) gene were amplified from the two isolates, respectively (Woudenberg et al. 2015). Sequence analysis of the two isolates showed 99 to 100% identity to that of A. alternata (MG182428 for ITS, MG598798 for endoPG, MG598796 for Alt a1, MG182429 for H3, KU738723 for EF1-α, KU738707 for RPB2, and KP851761 for gpd). Pathogenicity tests were conducted in a greenhouse. Sixty healthy 2-year-old P. ginseng seedlings grown in potting medium were tested in a greenhouse at 20/26°C and about 90% relative humidity with natural light. Of the plants, 30 were sprayed with spore suspension (1 × 10⁵ spores/ml) until most of the leaves were wet. Control treatments (30 plants) were treated with distilled water. The two isolates were tested, and all test plants were covered with clear plastic bags for 3 days to increase humidity. Each treatment had three replicate plants. Six days after inoculation, leaf spots similar to the original ones developed at inoculation sites for all isolates, and A. alternata was consistently reisolated from the induced symptoms. The pathogenicity test was performed three times. A. alternata causing leaf spot of American ginseng was reported in China (Hill and Hausbeck 2008). Also, leaf spot of Panax notoginseng caused by A. alternata was reported in China (Yang et al. 2018). To our knowledge, this is the first report of A. alternata on P. ginseng in China.

Ginseng (Panax ginseng C. A. Meyer, Araliaceae) hairy root and ginseng (P. ginseng C. A. Meyer, Araliaceae) root were steamed at 100°C for 3 h. Thereafter treatment, the content of ginsenosides, Rg1, Re, Ro, Rf, Rb1, Rc, Rb2, Rb3 and Rd decreased. On the other hand, the content of ginsenosides, Rg3, Rg2 and Rh1 increased. Two previously identified anticancer ginsenosides, Rg3 and Rh2 increased significantly in steamed ginseng hairy roots from 0.017 to 1.14 mg/g and not detected to 0.74 mg/g, respectively. In steamed ginseng root, Rg3 increased from 0.0062 to 0.75 mg/g, and Rh2 was not detected. These results indicated that steaming process may provide an effective method for ginseng hairy roots to conversion polar ginsenosides to non-polar ginsenosides Rg3 and Rh2. Key words: Panax ginseng, ginseng hairy roots, steaming, chemical composition, ginsenosides.